NCCN临床实践指南：HIV感染者癌症（2026.V1）

指南综合与多学科· 未分类与其他 · 2026

INTRODUCTION ${ }^{a, b, c, d, e, f, g}$

●People with human immunodeficiency virus(HIV)(PWH) have a higher incidence of many common cancers compared with the general population.

•'AIDS-defining cancers' is a historic term that included cervical cancer, non-Hodgkin lymphoma (NHL), and Kaposi sarcoma as cancers common in PWH than in the general population due to their association with higher levels of immunosuppression. Anal cancer is also more common in PWH and associated with immunosuppression, but it was not originally included as an AIDS-defining cancer.

●Dramatically improved treatment of HIV over the last two decades has led to a decrease in the risk of AIDS development, an increase in immune function and survival, and a decline in some cancers including human papillomavirus (HPV) and Kaposíar sarcoma-associated herpesvirus (SHVH)-associated cancers/cancers associated with immunosuppression in this population; however, the incidence of other cancers has increased because of longer life expectancies due to antiretroviral therapy (ART), accelerated aging as a consequence of HIV,and a higher prevalence of carcinogen exposure.

•Cancer in PWH should be co-managed by an oncologist, and HIV specialist, and PWH should receive cancer treatment as per standard guidelines. Although modifications to ART may be needed, HIV therapy should be continued during cancer therapy. Multidisciplinary

Aggressive NHL^h^ → See NCCN Guidelines for B-Cell Lymphomas Anal cancer in PWH (HIV-1) Cervical cancer Cervical Cancer Cervical Cancer in PWH (HIV-2) Classic Hodgkin lymphoma (CHL)→ Classic Hodgkin Lymphoma in PWH (HIV-3)Kaposi sarcoma →See NCCN Guidelines for Kaposi Sarcoma Non-small cell lung cancer (NSCLC)→Non-Small Cell Lung Cancer in PWH (HIV-4)Primary CNSM lymphoma →See NCCN Guidelines for B-Cell Lymphomas

a Principles of HIV Management While Undergoing Cancer Therapy (HIV-A).

b Principles of Systemic Therapy and Drug-Drug Interactions(HIV-B).

c Principles of Radiation Therapy(HIV-C).

d Principles of Surgery(HIV-D).

● Principles of Supportive Care（HIV-E）.

9 Refer to the NCCN Distress Thermometer and Problem List, which includes social determinants of health. See NCCN Guidelines for Distress Management (DIS-A).h Burkitt lymphoma; diffuse large B-cell lymphoma (DLBCL); KSHV-positive DLBCL,not otherwise specified (NOS); primary effusion lymphoma; and plasmablastic lymphoma.

NCCN

National Comprehensive Cancer in Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

Anal Cancer in PWH

●PWH are at higher risk of premalignant an epithelial changes compared to patients who are high(-hANQ and diagnosed with penal, vulvar,

●PWH have an approximately 15- to 20-fold increased likelihood of being diagnosed with anal cancer compared with individuals who are HIV-negative, and anal cancer accounted for approximately 5%-10% of cancers

●The International Anal Neoplasia Society(IANS) and the U.S.Department of Health and Human Services(DHHS) (see Human.Papilomair sections of Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV have been established guidance for anal cancer thancer's effects in PHW. Although the details of their recommendations differ for men, both organizations recommend with annual an cancer screening for men who have sex with men(MS)phines and transgender women with who have sex with men(MS)PWH who are 245 years. Screening methods include an anal cancer risk risk human papillomavirus testing, and digital anorectal exam(DARE).

●Anal cancer in PWH is often associated with persistent anal HPV diagnosed in a cancer in PWH is often associated with persistent anal HPV diagnosed in

●HPV-related disease in PHW is often associated with persistent anal HPV infection with anal cancer should be evaluated for the presence of vulvar, vaginal,or cervical disease.

●Non-magnon causes for lymphadenopathy should be considered in PWH. Suspicious PET-avid lymphadenopathy should be bioproposed to with HIV specialist). If negative for cancer, refer for an infectious disease workup.

●If an equal squamous intraepithelial lesions (iSEIL) of high ana rectifier and amelous cells of determined significance in intraepithelial lesion [HSIL], low-grade squamous intraepithelial [ASCUS] are identified by enducous cells of undetermined significance abnormal examinations, then high-resolution anoscopy (HRA) should be performed where available. a.2,c HRA capacity is limited, high-risk HIV status.

●Anal cancer in PWH should be co-managed by an oncologist and HIV Guidelines for Anal Carcinoma.

●Post-treatment surveillance of PWH should be as per the NCCN Guidelines for Anal Carcinoma.

●Anal cytology can be considered for the detection of anal dysplasia in survivors of anal cancer with HIV, although its value in detection of

●People who engage in receptive an intercourse should post-treatment pelvic physical therapy and analators with an appropriate care provider.

●Poor performance status in PWH and anal cancer may be from HIV, cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions should be

●There are multiple methods by which an axial dysplasia is treated: topical therapy (ie, fluorouracil, imiquimod), excision, and ablation. These treatments are safe in PWH and are associated with a decreased risk of progression to cancer even though treatment with a decreased risk PWH is associated with a high risk of recurrence. # DHHS Guidelines for p

In a randomized controlled trial of PHW who engage in receptive and a reasonable first-line to treatment of HSHI, since this treatment was used in a randomized controlled trial of PHW who engage in receptive antineurber therapy in the treatment of an axial disease, although recurrence rates were still high.

●Drug interactions can occur in patients with anal cancer and HIV. Both an

●Drug interactions can occur in patients with anal cancer and HIV. Both an Principles of Systemic Therapy and Drug-Drug Interactions in

●Even with screening and treatment, and treatment, there are high rates of progression of HSIL to cancer in PWH. b Therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore, therefore,

●Evolving data suggest that immune checkpoint inhibitors (HI-V). Generally safe and effective in PWH, with the following considerations: 2021 of the presence of cancer and cancer, which is increased to cases of cancer-related inflammatory synchrotron diseases such as multicentric syndrome (KICS) when ICIs are used. If the inflammatory cytookine Castleman disease (MCD) or KSHV-associated patient inflammatory cytookine and symptoms of KICS or MCD. ${}^{e}$

a Stier EA,et al.Int J Cancer 2024;154:1694-1702.

b Palefsky JM, et al. N Engl J Med 2022;386:2273-2282.

a Stier EA,et al.Int J Cancer 2024;154:1694-1702 a Palefsky JM,et al.N Engl J Med 2022;386:2273-2282 a Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents With HIV. U.S. Department of Health and Human Services, NIH Office of AIDS Research.Available at:https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-kuidelines-ad-adolescent-opportunistic-infections/whats-d 2024 a Politezlo, et al. Lancet Oncol 2013;14:346-353.

e Polizzotto MN,et al.Lancin Oncol 2013;14:346-353.

f Uldick TS,et al. JAMA Oncol 2019;5:1332-1393.

9 Fujita K, et al. Open Forum Infect Dis 2020;7:ofaa067.

Zaemes J,et al.Eur J Cancer 2020;132:168-175.

Suliman AM,et al.Cancer Immunol Immunothermolytun 2021;70:935-944.

The use of ICIs has been linked to opportunistic infections including Tuberculosis(TB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis(9) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactivation and flare of mycobacterial disease.g.H,i,j,k Tubularousis, TTB) reactiva

NCCN

National Comprehensive Cancer Network

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

Cervical Dysplasia and Cervical Cancer Screening in PWH

●PWH are at higher risk of HPV infection and premalignant cervical lesions compared to patients who are HIV-negative.

Cervical Cancer in PWH

●The risk of cervical cancer is elevated approximately 3- to 5-fold in PWH.

●The DHHS(see Human Papillomavoulus of the Results for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV have established guidance for cervical cancer screening in PWH.

●Premalant cervical lesions are common in PWH. Treatment of these lesions is generally safe and effective regardless of HIV status. However, endocervical extension is more frequent among PWH. Therefore, loop excision is less effective, with higher recurrence rates in PWH than in patients without HIV.

The DHHS guidance begins with cervical cytology at the time of HIV diagnosis for PHW aged 21 years. Co-testing for high-risk HPV can be considered for PHW aged≥25 years.However, transient HPV is highly prevalent after age 30 years, which may increase the likelihood of future age 30 colcoscopy in those aged 25 to 29 years.

●Non-malignant causes for lymphadenopathy should be considered in PWH. Suspicious or infectious etiology (consult with HIV specialist). If negative for cancer, refer for an infectious disease workup.

●PWH with cervical intraepithelial neoplasia(CIN) or invasive cervical cancer should be evaluated for field effect of HPV oncogenesis, including anal cancer(See NCCN Guidelines for Anal Cancer in Anal Canceroma)

If cytology results are normal, repeat cytology is recommended, with timing depend on HPV testing results.For those with ASCUS, high-risk HPV testing can be considered if not already performed. PWH with ASCUS who test positive for high-risk HPV should be evaluated by

●PWH who have cervical cancer should be referred to an HIV specialist to ensure they are on an effective ART regimen.

●PWH should be treated for cervical cancer as per the NCCN Guidelines for Cervical cancer, including use of concurrent chemotherapy for patients receiving definitive on HIV status.

●For those with ASCUS, high-risk HPV should be evaluated by colcopyos. If HPV testing is negative or not performed, cervical cytology should be repeated in 6 to 12 months.●For those with low- or higher-grade squamous

●Poor performance status in PWH who have cervical cancer may be from HIV, cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions. ART is recommended for all PWH and may improve performance status.

●In transectial lesion, colcopyos is recommended. primary screening modality in both PHW and the general populations. The WHO guidance includes partial colcopyos, visual inspection with acetic acid, or cytology for those who test positive for HPV.

●Drug interactions can occur in patients with cervical cancer and HIV. Both an HIV therapy and Drug-Drug-Drug Interactions (HIV-B).

●Excission(preferred) or ablative procedures such as cryotherapy are recommended for HSIL in the American Society of Coloptos and Cervical Pathology(ASCCP)-sponsored consensus guidelines(ASCCP)-sancer screening abnormalities" (endrolled by the American College of Obstetricsian and Gynecologists[ACOG] and other

●For recommendations regarding preventative HPV vaccination, see NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections.

●Evolving data suggest that ICIs are generally safe and effective in PWH, with the following

In persons with concurrent KSHV infection, there may be increased risk of KSHV-invasive immunization of KSHV-associated diseases, consider more frequent monitoring of signs and symptoms of KICS or MCD.e,

<EndOfPara>Unexplained fears should improve workup of MCD and KICS when ICIs are used. If the KSHV serum viral load, SPEP, IL-6, and IL-10. The diagnosis of KICS requires excisional biopsy of lymphadenopathy to exclude MCD.

The use of ICIs has been linked to TB reactivation and flare of mycobacterial disease.g.,K screening for latent TB infection can be considered before administration an ICl so that the patient can be monitored for TB symptoms and treatment of mycobacterial infection can be expedited.

e Polizzotto MN,et al.Clin Infect Dis 2016;62:730-738.

f Uldrick TS,et al.JAMA Oncol 2019;5:1332-1339.

g Fujita K,et al. Open Forum Infect Dis 2020;7:ofaa067.

h Bae S, et al. J Immunother Cancer 2021;9:e002960.

i Zaemes J, et al. Eur J Cancer 2020;132:168-175.

j Suliman AM,et al.Cancer Immunol Immunother 2021;70:935-944.

k Anidi IU, et al. Open Forum Infect Dis 2024;11:ofae183.

l Bouvard V, et al. N Engl J Med 2021;385:1908-1918.

m WHO guideline for screening and treatment of cervical pre-cancer lesions for cervical cancer prevention, 2nd edition.

Perkins RB,et al.J Low Genit Trac Dis 2020;24:102-131.

O Kocken M, et al. Lancet Oncol 2011;12:441-450.

NCCN

NCCN Cancer Network®

NCCN Guidelines Version and HIV

Classic Hodgkin Lymphoma (CHL) in PWH

Classic Hodgkin Lymphoma (CHL) in PWH.PH are 5 to 14 times more likely to be diagnosed with CHL than individuals who are HIV-negative, and CHL accounts for approximately 4% of cancer diagnosed in the PWH-polymeride.

●Compared with people without HIV, PHW for commonly present with mixed cellularity or lymphocyte-depleted histologies of CHL. Ninety percent of cases of CHL in PWH are Epstein-Barr virus(EBV)-associated. PHW often present with more advanced disease, including intranodal disease and bone marrow involvement. Bone-marrow-only presentations sometime occur. B symptoms (ie, lever, night sweats, weight loss) are also more common in this population, and should always prompt investigation of opportunistic infection. In contrast to NHL in PHW, central nervous system (CNS)involvement is rare with CHL.

●Interpretation of diagnostic and staging imaging may be complicated by the increased incidence of non-malignant lesions that may be mistaken for cancer spread or modifications to cancer treatments should not be made based solely on HIV status.

●Patients should be treated as per the NCCN Guidelines for Hodgkin Lymphoma, and modifications to cancer treatment should not be made based solely on HIV status.

●All of the standard CHL regimens have been studied in PWH.

Brentuximab vedotin with AVD(BV-AVD) is a safe and effective option in PHW with attention to drug-drug interactions. B2016 and has been shown to increase CD4+ T-cell counts in individuals with HIV-associated CHL.

●Nivolumab-AVD can be considered as a safe option in KHV and mycobacterial infections. QCHL with attention to presence of concurrent growth is not recommended during ABVD treatment in the NCCN Guidelines for Hodgkin Lymphoma because of concerns with possible required in PWH, especially if Hodgkin Lymphoma or neutropy, growth factors may be severe neutropenia or neutropenic fever.

Similarly, whereas dose reduction is not recommended for neutropenia with ABVD in the NCCN Guidelines for Hodgkin Lymphoma, dose reductions for neutropenia with ABVD in the severe neutropenia or neutropenic fever.

with severe and prolonged cytopenias.

Pneumocystis jirovecii (PJP) prophylaxis is strongly may be recommended.

e Polizzotto MN,et al.Clin Infect Dis 2016;62:730-738.

f Uldrick TS, et al. JAMA Oncol 2019;5:1332-1339.

9 Fujita K,et al. Open Forum Infect Dis 2021;9:e00260.

h Bae S,et al.J.Immunol Cancer 2020;19:532-139.

iZaemes J,et al.Eur J Cancer 2020;132:168-175.

j Suliman AM, et al. Cancer Immunol Immunother 2021;70:935-944.

K Anidi IU,et al. Open Forum Infect Dis 2024;11:ofae183.

P Rubinstein P, et al. Lancet 2024;391:1379-1389.

r Alvarnas JC,et al. Blood 2016;128:1050-1058.

Note: All recommendations are category 2A unless otherwise indicated.

Prophylaxis for other opportunistic infections including gram-negative bacteria can be considered, particularly for patients with more advanced immunosuppression. See Guidelines for the Prevention for the Prevention of immunosuppression. See Guidelines for HIV.

●FDG-PET/CT-guided therapy in HIV-associated CHL is feasible; however,care should be taken to recognize potential confounding factors (ie, non-malignant causes for PET-avoid regions).

●Relapsed/refactory CHL should be treated as per the NCCN Guidelines for Hodgkin Lymphoma based on currently available evidence, and there is support for feasibility and efficacy of autologous and allogenic hematopoietic cell transplant.

●Evolving data suggest that ICLs are generally safe and effective in PWH, with the following considerations:

In persons with concurrent KSHV infection, there may be increased risk of KSHV-associated inflammatory syndromes such as MCD or KICS when ICSK SHV-associated inflammatory of KSHV-associated diseases, consider are used. If the patient has a history of symptoms of KICS or MCD.1,4 more frequent monitoring of signs and symptoms of KICS or KICS with Unexplained fevers should prompt workup of MCD and KICS with C-reactive protein, KSHV serum viral biopsy of lymphadenopathy to diagnosis of KICS requires excisional biopsy of lymphadenopathy to exclude MCD.

The use of the RIBIC has been linked to opportunistic infections including TB reactivation and flare of mycobacterial disease. 9,13,13,2024 R is screening for latent infection can be considered before administering an ICl so that the TB infection can be considered before administering of Mycobacterial

●Poor performance in PWH and CHL may be from HIV, cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions. ART is recommended for all PHW and may improve performance status.

●Drug interactions can occur in patients with CHL and HIV. Both an HIV pharmacist and an oncology pharmacist should be consulted.$\!$ Adverse reactions due to drug inhibitors, and these antiretrovins(ARVs)$\!$ cobicatist, and protease inhibitors, and these antiretrovins is preferred using itonavir,$\!$ In patients with CHL and HIV. Both an HIV cancer, it has been a novel and a new new new new new new new new new new new new new new new new new new new new new new new new new new new new new new

NCCN

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

Non-Small Cell Lung Cancer in PWH

●The risk of lung cancer is 2 to 5 times higher in PWH than in individuals who are HIV-negative, and lung cancer accounts for approximately 11% of cancers diagnosed in this population.

●Screening for lung cancer with low-dose CT should be performed in PWH as per the NCCN Guidelines for Lung Cancer Screening. However,it should be noted that PWH may develop lung cancer at a younger age compared to the general population.sJ investigations are ongoing to determine if modifications to screening guidelines for PWH are warranted.

●Smoking cessation should be discussed (See NCCN Guidelines for Smoking Cessation).

●NSCLC in PWH should be co-managed by an oncologist and HIV specialist, and PWH should be treated for NSCLC as per the NCCN Guidelines for Non-Small Cell Lung Cancer. Modifications to cancer treatment should not be made solely based on HIV status.

●PWH may be more likely to have benign lung nodules than patients without HIV. An infectious disease workup should be performed when indicated. Treatment for possible non-malignant diagnoses can be considered before biopsy. If concurrent pulmonary Kaposi sarcoma is

●Lung biopsies should be cultured and stained for bacteria,fung, and mycobacteria.

●Non-malignant causes for lymphadenopathy should be considered in PWH. Suspicious PET-avid lymphadenopathy should be biopsied to differentiate between nodal metastasis or infectious etiology(consult with HIV specialist). If negative for cancer, refer for an infectious disease workup.

●Workup of brain lesions in patients with NSCLC and advanced HIV-related immunosuppression should include consideration of consultation with HIV specialist and an evaluation to rule out infectious processes(eg, toxoplasmosis) or other malignancies such as NHL. Consideration of relative risks based on viral load and CD4+ T-cell count may further inform these assessments.

●Poor performance status in PWH and NSCLC may be from HIV, cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions. ART is recommended for all PWH and may improve performance status.

●Drug interactions can occur in patients with NSCLC and HIV. Both an HIV pharmacist and an oncology pharmacist should be consulted. See Principles of Systemic Therapy and DrugDrug-Drug Interactions(HIV-B).

●Evolving data suggest that Icls are generally safe and effective in PWH, with the following considerations:

In persons with concurrent KSHV infection, there may be increased risk of KSHV-associated inflammatory syndes or MCD or KICS when ICIs are used. If the patient has a history of KSHV-associated diseases, consider more frequent monitoring of signs and symptoms of KICS or MCD.e,f

Unexplained fevers should prompt workup of MCD and KICS with C-reactive protein, KSHV serum viral load, SPEP, IL-6, and IL-10. The diagnosis of KICS requires excisional biopsy of lymphadenopathy to exclude MCD.

The use of ICIs has been linked to opportunistic infections including TB reactivation and flare of mycobacterial disease.g,h,i,j,k Screening for latent TB infection can be considered before administering an ICl so that the patient can be monitored for TB symptoms and treatment of mycobacterial infection can be expedited.

h Bae S,et al.J Immunother Cancer 2021;9:e002960.

i Zaemes J, et al. Eur J Cancer 2020;132:168-175.

Suliman AM, et al. Cancer Immunol Immunother 2021;70:935-944.

k Anidi IU, et al. Open Forum Infect Dis 2024;11:ofae183.

Sigel K,et al. Curr HIV/AIDS Rep 2011;8:142-152.

NCCN Guidelines Version 1.2026 Cancer in People with HIV

Version 1.2026, 09/05/25 © 2025 National Comprehensive Cancer Network® (NCCN®), All rights reserved. NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN.

NCCN Guidelines Index Table of Contents Discussion

PRINCIPLES OF HIV MANAGEMENT WHILE UNDERGOING CANCER THERAPY

HIV-A 1 OF 2

• Linkage to HIV care from cancer providers

All patients should be offered HIV screening at least once during their lifetime. Consider HIV testing in patients with a new cancer diagnosiswho have not been recently screened.1,2 Cancer in PWH should be co-managed by an oncologist and HIV specialist.

HIV therapy should be initiated or continued during cancer therapy.

ART may require modification by an HIV specialist in conjunction with an HIV pharmacist and an oncology pharmacist to minimize drug-drug interactions (DDIs) and toxicities.

ART interruptions should be avoided because of the risk of immunologic compromise, opportunistic infection, and death.3 Continuation of ART might result in better tolerance of cancer treatment, higher response rates, and improved survival. ART should not be discontinued unless in consultation with an HIV specialist.

Cancer treatment should not be delayed for HIV workup and treatment, if possible.

• Routine HIV care in conjunction with HIV specialist during cancer therapy

ART should be offered immediately (if the patient is not already receiving it), but may need to be adapted according to the cancer treatmentplan.4,5 See Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV. To facilitate separate assessment of tolerability of ART and cancer treatment, consider initiating ART ≥7 days prior to the start of cancer treatment or after cancer therapy has been initiated long enough for tolerance to be established. There may be circumstances when ART should be started immediately, regardless of the cancer therapy timing, such as with the diagnosis of progressive multifocal leukoencephalopathy (PML). ◊ INSTI based regimens are preferred because they have fewer DDIs (See Principles of Systemic Therapy and Drug-Drug Interactions[HIV-B]).

All patients with HIV should be tested for hepatitis B and hepatitis C. Testing may be necessary prior to initiation of chemotherapy to avoid hepatic toxicity. For hepatitis B, core antibodies should be checked in addition to surface antibodies and antigens. See Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV.

In PWH who also have chronic hepatitis B infection (positive hepatitis B surface antigen), an ART regimen that treats both HIV and hepatitis B should be initiated. (See Special Circumstances, HIV-E, 2 of 2).

Laboratory testing should be scheduled for both before and after initiation of ART (See Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV). HIV viral load and CD4+ T-cell count monitoring (See Table 4 of Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV):◊ If there are potential interactions between ART and cancer-related or other supportive care therapies leading to decreased effectiveness ofART, more frequent HIV viral load testing (eg, once a month for the first 3 months and then every 3 months6) may be needed.◊ Consider measuring the CD4+ T-cell count more frequently in patients receiving cancer treatments anticipated to cause lymphopenia.Decreases in CD4+ T-cell counts attributable to cancer therapy are not necessarily reflective of HIV control, which is better measured byHIV viral load. A decrease in CD4+ T-cell count can still predict increased risk for opportunistic infections. Additional risk beyond thatpredicted by CD4+ T-cell counts may occur due to effects of cancer-related therapy on immune function.

Smoking cessation should be discussed.7,8 (See NCCN Guidelines for Smoking Cessation).

• Patients with head and neck cancer have difficulty with oral drug administration due to feeding tubes, which could be problematic for ART.Consider prescribing formulations such as liquids, capsules that may be opened, tablets that may be crushed, or injectable ART. Refer to theprescribing information for individual drugs regarding feeding tube administration.• Primary and secondary prophylaxis for opportunistic infections during cancer treatment Patients should receive the prophylaxis indicated by their HIV status and cancer treatment. See Principles of Supportive Care (HIV-E).References on

Note: All recommendations are category 2A unless otherwise indicated.

HIV-A 2 of 2

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

Note: All recommendations are category 2A unless otherwise indicated.

HIV-A 2 OF 2

1 Branson BM, Handsfield HH, Lampe MA, et al. Revised recommendations for HIV testing of adults, adolescents, and pregnant women in health-care settings. MMWR Recomm Rep 2006;55(RR-14):1-17.

2 Rizza SA, MacGowan RJ, Purcell DW, et al. HIV screening in the health care setting: status, barriers, and potential solutions. Mayo Clin Proc 2012;87:915-924.3 El-Sadr WM, Lundgren J, Neaton JD, et al. CD4+ count-guided interruption of antiretroviral treatment. Strategies for management of Antiretroviral Therapy (SMART) Study Group. N Engl J Med 2006;355:2283-2296.

4 Hessol NA, Pipkin S, Schwarcz S, et al. The impact of highly active antiretroviral therapy on non-AIDS-defining cancers among adults with AIDS. Am J Epidemiol

2007;165:1143-1153.

5 Kitahata MM, Gange SJ, Abraham AG, et al. Effect of early versus deferred antiretroviral therapy for HIV on survival. N Engl J Med 2009;360:1815-1826.6 Torres HA, Mulanovich V. Management of HIV infection in patients with cancer receiving chemotherapy. Clin Infect Dis 2014;59:106-114.7 Anthonisen NR, Skeans MA, Wise RA, et al. The effects of smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern Med

2005;142:233-239.

8 Clinical Practice Guideline Treating Tobacco Use and Dependence 2008 Update Panel, Liaisons, and Staff. A clinical practice guideline for treating tobacco use and

dependence: 2008 update. A U.S. Public Health Service report. Am J Prev Med 2008;35:158-176.

PRINCIPLES OF HIV MANAGEMENT WHILE UNDERGOING CANCER THERAPY REFERENCES

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

PRINCIPLES OF SYSTEMIC THERAPY AND DRUG-DRUG INTERACTIONS

Drug-Drug Interactions (DDIs)

• Oncology and HIV clinicians, along with both an oncology pharmacist and HIV pharmacist, if available, should review proposed cancer

therapy, supportive care medications, and ART for possible DDIs and overlapping toxicities prior to initiation. Coordinated care by an

oncologist and HIV clinician is recommended for the duration of therapy.

• These Guidelines provides general guidance, but comprehensive resources for ART drug-drug interactions should be consulted for patients with HIV and cancer. These resources include:

The DHHS Panel on Antiretroviral Guidelines provide comprehensive information on mechanisms of antiretroviral-associated drug

interactions as well specific drug-drug interaction guidance (https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-andadolescent-arv/drug-interactions-overview). Of note, these guidelines do not incorporate many systemic cancer therapies. A preferred

resource that does provide an interaction checker that includes cancer therapies is the University of Liverpool HIV Drug Interactions site

(https://www.hiv-druginteractions.org).

• Select ARVs can be administered safely with systemic cancer therapies. With continued development of new ARVs, effective alternatives are almost always available to patients when the existing ART is expected to affect metabolism or transport of, or share toxicities with, systemic cancer therapies. Small case series favor integrase inhibitor-based ART during cancer therapy.1,2 HIV regimens containing INSTIs without

pharmacologic boosters are favored in the setting of malignancy, due to a lower potential for DDI.

• The possibility that DDIs may enhance treatment toxicity or decrease efficacy needs to be considered. In general, CYP450 (or any enzyme or drug transporter) inhibitors increase the substrate exposure resulting in increased toxicity, while inducers decrease the exposure resulting in decreased efficacy. The exception to this is a prodrug where the metabolite is active and the opposite effect would be observed.

• Select major considerations with ARVs include:

ARV interaction mechanisms span most metabolic pathways and transporters, including CYP enzymes, P-gp, and UGT1A1.

The greatest concern for DDIs is with ART regimens containing pharmacologic boosters (ie, ritonavir, cobicistat) and protease inhibitors.

These drugs inhibit CYP3A4 and thus may significantly interact with agents metabolized by that pathway.

NNRTIs, except for rilpivirine and doravirine, induce CYP3A4 and thus may cause the opposite DDI from the inhibitors. Ritonavir is also an

inducer of certain enzymes, most notably CYP2C19.

ART treatment guidelines caution against use of ritonavir- and cobicistat-boosted regimens and some NNRTIs in the context of cancer

treatment. (See Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV).

Medications and supplements with polyvalent cations (multivitamins, supplements, antacids, etc) can bind to integrase inhibitors and

reduce their absorption.

Acid-reducing agents (antacids, H-2 antagonists, proton pump inhibitors, etc) can reduce the absorption of atazanavir and rilpivirine.

When cancer therapy is expected to be myelosuppressive, zidovudine is contraindicated due to its likelihood to cause or exacerbate

myelosuppression.

Note: All recommendations are category 2A unless otherwise indicated.

HIV-B 1 OF 2

1 Torres HA, et al. Clin Microbiol Infect 2014;20:O672-679.2 Casado JL, et al. Antivir Ther 2015;20:773-777.

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NCCN Guidelines Index Table of Contents Discussion

Note: All recommendations are category 2A unless otherwise indicated.

HIV-B 2 OF 2

DDIs (continued)

• If a potential DDI or overlapping toxicity exists, options include (in order of preference):

1. Substituting a different ARV with less DDI potential;

2. Selecting an alternative cancer therapy regimen with less DDI potential

If the above two options do not seem feasible, consult with an HIV specialist.

• Drugs used to prevent and/or treat opportunistic infections in PWH may also interact with cancer therapies. Some examples of concern

include rifamycins (via induction of hepatic metabolism), clarithromycin (via inhibition of CYP3A4), azole antifungals (via inhibition of

various hepatic metabolic processes), and trimethoprim/sulfamethoxazole treatment with methotrexate (via inhibition of methotrexate renal

excretion and compound risk of bone marrow suppression). See Significant Pharmacokinetic Interactions between Drugs Used to Treat

or Prevent Opportunistic Infections (https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunisticinfections/significant-drug-interactions?view=full) for more information.

Immune Checkpoint Inhibitors

• Evolving data suggest that ICI are generally safe and effective in PWH,3 with the following considerations:

In persons with concurrent KSHV infection, there may be increased risk of KSHV–associated inflammatory syndromes such as MCD

or KICS when ICIs are used. If the patient has a history of KSHV-associated diseases, consider more frequent monitoring of signs and

symptoms of KICS or MCD.4,5

Unexplained fevers should prompt workup of MCD and KICS with C-reactive protein, KSHV serum viral load, SPEP, IL-6, and IL-10. The

diagnosis of KICS requires excisional biopsy of lymphadenopathy to exclude MCD.

The use of ICIs has been linked to TB reactivation and flare of mycobacterial disease.6-10 Screening for latent TB infection can be

considered before administering an ICI so that the patient can be monitored for TB symptoms and treatment of mycobacterial infection can

be expedited.

PRINCIPLES OF SYSTEMIC THERAPY AND DRUG-DRUG INTERACTIONS

3 Shah N, et al. J Immunother Cancer 2019;7:353.4 Polizzotto MN, et al. Clin Infect Dis 2016;62:730-738.5 Uldrick TS, et al. JAMA Oncol 2019;5:1332-1339. 6 Fujita K, et al. Open Forum Infect Dis 2020;7:ofaa067.

7 Bae S, et al. J Immunother Cancer 2021;9:e002960.8 Zaemes J, et al. Eur J Cancer 2020;132:168-175.9 Suliman AM, et al. Cancer Immunol Immunother 2021;70:935-944.10 Anidi IU, et al. Open Forum Infect Dis 2024;11:ofae183.

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

PRINCIPLES OF RADIATION THERAPY1

Note: All recommendations are category 2A unless otherwise indicated.

HIV-C

• HIV status alone should not be a criterion for decision-making regarding radiation therapy (RT) indications or dose. RT should be offered as

part of the cancer management approach when indicated.

• Dose fractionation and treatment volumes are recommended as per NCCN Clinical Practice Guidelines by disease site.

• RT can be administered for cure or palliation.

• More modern data suggest RT is effective and well-tolerated for certain cancers (eg, anal cancer); in other cancers, data are insufficient to recommend a change from standard therapy (eg, lung cancer).

• Additional clinical monitoring may be required with concurrent chemoradiotherapy.

• Particular attention should be paid to limit dose to the following structures using conformal techniques like intensity-modulated radiation therapy (IMRT), proton therapy, brachytherapy, or stereotactic body RT (SBRT) when deemed appropriate by the treating provider2,3:

Mucosal membranes2,3

Skin

Bone marrow

• Nutritional support, pain control, and other supportive measures should be used to minimize radiotherapy interruptions.

1 Alongi F, Giaj-Levra N, Sciascia S, et al. Radiotherapy in patients with HIV: Current issues and review of the literature. Lancet Oncol 2017;18:e379-e393. 2 Bryant AK, Huynh-Le MP, Simpson DR, et al. Association of HIV status with outcomes of anal squamous cell carcinoma in the era of highly active antiretroviral therapy. JAMA Oncol 2018;4:120-122.

3 Bryant AK, Mudgway R, Huynh-Le MP, et al. Effect of CD4 count on treatment toxicity and tumor recurrence in HIV positive patients with anal cancer. Intl J

Rad Onc Biol Phys 2018;100:478-485.

Abstract

Note: All recommendations are category 2A unless otherwise indicated.

NCCN Guidelines Index Table of Contents Discussion

• HIV status alone should not be a criterion for decision-making regarding surgical intervention, regardless of the procedure.

References

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NCCN Guidelines Index Table of Contents Discussion

Note: All recommendations are category 2A unless otherwise indicated.

HIV-E 1 OF 2

• The risk of infectious complications in PWH is reduced with improved HIV control and aggressive infection prophylaxis; therefore, ART

should be initiated and/or continued during cancer therapy.

• Select ARTs can be administered safely with systemic cancer therapy. With continued development of new ARVs, effective alternatives are often available to patients when the existing ARVs are expected to affect metabolism of or share toxicities with systemic cancer therapies.

All ART initiation or changes should be done in consultation with an HIV specialist. See Principles of Systemic Therapy and Drug-Drug

Interactions (HIV-B).

• Long-term steroid use should be limited in PWH because of the risk of opportunistic infections and other complications.

• PWH have an increased risk of oral mucositis, esophagitis, and colitis. A high index of suspicion of and early testing for opportunistic

infections, including fungal infections, cytomegalovirus (CMV), and TB, is appropriate; early consultation with an HIV specialist is

appropriate. See Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV.

• Patients desiring fertility preservation should be referred to oncofertility for a discussion of options.

Other Supportive Care Measures:

• For most supportive care situations related to cancer treatment, PWH should receive care as per the appropriate NCCN Guidelines for

Supportive Care (available at www.NCCN.org), including:

NCCN Guidelines Adult Cancer Pain

NCCN Guidelines Antiemesis

NCCN Guidelines Cancer-Related Fatigue

NCCN Guidelines Distress Management

NCCN Guidelines Palliative Care

NCCN Guidelines Survivorship

• For general recommendations for vaccination in patients with cancer, see NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections and DHHS Guidelines Immunizations for Preventable Diseases in Adults and Adolescents with HIV.

Generally, live virus vaccines should not be administered to PWH with CD4+ T-cell counts <200 cells/μL.

PRINCIPLES OF SUPPORTIVE CAREa

• For recommendations regarding infectious prophylaxis in PWH receiving cancer therapy, see HIV-E (2 of 2).

a Refer to the NCCN Distress Thermometer and Problem List, which includes social determinants of health. See NCCN Guidelines for Distress Management (DIS-A).

NCCN

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

PRINCIPLES OF SUPPORTIVE CARE

●PW should receive the prophylaxis indicated by their HIV status and cancer treatment.CD4 thresholds for prophylaxis may be higher in patients starting an immunosuppressive regimen. Also see the NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections and Guidelines for Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV.

●For PWH receiving cancer therapy where profound immunosuppression/myelosuppression is anticipated, the Panel recommends the following:

●Myeloid growth factor support(per NCCN Guidelines for Hematopoietic Growth Factors or NCCN treatment guidelines with specific recommendations)

Myeloid growth factor support is required in regimens that are high risk for febrile neutropenia, strongly recommended in regimens that are intermediate risk for febrile neutropenia, and should be strongly considered in regimens that are low risk for febrile neutropenia in PWH. Pre-existing neutropenia and/or low CD4+ T-cell counts(<200 cells/μL) increase risk of chemotherapy-associated neutropenic fever; myeloid growth factor support is strongly recommended with these risk factors.

Gram-negative infection prophylaxis

Fluorquinolone prophylaxis or equivalent during periods of neutropenia

Gc,Fiproloxacin00-750 mg PO every 12 hours QR levofloxacin500-750 mg PO daily

Herpes simplex virus(HSV)/varicella-zosteror virus(VZV) prophylaxis

Continue until completion of cancer therapy

Gg,Acyclovir 400-800 mg PO twice daily QR valycovlin 500 mg PO twice daily daily

PJP prophylaxis and toxoplasmosis prophylaxisb

◆Continue until CD4+ T-cell counts recovered to≥200 cells/uL for≥3 months duration post completion of cancer therapy

-Use caution when administering trimethophrim-sulfamethoxazole (TMP/MSX) while the patient is on methotrexate

- G6PD deficiency screening should be performed prior to initiation of dapsone

Mycobacterium avium complex(MAC) prophylaxisb

PWH who have CD4+ T-cell counts<50 cells/μL and are not on ART.

Disseminated MAC disease should be ruled out before starting prophylaxis.

<Eg,Azithromycin 1200 mg PO once a week

Candida prophylaxis

<Eg,Fluconazole and/or nystatin

Antifungal prophylaxis

\Box During periods of prolonged neutropenia(27 days)

![](827,272,856,296) Azole antifungals may interact with ART and chemotherapy.Azoles should typically be held a minimum of 24 hours prior to and through 24 hours after administration of cancer therapy that is metabolized via CYP3A4.

<Eg,Fluconazole 400 mg PO daily QR posaconazole(delayed-release tablets) 300 mg PO twice daily on day 1 followed by 300 mg PO daily thereafter QR voriconazole 200 mg PO twice daily

<EndOfPara> In certain geographic areas: histoplasmosis, coccidioidomyosis, or Talaromyces marnefei

·Consultation with an HIV specialist is strongly recommended in patients with hepatitis co-infection or other opportunistic infection.Consultation with a hepatologist should also be considered in the setting of advanced liver disease.

Hepatitis B virus(HBV)

All PWH should be tested for hepatitis B by 3 tests: hepatitis B surface antigen (HBsAg), hepatitis B core antibody (anti-HBc)total immunoglobulin(Ig) or IgG, and antibody to hepatitis B surface antigen. Testing is required prior to initiation of systemic therapy to avoid hepatic toxicity but anticancer therapy should not be delayed. See Hepatitis B Virus Screening and Management for Patients With Cancer Prior to Therapy: ASCO Provisional Clinical Opinion Update and Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV.

All patients should be on fully suppressive HIV ART. Ideally, the ART should include drugs that treat HBV as well as HIV.

-If not able to include drugs in ART that treat both HIV and HBV,HBV therapy will be directed by an HIV specialist.

-If the prophylaxis is not part of ART, the duration of therapy should be 1-year post-transplant, post-B cell depleting antibodies, or post cell-based therapy.

●For Unexplained Fever or Other Infectious Episode: Consultation with an HIV specialist is strongly recommended for febrile neutropenia in the context of appropriate prophylaxis. Opportunistic infections including PJP and CMV as cause of fever are more likely in PWH receiving cancer chemotherapy; a high index of suspicion and early testing for opportunistic infections in consultation with an HIV specialist is appropriate.

b These are specifically for prophylaxis. Refer to the Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV for patients with a recent history of or current active infection.

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

PRINCIPLES OF IMAGING

HIV-F

• Interpretation of imaging for the workup, staging, and surveillance of PWH who have cancer is complicated by the increased incidence of

non-malignant lesions that may be mistaken for cancer spread or recurrence.

Lymphadenopathy seen on 18F-FDG PET/CT can be malignant or can result from opportunistic infections or HIV directly.1

Lung lesions may be malignant or may result from opportunistic infections, drug reactions, or immune activation.

Brain lesions may be malignant or may result from opportunistic infections, vascular complications, or hydrocephalus.

• Opportunistic infections and HIV-related adenopathy are more common in patients with higher viral loads and lower CD4+ T-cell counts.

• Consultation with an HIV specialist and an evaluation to rule out infectious processes (eg, toxoplasmosis) or additional malignancies should be considered as clinically appropriate for PWH whose imaging shows lymphadenopathy or lesions in the spleen, lungs, brain, bone, liver,and gastrointestinal tract, especially in the presence of a low CD4+ T-cell count and concurrent B symptoms.

• Lesions of uncertain etiology should be biopsied to confirm cancerous histology.

1 Davison JM, Subramaniam RM, Surasi DS, et al. FDG PET/CT in patients with HIV. AJR Am J Roentgenol 2011;197:284-294.

Note: All recommendations are category 2A unless otherwise indicated.

NCCN

National Comprehensive Cancer Network

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

ABBREVIATIONS

ART

antiretroviral therapy

ARV

antiretroviral

ASCUS

atypical squamous cells of undetermined significance

CHL

classic Hodgkin lymphoma

CIN

cervical intraepithelial neoplasia

CMV

cytomegalovirus

CNS

central nervous system

DARE

digital anorectal exam

DDI

drug-drug interaction

DHHS

Department of Health and Human Services

DLBCL

diffuse large B-cell lymphoma

DLCO

diffusing capacity of the lung for carbon monoxide

EBV

Epstein-Barr virus

HBc

hepatitis B core

HBsAg

hepatitis B surface antigen

HBV

hepatitis B virus

HIV

human immunodeficiency virus

HPV

human papillomavirus

HRA

HSIL

HSV

IANS

ICI

IMRT

INSTI

KICS

KSHV

LSIL

MAC

MCD

MSM

NHL

NSCLC

NNRTI

NOS

PJP

PML

PWH

SBRT

SPEP

VZV

NSCLC non-small cell lung cancer

non-small cell lung cancer

NNRTI non-nucleoside reverse transcriptase inhibitor

NOS not otherwise specified

PJP pneumocystis jirovecii pneumonia

PML progressive multifocal leukoencephalopathy

PWH people with HIV

SBRT

SBRT stereotactic body radiation therapy

SPEP serum protein electrophoresis

TB tuberculosis

VZV varicella zoster virus

NCCN

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

NCCN Guidelines Index Table of Contents Discussion

||NCCN Categories of Evidence and Consensus| |---|---| |Category 1|Based upon high-level evidence (≥1 randomized phase 3 trials or high-quality, robust meta-analyses), there is uniform NCCN consensus (≥85% support of the Panel) that the intervention is appropriate.| |Category 2A|Based upon lower-level evidence, there is uniform NCCN consensus (≥85% support of the Panel) that the intervention is appropriate.| |Category 2B|Based upon lower-level evidence, there is uniform NCCN consensus (≥50%, but <85% support of the Panel) that the intervention is appropriate.| |Category 3|Based upon any level of evidence, there is major NCCN disagreement that the intervention is appropriate.|

All recommendations are category 2A unless otherwise indicated.

|NCCN Categories of Preference|| |---|---| |Preferred|Interventions that are based on superior efficacy, safety, and evidence; and, when appropriate, affordability.| |Other recommended|Other interventions that may be somewhat less efficacious, more toxic, or based on less mature data; or significantly less affordable for similar outcomes.| |Useful in certain circumstances|Other interventions that may be used for selected patient populations (defined with recommendation).|

All recommendations are considered appropriate.

National Comprehensive Cancer Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

Discussion

This discussion corresponds to the NCCN Guidelines for Cancer in People With HIV. Last updated: August 11, 2025

|Overall Statements Update Methodology 3|| |---|---| |Literature Search Criteria.|| |Sensitive /Inclusive Language Usage|MS-3| |Disparities in Cancer Care for PWH|MS-3| |HIV Management During Cancer Therapy|MS-3| |HIV Screening.|MS-4| |Linkage to HIV Care.|MS-4| |HIV Therapy During Cancer Treatment|MS-4| |Opportunistic Infection Prophylaxis|MS-5| |Smoking Cessation in PWH Who Have Cancer|MS-6| |Recommendations for Cancer Management in PWH|MS-6| |Cancer Workup in PWH|MS-6| |Systemic Therapy and Drug-Drug Interactions|MS-7| |Immune Checkpoint Inhibitors|MS-8| |Radiation Therapy in PWH|MS-9| |Cancer Surgery in PWH|MS-9| |Supportive Care During Cancer Therapy in PWH|MS-10| |Recommendations for Specific Cancers in PWH|MS-11| |Anal Cancer in PWH|MS-11| |Cervical Cancer in PWH|MS-14| |Hodgkin Lymphoma in PWH|MS-15| |Kaposi Sarcoma in PWH|MS-18| |Lung Cancer in PWH|MS-18| |NHL in PWH|MS-20| |Management of Cancer in PWH in Lower Resource Settings|MS-20| |Summary.|MS-21| |References.|MS-22|

![NCCN\nNCCN\nConcom\n](2/aj0YEe4oUhYkBdfpda0fYP/figure74b854d6b5e44444ad2b2be55055a583_0_1.png)

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

Overview

More than 1.2 million people in the United States were estimated to be living with human immunodeficiency virus(HIV) infection in October 2022.1 Cancers arising in the context of HIV have historically been categorized as AIDS-associated and non-AIDS-associated malignancies with the former including aggressive non-Hodgkin lymphomas(NHLs), Kaposi sarcoma, and invasive cervical cancer.2,3 With increasing recognition of the role of immunity in cancer development and control, as well as associations between HIV and other cancers, we use the term“HIV-associated” for all cancers occurring in people with HIV (PWH). Dramatic improvements in and access to treatment of HIV over the last two decades has decreased the risk of AIDS-defining conditions, improved immune function and survival, and led to a decline in the incidence of cancers historically categorized as AIDS-defining, including human papillomavirus (HPV)-associated cancers and cancers associated with immunosuppression.4-6 PWH are living longer and healthier lives; however, they are experiencing an increased risk of many solid tumors associated with aging.7-13 The proportion of mortality due to cancers in PWH has increased from 5% during 1996 to 1999 to 19% during 2016 to 2020,while the proportion of AIDS-related mortality in this population dropped from 49% to 16% over the same time period. 14

An estimated 7490 PWH were diagnosed with cancer in the United States in 2020.15 Projections indicate a decline in this figure to an estimated 6690 by 2030. Studies have noted a higher risk for developing many cancers in PWH than in the general population, likely due to underlying immune deficiency, accelerated aging, and co-infection with viruses such as HPV, Kaposi sarcoma herpesvirus(KSHV; also called human herpesvirus 8 or HHV8), hepatitis B virus(HBV), hepatitis C virus(HCV), and Epstein-Barr virus(EBV).16-20 In

<EndOfPara>addition, the prevalence of other cancer risk factors in the HIV population(eg, smoking) likely play a role. ${ }^{21-25}$

The estimated proportions of each major cancer type among total incident cancer cases occurring in PWH in the United States during 2020 were15:

● Prostate cancer 18%

● Lung cancer $\boxed{12}$

● NHL 10%

● Kaposi sarcoma 7%

● Anal cancer 7%

● Liver cancer 6%

● Oropharyngeal cancer 4%

● Colorectal cancer 3%

● Hodgkin lymphoma 3%

● Breast cancer 3%

● Cervical cancer 1%

Deaths due to cancer in the U.S. HIV population occurred at a rate of 484 and 314 per 100,000 person-years in 2001 to 2005 and 2011 to 2015, respectively. ${ }^{26}$ Approximately 9.2% of deaths in PWH in the United States were attributable to non-AIDS-defining cancers and 5.0%

These NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Cancer in People with HIV provide treatment recommendations for PWH who develop non-small cell lung cancer(NSCLC), anal cancer, Hodgkin lymphoma, and cervical cancer. In addition, the Panel outlines general advice for this population regarding HIV management during cancer therapy; drug-drug interactions(DDIs);and workup, radiation therapy, surgical management, and supportive care in PWH who have cancer. The Panel based its recommendations

![NCCN\nNational\nComprehensive\nCancer\nNetwork®\n](2/aj0YEe4oUhYkBdfpda0fYP/figureda018a10e39342c08ecbec28de97bf43_0_1.png)

National Comprehensive Cancer in Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

on relevant data when available and on expert consensus for situations where data were not available.These guidelines are intended to assist health care providers with clinical decision-making for PWH who have cancer. This Discussion elaborates on the guidelines and provides an overview of the literature supporting the included recommendations.

Guidelines Update Methodology

The complete details of the Development and Update of the NCCN Guidelines are available on the NCCN website at www.NCCN.org.

Literature Search Criteria

Prior to the update of the NCCN Guidelines for Cancer in People with HIV, an electronic search of the PubMed database was performed to obtain key literature in the field, using the following search terms:(cancer or malignancy or carcinoma or adenocarcinoma or lymphoma or leukemia or melanoma or sarcoma or neoplasia) and(HIV or AIDS).The PubMed database was chosen because it remains the most widely used resource for medical literature and indexes peer-reviewed biomedical literature.27

The search results were narrowed by selecting studies in humans published in English. Results were confined to the following article types: Case Reports, Clinical Study, Clinical Trial, Phase II; Clinical Trial,Phase III; Clinical Trial,Phase IV; Controlled Clinical Trial;Evaluation Study; Guideline; Multicenter Study; Observational Study;Practice Guideline; Randomized Controlled Trial; Meta-Analysis;Systematic Reviews; and Validation Studies.

The data from key PubMed articles as well as articles from additional sources deemed as relevant to these guidelines as discussed by the Panel during the Guidelines update have been included in this version of the Discussion section. Recommendations for which high-level

evidence is lacking are based on the Panel's review of lower-level evidence and expert opinion.

Sensitive /Inclusive Language Usage

NCCN Guidelines strive to use language that advances the goals of equity,inclusion,and representation.28 NCCN Guidelines endeavor to use language that is person-first; not stigmatizing; anti-racist, anti-classist, anti-misogynist, anti-ageist, anti-ableist, and anti-weight-biased; and inclusive of individuals of all sexual orientations and gender identities.NCCN Guidelines incorporate non-gendered language,instead focusing on organ-specific recommendations. This language is both more accurate and more inclusive and can help fully address the needs of individuals of all sexual orientations and gender identities.NCCN Guidelines will continue to use the terms men, women, female,and male when citing statistics, recommendations, or data from organizations or sources that do not use inclusive terms. Most studies do not report how sex and gender data are collected and use these terms interchangeably or inconsistently. If sources do not differentiate gender from sex assigned at birth or organs present, the information is presumed to predominantly represent cisgender individuals. NCCN encourages researchers to collect more specific data in future studies and organizations to use more inclusive and accurate language in their future analyses.

Disparities in Cancer Care for PWH

In general, PWH who develop cancer have a higher mortality rate compared with the general cancer population.29-34 Reasons for this increased mortality include delayed diagnoses, advanced cancer stage,other comorbidities, and immunosuppression in PWH.30,35-38 In fact, one study showed that PWH had fewer comorbidity-free years at 21 years of age than matched adults without HIV.39 However, there is also significant disparity in cancer treatment between PWH and the general

![NCCN\n](2/aj0YEe4oUhYkBdfpda0fYP/figure6cc1ec0c7e8e4135aebf745d7335e4ff_0_1.png)

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

cancer population, with many PWH not receiving any cancer treatment.40-44 Results of a survey of 500 medical and radiation oncologists in the United States published in 2015 suggest that lack of consensus guidelines and provider education contribute to the substandard cancer care often offered to PWH who have cancer.45 An analysis of the HIV/AIDS Cancer Match Study(2001-2019)demonstrated persistent disparities in cancer treatment among PWH.46 It is the hope of the NCCN Panel that these guidelines can help to fill that gap in education and enable health care providers to provide optimal cancer care to PWH.

HIV Management During Cancer Therapy

In the United States, 13% of PWH are not aware of their HIV status.PWH who are unaware of their HIV status do not receive the clinical care they need to reduce HIV-associated morbidity and mortality and may unknowingly transmit HIV.47 To detect HIV early, the Centers for Disease Control and Prevention(CDC) recommends HIV screening for everyone aged 13 to 64 years at least once, and annual testing for people with certain risk factors.48

HIV testing may be particularly important in patients with cancer,because identification of HIV infection has the potential to improve clinical outcomes.49 In a multicenter prospective cohort study of >3000 patients diagnosed with cancer, 1.1% tested positive for HIV.50 Results of a retrospective cohort study at MD Anderson Cancer Center revealed, however, that the rate of HIV testing in cancer clinics from 2007 to 2009 was only 19.3%.51 Analysis of data from the 2009 Behavioral Risk Factor Surveillance System showed that only 41% of U.S. cancer survivors <65 years of age reported ever being tested for HIV.52 Race, other demographic characteristics, and tumor type influenced the likelihood of receiving an HIV test in both studies.

All patients should be offered HIV screening once during their lifetime.The NCCN Panel believes that HIV testing should be considered in patients with a new cancer diagnosis who have not been recently screened. Testing is particularly important in the context of suspected or confirmed Kaposi sarcoma or primary central nervous system(CNS)lymphoma, given the risk of these cancers in the United States is approximately 250- to 500-fold higher in PWH compared to those without HIV.9,19

Linkage to HIV Care

The HIV Care Continuum Initiative indicates that all patients diagnosed with HIV should be referred to an HIV specialist.53 Linkage to care and initiation of antiviral therapy have been shown to improve viral suppression.54,55 Early initiation of antiretroviral therapy (ART) has also been shown to improve survival in PWH and lower incidence of HIV-associated malignancies. 56-59 Linkage to HIV care is essential for PWH who have cancer to optimize HIV control as well as prevention and treatment of opportunistic infections; therefore, the oncology team should refer all PWH who have cancer to an HIV specialist if they do not already have one. The HIV.gov website has a map that can be used to locate HIV services:https://locator.hiv.gov.

Consultation with a hepatologist should also be considered in the setting of viral hepatitis or advanced liver disease(see Supportive Care During Cancer Therapy in PWH, below).

HIV Therapy During Cancer Treatment

HIV treatment for PWH who have cancer should be initiated and maintained by an HIV specialist, in collaboration with the oncology team. If the patient has already started ART, it should be continued during cancer treatment, although modifications may be needed. For patients who have not yet started ART, it should ideally be initiated

![NCCN\nNCC\n](2/aj0YEe4oUhYkBdfpda0fYP/figure0905623fd7424d3a9e9f3412950ac1e5_0_1.png)

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

either≥7 days prior to the start of cancer treatment or long enough after cancer therapy has been initiated that it is possible to distinguish between adverse effects attributable to chemotherapy versus those attributable to ART.

ART interruptions during cancer treatment should be avoided, because they increase the risk of immunologic compromise, opportunistic infection, and death. ${}^{60}$ ART should not be discontinued unless in consultation with an HIV specialist. Continuation of ART may also result in better tolerance of cancer treatment, higher response rates, and improved survival.61,62 ART can be modified as needed based on DDIs or overlapping toxicities with cancer therapy(see Systemic Therapy and Drug-Drug Interactions, below).

Laboratory testing, HIV viral load, and CD4+ T-cell monitoring should generally be performed in PWH with cancer as per normal schedules for PWH.63 More frequent viral load and CD4+ T-cell testing may be needed with use of cancer or supportive therapies, which may reduce the effectiveness of ART or cause lymphopenia. A study showed that radiation and/or chemotherapy is associated with significantly reduced initial CD4+ T-cell counts compared with surgery or other treatment in PWH.64 Other data also show that certain chemotherapy regimens can cause a sustained drop in CD4+ T-cell counts and an increased risk of opportunistic infections. ${}^{65}$ In the setting of radiation or chemotherapy-associated lymphopenia, HIV viral load monitoring more accurately reflects control of HIV compared with CD4+ T-cell count. Monitoring the depth of CD4+ T-cell suppression prior to and during cancer therapy is important for informing the risk of opportunistic infections and appropriate prophylaxis.

Opportunistic Infection Prophylaxis

The occurrence of opportunistic infections in PWH has decreased in the ART era, mainly because effective ART reduces infection risk as CD4+T-cell counts rise.6,66-68 Furthermore, improvements in prophylaxis and treatment of opportunistic infections in PWH has further reduced risk.68,69 Still, opportunistic infections represent a major cause of morbidity and mortality in PWH.68,69

The risk of bacterial, fungal, and viral infections is elevated in patients with cancer, who may experience immunosuppression resulting from cancer treatment and sometimes from the disease itself(eg,hypogammaglobulinemia in chronic lymphocytic leukemia or multiple myeloma).70-74 In particular, chemotherapy can cause neutropenia,which is a major risk factor for the development of infections.75 The frequency and severity of infection are inversely proportional to the neutrophil count, with the risks of severe infection and bloodstream infection greatest(approximately 10%-20%) at neutrophil counts<100 cells/mCL.76 Certain novel targeted agents are also associated with immunosuppression and increased infection risk.77

PWH may be more susceptible to infectious complications following certain chemotherapy regimens compared to individuals without HIV,78 and low CD4+ T-cell counts appear to increase the risk of febrile neutropenia.79 Persons with advanced immunosuppression due to HIV are at higher risk of cytopenias regardless of cancer status. However,HIV status alone does not differentially impact the risk of myelosuppression and infectious complications in all cancer regimens.80

Overall, the NCCN Panel recommends that PWH who have cancer should receive the prophylaxis indicated by their HIV status and cancer treatment, with consideration given to the potential for increased risk of febrile neutropenia or more advanced lymphopenia in PWH, particularly

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National Comprehensive Cancer in Cancer

NCCN Guidelines Version 1.2026 Cancer in People with HIV

with low CD4+ T-cell counts. Specific recommendations for PWH receiving cancer therapy for which profound immunosuppression/myelosuppression is anticipated are outlined in the guidelines above(see Principles of Supportive Care in the algorithm).The U.S. Department of Health and Human Services'(DHHS')Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents With HIV(available at https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/whats-new) and the NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections(available at www.NCCN.org) also contain recommendations that may be relevant to this population. If febrile neutropenia occurs in spite of prophylaxis, consultation with an HIV specialist is strongly recommended.

Smoking Cessation in PWH Who Have Cancer

A study found that in the United States, 42% of PWH use tobacco.8.1 Help with smoking cessation should be offered to PWH who smoke and have cancer (see the NCCN Guidelines for Smoking Cessation,available at www.NCCN.org). Smoking cessation after a cancer diagnosis in the general population has been linked with improved general health and well-being, reduced treatment-related complications,decreased cancer recurrence, fewer second primary tumors, and improved survival.82-89 Data on the effects of smoking cessation specific to PWH after a cancer diagnosis are lacking. The Infectious Diseases Society of America recommends implementing an Ask-Advise-Connect framework to initiate smoking cessation, prescribe pharmacotherapy(preferably varenicline), and provide a direct connection to behavioral therapy to increase the likelihood of successful cessation in PWH.81 The National Cancer Institute has begun an initiative to advance research into smoking cessation treatment for PWH.90

Recommendations for Cancer Management in PWH

Special considerations for cancer management in PWH and recommendations for the management of specific cancers in PWH are discussed herein. Overall, the NCCN Panel recommends that most PWH who develop cancer should be offered the same cancer therapies as those without HIV. Modifications to cancer treatment should not be made solely based on HIV status. Inclusion of PWH in cancer clinical trials should be encouraged whenever feasible.

Cancer Workup in PWH

Workup for PWH who have cancer is complicated by the increased incidence of non-malignant lesions that may be mistaken for cancer spread or recurrence.91,92 For example, HIV viremia and opportunistic infections commonly cause lymphadenopathy in PWH, which can be seen on F-18 fluorodeoxyglucose(FDG)-PET/CT.93,94 Nonmalignant causes of lymphadenopathy are more common in patients with higher viral loads and lower CD4+ T-cell counts.95 Therefore, PWH who have cancer should have an infectious disease workup for lymphadenopathy as clinically indicated.

Similarly, consultation with an HIV specialist and an evaluation to rule out infectious processes(eg, toxoplasmosis) or additional malignancies should be considered for PWH with cancer who develop splenic, brain,lung, liver, or gastrointestinal lesions, especially in the presence of a low CD4+ T-cell count and concurrent B symptoms. Opportunistic infections in the lung include Mycobacterium tuberculosis(Mtb), cytomegalovirus(CMV), and Pneumocystis carinii pneumonia(PCP).96 Furthermore,non-infectious, non-malignant pulmonary manifestations of HIV can be difficult to interpret on imaging studies, including drug reactions and immune activation.96,97 Brain lesions seen in PWH may result from cancers such as CNS lymphoma, but opportunistic infectious causes are more common, including viral encephalitis, aspergillosis,

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toxoplasmosis, cryptococcus,bacterial meningitis, tuberculosis(TB),and progressive multifocal leukoencephalopathy.98-100 Benign, non-infectious brain lesions can also occur in PWH(eg, vascular complications, hydrocephalus).98,99 Bone lesions may occur with Mtb infection, bacillary angiomatosis, and use of tenofovir.101-103 Gastrointestinal lesions commonly occur during infection with CMV,Candida, and Cryptosporidium.104 Liver lesions may be caused by multiple organisms including Mtb, Mycobacterium avium complex(MAC), and CMV.105 Lesions of uncertain etiology should be biopsied to confirm cancerous histology.

Systemic Therapy and Drug-Drug Interactions

DDIs between anticancer therapy and antiretrovirals(ARVs) were first noted with the increased incidence of mucositis in PWH who had NHL who were treated with both the protease inhibitor saquinavir and the chemotherapy regimen cyclophosphamide, doxorubicin, and etoposide.106 DDIs depend on a variety of factors, including the route of elimination and the effect on CYP450 and other drug transporter or drug-metabolizing enzymes of both of the drugs involved.107,108 Depending on the mechanism of the interaction, DDIs can result in: 1)decreased exposure and reduced efficacy of the anticancer or antiretroviral agent; or 2) increased exposure and increased toxicity of the anticancer or antiretroviral agent. In general, enzyme inhibitors increase the substrate exposure and thus increase toxicity, whereas enzyme inducers decrease the substrate exposure and reduce efficacy.The exception to this rule is for prodrugs, where the metabolite is the active agent. In these cases, the DDIs would be reversed(ie, enzyme inhibitors decrease efficacy; enzyme inducers increase toxicity). These Guidelines provide general guidance, but comprehensive resources for ARV DDIs are available and should be consulted for PWH and cancer.The DHHS Panel on Antiretroviral Guidelines provides information on the mechanisms of ARV-associated drug interactions and guidance on

specific DDIs(https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/drug-interactions-overview).However, these guidelines do not incorporate many systemic cancer therapies. A preferred resource that provides an interaction checker including cancer therapies is the University of Liverpool HIV drug interactions site(https://www.hiv-druginteractions.org).

The greatest concern for DDIs is with ART regimens containing pharmacologic boosters (ie, ritonavir, cobicistat) and protease inhibitors (eg, atazanavir, darunavir, saquinavir), which strongly inhibit CYP3A4.Protease inhibitors are also substrates of CYP3A4; therefore, ritonavir and cobicistat increase the exposure of protease inhibitors and thus the effectiveness of ART.109 Pharmacologic boosters may also increase exposure to and toxicity associated with any drug, including anti-cancer agents metabolized by CYP3A. In fact, preclinical studies in mice show that CYP3A inhibitors can alter exposure to erlotinib and docetaxel. 110,111 A recent phase I pharmacokinetic study found that exposure of erlotinib 75 mg combined with ritonavir is similar to erlotinib 150 mg. 112 A phase I pharmacokinetic study in 19 PWH with cancer found that those participants receiving ritonavir-based ART experienced greater toxicity at a lower dose of unitinib than those receiving non-ritonavir-based ART.113 Furthermore, a retrospective analysis of PWH treated for Hodgkin lymphoma showed that concomitant ritonavir-based HIV therapy and vinblastine can result in irreversible neurologic toxicity. 114-116

Another type of ART that can cause DDls with cancer therapy is non-nucleoside reverse transcriptase inhibitors, which induce CYP3A. These drugs may thus decrease exposure and efficacy of cancer agents metabolized by CYP3A. A preclinical mouse study showed that a CYP3A inducer decreased erlotinib exposure. ${}^{110}$

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HIV regimens containing integrase inhibitors without pharmacologic boosters are favored in the setting of malignancy because of their lower potential for DDIs. Small case series have shown that integrase inhibitor-based ART is superior to other ART regimens during cancer therapy.117,118 In one of these studies, data from 154 PWH with cancer who received care at the University of Texas MD Anderson Cancer Center between 2001 and 2012 were reviewed.118 Non-nucleoside reverse transcriptase inhibitors and integrase strand-transfer inhibitors(ISTI) had comparable antiviral efficacy. The activity of these two classes was superior to the antiviral activity of protease inhibitors, but the integrase inhibitors were better tolerated during cancer therapy.

ART regimens and cancer therapies that are not involved in the same metabolic pathways can still be problematic to coadminister because of overlapping toxicities. One major concern is for neuropathy, which is associated with many cancer drugs(eg, platinum agents, taxes, vinca alkaloids, treventiamab vedotin, proteasome inhibitors) and certain nucleoside reverse transcriptase inhibitors(eg, didanosine,stavudine).119 Another example is neutropenia, which can be a side effect of zidovudine, boosted protease inhibitors, and integrase inhibitors and is a common side effect of many chemotherapy regimens.120,121 Other overlapping toxicities of cancer therapy and ART can affect the liver, cardiovascular system, and kidneys.108,122-124

Despite the possibility for DDIs and overlapping toxicities,ARVs can be safely coadministered with chemotherapy. In general, ISTI-based regimens are preferred because they have fewer DDIs. Oncology and HIV clinicians, along with HIV and oncology pharmacists, if available,should review proposed cancer therapy, supportive care medications,and ART for possible DDIs and overlapping toxicity concerns prior to initiation of therapy. Consultation of the drug package inserts for further information is also recommended. Modification of ART or cancer

therapy or increased monitoring may be required. With the continued development of new ART, effective alternatives are often available to patients when the currently used ART is expected to affect the metabolism of or share toxicities with systemic cancer therapies.

If a potential DDI exists, the Panel lists the following options(in order of preference):

1.Substitution of a different antiretroviral with less DDI potential

2.Selection of an alternative cancer therapy regimen with less DDI potential

If the above two options do not seem feasible, consultation with an HIV specialist is recommended.

Drugs used to prevent and/or treat opportunistic infections in PWH may also interact with cancer therapies. Some examples of concern include rifamycins (via induction of hepatic metabolism), clarithromycin (via inhibition of CYP3A4), azole antifungals (via inhibition of various hepatic metabolic processes), trimethoprim/sulfamethoxazole treatment with methotrexate (impact on methotrexate clearance), and dapsone(compound risk of neutropenia). For more information, see Significant Pharmacokinetic Interactions between Drugs Used to Treat or Prevent Opportunistic Infections (https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/significant-drug-interactions?view=full).

Immune Checkpoint Inhibitors

Evidence suggests that immune checkpoint inhibitors (ICls) are generally safe and effective in PWH, ${}^{125}$ though in persons with KSHV infection, there may be increased risk of life-threatening KSHV-

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associated inflammatory syndromes such as multicentric Castleman disease(MCD) or KSHV-associated inflammatory cytokine syndrome(KICS) when ICIs are used. Consider screening for seropositivity for KSHV. If the patient has a history of KSHV-seroposivity or KSHV-associated conditions, consider more frequent monitoring of signs,symptoms(eg,fevers,lymphadenopathy, splenomegaly,pancytopenia),and laboratory findings(eg, elevated C-reactive protein, interleukin-6[IL-6], 4+ log copies/mL KSHV viremia) consistent with KICS or MCD.126-136

In a phase I study, pembrolizumab demonstrated an acceptable safety profile in PWH and advanced cancer.137 Most treatment-emergent adverse events possibly attributed to pembrolizumab were grade 1(20%) or grade 2(53%). The most common adverse events included anemia, fatigue, nausea, and hypothyroidism.

The use of ICls has also been linked to opportunistic infections including TB reactivation and flair of mycobacterial disease.138-142 Screening for latent TB infection can be considered before administering in ICl so that the patient can be monitored for TB symptoms and treatment of mycobacterial infection can be expedited.

Radiation Therapy in PWH

Modern data suggest that radiation therapy for certain cancers (eg, anal cancer; see below) is effective and well-tolerated in PWH. For other cancers, however, data on the safety and efficacy of radiation therapy specific to PWH are limited (eg, lung cancer). ${ }^{143}$

The data on the use of radiation in PWH who have anal cancer are particularly strong, with>20 clinical studies published.143 One retrospective cohort study included 175 PWH and 1009 people without HIV who had anal cancer in the ART era.144 No differences were seen in survival after chemoradiation treatment based on HIV status. In

addition, a prospective study of 36 patients with anal cancer that included 14 PWH found no differences in overall survival or in acute or late toxicities.145

In summary, when radiation therapy is indicated in the care of patients with cancer, HIV status alone should not be a criterion for decision-making regarding treatment indications or dose. Dose fractionation and treatment volumes are recommended per NCCN Guidelines Treatment by Cancer Type (available at www.NCCN.org). The Panel recommends that particular attention be paid to limit dose to mucosal membranes,skin, and bone marrow using conformal techniques like intensity-modulated radiation therapy (IMRT), proton therapy, brachytherapy, or stereotactic body radiation therapy (SBRT) for PWH, as deemed appropriate by the treating provider. The Panel also notes that additional clinical monitoring may be required with use of concurrent chemoradiation in PWH. Furthermore, nutritional support, pain control,and other supportive measures should be used to minimize radiation therapy interruptions in this population.

Cancer Surgery in PWH

Older data from anorectal surgery for benign disease(eg, hemorrhoids,fistulas) indicate that PWH can experience delayed wound healing,especially if the CD4+ T-cell count is<50/μL.146 Other reports, however,demonstrate that PWH who undergo anorectal surgery have uncomplicated wound healing.147 Furthermore, a study of PWH who required invasive procedures found that wound infection rates were not associated with HIV status.148 In addition, studies evaluating surgical outcomes in PWH demonstrate that clinical outcomes, length of stay,and complications are similar between PWH and patients without HIV for most surgical procedures.149,150

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Studies have also shown that surgery for common malignancies(eg,anal cancer, prostate cancer, colorectal cancer) in PWH is safe and effective.151-156 In particular, ample data suggest that surgical management in PWH with early-stage anal cancer or recurrent anal cancer is safe and effective.151-153 For example, a retrospective review of 1725 U.S. patients with anal cancer(18% HIV-positive) who received an abdominoperineal resection (APR) saw no differences in mortality,length of hospital stay, or hospitalization costs based on HIV status.152 However, postoperative hemorrhage occurred more frequently in the PWH group (5.1% vs.1.5%;P=.05). Liver transplantation for hepatocellular carcinoma in the setting of HIV infection also appears to be feasible. A multicenter study in Italy compared the outcomes of liver transplantation in 30 PWH and 125 patients without HIV who had hepatocellular carcinoma.157 HIV status did not affect overall survival or cancer recurrence rates.

PWH should be treated with standard universal precautions, and no additional pre- or postoperative laboratory testing is needed specific to PWH beyond the normal workup and follow-up for a patient undergoing surgery. Overall health (eg, organ dysfunction, nutritional state) has been found to be a more reliable predictor of surgical outcome than CD4+ T-cell counts or HIV viral loads in PWH. Data showing that low CD4+ T-cell counts are associated with poorer prognosis have been inconsistent, and viral suppression has not been conclusively shown to improve surgical outcomes.158-162

Overall, the Panel recommends that HIV status alone should not be a criterion for decision-making regarding surgical interventions in patients with cancer, regardless of the procedure being considered.

Supportive Care During Cancer Therapy in PWH

Patients with advanced HIV often suffer from fatigue, weight loss, pain,anorexia, and anxiety.163 ART may cause side effects including nausea/vomiting,diarrhea,constipation,cough,dyspnea,insomnia,and depression.163 Cancer and its treatment can also cause all of these symptoms and PWH report greater cancer treatment toxicity.164 Managing these symptoms can be critical, because studies show that treatment side effects may decrease completion of cancer treatment in PWH and compromise cancer outcomes.164-166

For most supportive care situations related to cancer treatment, PWH should be cared for as per the appropriate NCCN Guidelines for Supportive Care (available at www.NCCN.org), including:

● NCCN Guidelines for Adult Cancer Pain

● NCCN Guidelines for Palliative Care

● NCCN Guidelines for Antiemesis

● NCCN Guidelines for Cancer-Related Fatigue

● NCCN Guidelines for Distress Management

● NCCN Guidelines for Survivorship

In addition,recommendations for fertility preservation can be found in the NCCN Guidelines for Adolescent and Young Adult (AYA) Oncology,and vaccination recommendations can be found in the NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections(both available at www.NCCN.org) and DHHS' Guidelines for he Prevention and Treatment of Opportunistic Infections in Adults and Adolescents With HIV, available at https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/immunizations).

The Panel notes some special considerations for PWH who have cancer. For instance, long-term steroid use should be limited in PWH

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because of the increased risk of opportunistic infections and other complications.

All PWH should be tested for hepatitis B by 3 tests: hepatitis B surface antigen (HBsAG), hepatitis B core antibody (anti-HBc) total immunoglobulin (Ig) or IgG, and antibody to HBsAG. Testing is required prior to the initiation of systemic therapy to avoid hepatic toxicity, but anticancer therapy should not be delayed. See Hepatitis B Virus Screening and Management for Patients With Cancer Prior to Therapy:ASCO Provisional Clinical Opinion Update and Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV.167,168

In addition, the risk of infections in PWH is increased during cancer treatment.70-74,77 Opportunistic infection prophylaxis thus plays a critical role in the supportive care of PWH who have cancer (see Opportunistic Infection Prophylaxis, above).

Recommendations for Specific Cancers in PWH

Anal Cancer in PWH

Anal cancer in PWH is often associated with persistent anal HPV infection, which is likely due to immune suppression.169 A meta-analysis of anal cancer burden across major groups known to be at elevated risk showed that anal cancer risk is highest among men who have sex with men(MSM) living with HIV, with incidence rates up to 85 times higher than in the general population (85 cases per 100,000 person-years vs.1-2 per 100,000, respectively). 170 Analysis of the French Hospital Database on HIV also showed a highly elevated risk of anal cancer in PWH, including in those who were on ART and whose CD4+ T-cell counts were high.171 In this analysis, the standardized incidence ratio(SIR) between MSM living with HIV compared to the general population was 109.8 (95% CI, 84.6-140.3) in the years 2005 to 2008. Between other men with HIV and the general population, it was 49.2 (95% CI,

33.2-70.3).For women with HIV, the corresponding SIR was 13.1(95%CI,6.8-22.8) compared to the general population. Overall, anal cancer accounts for approximately 7% of cancers diagnosed in PWH,15 and the current risk of anal cancer in PWH is elevated approximately 19-fold over the general U.S. population.19,172

Anal cancer is preceded by precursor lesions called anal intraepithelial neoplasia (AIN), which can be further subdivided into high-grade AlN (or high-grade squamous intraepithelial lesion, HSIL) and low-grade AlN (or low-grade squamous intraepithelial lesion, LSIL).173 Some evidence suggests that ART may be associated with a decrease in the incidence of high-grade AlN and its progression to anal cancer.174-176 However, the incidence of anal cancer in PWH has not decreased much, if at all, over time.10,19,171,172

Recommendations for the management of anal cancer are presented in the NCCN Guidelines for Anal Carcinoma(available at www.NCCN.org)and the NCCN Guidelines for Anal Carcinoma: Sub-Saharan Africa(available at www.NCCN.org/international-adaptations).

Screening for and Management of High-Grade Squamous Intraepithelial Lesions in PWH

PWH are at higher risk of HSIL compared to those without HIV.177 HSIL can be a precursor to anal cancer, 178-181 and treatment of HSIL may prevent the development of anal cancer by 57%.182 Based on the ANCHOR data, the International Anal Neoplasia Society(IAN) and DHHS have published guidelines recommending routine screening and treatment of HSIL in PWH.168,183 Although the details of their recommendations differ, there is consensus in initiating screening at age 35 years for MSM living with HIV and transgender women living with HIV, and at age 45 years for all other PWH. Additionally, the Panel recommends that PWH diagnosed with penile, vulvar, vaginal, or cervical disease undergo screening for anal cancer. Screening methods

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include anal cytology, high-risk HPV(hrHPV) testing, and digital anorectal exam(DARE). Some data suggest that screening protocols that include both cytology and HPV testing are most effective.184 If anal squamous intraepithelial lesions are identified by cytology or if there are anal symptoms or abnormal examinations, then high-resolution anoscopy(HRA) should be performed if available. Standard anoscopy is recommended if HRA is not available.

Multiple methods are used to treat anal dysplasia, including topical therapy(ie, fluorouracil, imiquimod), excision, and ablation.185-188 These treatments are safe in PWH and are associated with a decreased risk of progression to cancer.189-192 However, treatment of anal dysplasia in PWH is associated with a higher risk of recurrence compared to those without HIV.189,193 Due to this, a randomized, double-blind, placebo-controlled trial investigated if HPV vaccination could prevent high-grade AlN recurrence in MSM living with HIV, but found no preventive effect.194 In a randomized controlled trial of MSM who are HIV-positive,electrocautery(ablation) was found to be better than topical therapy in the treatment of anal dysplasia, even though recurrence rates were still high.195 Perianal AlN appeared to respond better to imiquimod than intra-anal AlN. An AIDS Malignancy Consortium trial randomized 120 patients with high-grade AlN to ablation or active monitoring.196 Complete or partial lesion clearance was more common in the treatment group(82% vs.47%;95% CI,16%-50%;P<.001). Adverse events included mild or moderate anal pain and bleeding.

The Anal Cancer/HSIL Outcomes Research(ANCHOR) study, a phase III trial, included 4446 PWH≥35 years with HSILs.192 Participants were randomized into two groups: treatment of the HSIL or active monitoring of HSIL without treatment. Study results found that the rate of progression to cancer was lower in the treatment group than in the active monitoring group by 57%(95% CI, 6-80; P=.03). The observed

rate of progression in the treatment group was 173 per 100,000 person-years (95% CI,90-332), compared to 402 per 100,000 person-years (95% CI,262-616) in the active monitoring group. Office-based electroacryation ablation (primarily hyfrecation) was the most frequent treatment modality in the trial(83.6% of patients). While the trial did not compare the efficacy of different methods to treat HSIL, the DHHS considers office-based hyfrecation to be a reasonable first-line treatment due to its low rate of serious adverse events observed in the trial.168

Furthermore, even with screening and treatment, there are high rates of progression of HSIL to cancer in PWH.192 HPV vaccination has been shown to reduce the rate of HPV type-associated HSILs; therefore,prevention of HPV acquisition and the subsequent development of anal HSIL in PWH are important.197,198 For recommendations regarding preventive HPV vaccination, see the NCCN Guidelines for Prevention and Treatment of Cancer-Related Infections (available at www.NCCN.org).

Workup for Anal Cancer in PWH

The NCCN Panel recommends that all patients with anal cancer should be tested for HIV if not already known to have a documented HIV infection. Viral load and CD4+ T-cell counts should be determined in PWH who have anal cancer. Low CD4+ T-cell counts prior to anal cancer treatment have been shown to be associated with an increased risk for acute hematologic toxicity.199,200 PWH with anal cancer should be referred to an HIV specialist if HIV care has not yet been established(see HIV Management During Cancer Therapy, above).

Additional workup for anal cancer in PWH should be performed as described in the NCCN Guidelines for Anal Carcinoma(available at www.NCCN.org).HPV-related disease in PWH is often multifocal.Therefore, PWH diagnosed with anal cancer should be evaluated for

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the presence of vulvar, vaginal, or cervical disease. Non-malignant causes for lymphadenopathy should be considered. Suspicious PET-avid lymphadenopathy should be biopsied to differentiate between nodal metastasis or infectious etiology(consult with an HIV specialist). If negative for cancer, refer for an infectious disease workup.

Management of Anal Cancer in PWH

Most evidence regarding outcomes in PWH with anal cancer comes from retrospective comparisons, a few of which found worse outcomes in PWH.201-204 Most studies, however, have found outcomes to be similar in PWH and those without HIV.144,151,152,200,205-208 For example,in a retrospective cohort study of 1184 veterans diagnosed with squamous cell carcinoma of the aus between 1998 and 2004(15% of whom tested positive for HIV), no differences with respect to receipt of treatment or 2-year survival rates were observed for PWH compared with patients without HIV.144 Furthermore, a population-based study of almost 2 million patients with cancer, 6459 of whom were living with HIV, found no increase in cancer-specific mortality for anal cancer in PWH.30 Some phase II studies in anal cancer have included PWH.209,210 Although the numbers of PWH in these trials have been small, the efficacy and safety results appear similar regardless of HIV status.

Based on these data, the NCCN Panel recommends that PWH should be treated for anal cancer as per the NCCN Guidelines for Anal Carcinoma (available at www.NCCN.org), and that modifications to cancer treatment should not be made solely on the basis of HIV status.Additionally, non-malignant causes for lymphadenopathy should be considered in PWH, with referral for an infectious disease workup if suspicious/PET-avid nodes are seen (also see Cancer Workup in PWH,above). Poor performance status in PWH and anal cancer may be from HIV, cancer, or other causes. The reason for poor performance status

should be considered when making treatment decisions. ART is recommended for all PWH and may improve performance status.

The phase II AIDS Malignancy Consortium 045 (AMC045) trial evaluated the safety and efficacy of cetuximab with cisplatin/5-FU and radiation in PWH with anal squamous cell carcinoma. Preliminary results from this trial and a similar trial in immunocompetent patients(Eastern Cooperative Oncology Group [ECOG] 3205), reported in 2012,were encouraging with acceptable toxicity and 2-year progression-free survival (PFS) rates of 92% (95% CI, 81%-100%) and 80% (95% CI,61%-90%) in the immunocompetent and PWH populations,respectively.211 Longer-term results from E3205 and AMC045 were published in 2017. In a post hoc analysis of E3205, the 3-year locregional failure rate was 21% (95% CI, 7%-26%).212 The toxicities associated with the regimen in ECOG 3205 (patients who were immunocompetent) were substantial, with grade 4 toxicity occurring in 32% of the study population and 3 treatment-associated deaths (5%). In AMC045 (PWH), the 3-year locregional failure rate was 20% (95% CI,10%-37%) by Kaplan-Meier estimate.213 Grade 4 toxicity and treatment-associated rates were similar to that seen in E3205, at 26% and 4%,respectively. The addition of cetuximab to standard chemoradiation is therefore not recommended in PWH or those without HIV with anal cancer at this time.

Surveillance and Survivorship in PWH Treated for Anal Cancer Surveillance following treatment of anal cancer in PWH should be performed as described in the NCCN Guidelines for Anal Carcinoma(available at www.NCCN.org). A small retrospective study of 93 patients with anal cancer found that recurrence rates were not affected by HIV status.207 However, a nationwide retrospective cohort study of 142 veterans with HIV with stage I-III anal cancer found that those with

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lower post-treatment CD4+ T-cell counts had an increased risk for cancer recurrence.199

Regular anal cytology can also be considered for the detection of anal dysplasia in survivors of anal cancer with HIV, although data informing its value in detection of recurrent anal cancer are lacking. If high-grade AIN is identified, then HRA should be performed if available.

PWH diagnosed with anal cancer should be counseled on infertility risks and referred for fertility counseling as appropriate. PWH who engage in receptive anal intercourse should discuss post-treatment pelvic physical therapy and anal dilators with an appropriate health care provider.

Cervical Cancer in PWH

Persistent infection with hrHPV, the etiologic agent of cervical cancer, is more likely in PWH than individuals without. 214-216 Furthermore, the incidence of cervical cancer in PWH is about 3 to 6 times higher than that in those without HIV.8,19,217-219 Some evidence suggests that ART lowers the risk of persistent HPV infection and the prevalence of cervical intraepithelial neoplasia (CIN), precursors of cervical cancer.220-224 In addition, initiation of ART may reduce the progression of CIN and incidence of cervical cancer.223,225 However, evidence that the incidence of cervical cancer in PWH has decreased significantly in the modern ART era is lacking. 8,10,12,19,226-228 In 2020, cervical cancer accounted for about 1% of cancers diagnosed in the HIV population. 229 This number is likely low because the U.S. HIV population is predominately male.Cervical cancer is a major health problem in low- and middle-income countries (LMIC) struggling with high HIV and HPV prevalence.

Recommendations for the management of cervical cancer in PWH are presented in the NCCN Guidelines for Cervical Cancer(available at www.NCCN.org). For recommendations for patients in sub-Saharan Africa, please see the NCCN Guidelines for Cervical Cancer: Sub-

Saharan Africa (available at www.NCCN.org/international-adaptations).For recommendations for other lower-resource areas, please see the NCCN Framework for Resource Stratification of NCCN Guidelines (NCCN FramworkTM) for Cervical Cancer (available at www.NCCN.org/framework).

Management of Precancerous Cervical Lesions in PWH Treatment options for CIN include cryotherapy, loop electrosurgical excision procedure (LEEP), and cold knife conization.230,231 These options are generally safe and effective for PWH.232-237 However,endocervical extension is more frequent among PWH.238 Therefore,loop excision is less effective and recurrence rates are higher in PWH than in those without HIV.238-241 A single-center randomized trial in Kenya, however, showed that LEEP for high-grade CINs (CIN2+)resulted in a significantly lower rate of cervical neoplasia recurrence over 24 months than cryotherapy in 400 PWH.242 A secondary subgroup analysis of this randomized controlled trial also found that LEEP was more likely to clear hrHPV infection compared to those undergoing cryotherapy.243 Persistent hrHPV infection is strongly associated with recurrent CIN2+, indicating that the benefits of LEEP may be attributed to its effectiveness in clearing hrHPV infection.

Additionally, a randomized, double-blind, placebo-controlled trial investigated if HPV vaccination prior to LEEP could prevent CIN2+recurrence in PWH but found no preventive effect.244

Workup for Cervical Cancer in PWH

The NCCN Panel recommends all patients with cervical cancer be tested for HIV if they are not already known to have a documented HIV infection. As in all cancers, PWH should be referred to an HIV specialist(see HIV Management During Cancer Therapy, above).

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Additional workup for cervical cancer in PWH should be performed as described in the NCCN Guidelines for Cervical Cancer (available at www.NCCN.org).In addition, PWH with CIN or invasive cervical cancer should also be evaluated for field effects of HPV oncogenesis, namely anal and vulvar cancer. Non-malignant causes for lymphadenopathy should be considered. Suspicious PET-avid lymphadenopathy should be biopsied to differentiate between nodal metastasis or infectious etiology (consult with HIV specialist). If negative for cancer, refer for an infectious disease workup.

Management of Cervical Cancer in PWH

A systematic review published in 2015 identified only 8 studies (3 prospective and 5 retrospective) addressing the management of cervical cancer in PWH.245 Hematopoietic grade 1 and 2 toxicity rates were higher in PWH than in patients without HIV. Grade 3 and 4 events that differed by HIV status were anemia (4% in PWH vs. 2%) and gastrointestinal reactions (5% in PWH vs. 2%). This systematic review also found that PWH who started ART early were more likely to complete cancer treatment. Additional data following the 2015 systematic review also suggest that PWH who have cervical cancer are more likely to experience hematologic toxicity and less likely to complete a full course of chemotherapy than patients without HIV. ${}^{246}$

A prospective cohort study of 348 patients with cervical cancer in Botswana compared outcomes between the 66% who were living with HIV and those who were not.37 The PWH had a median CD4+ T-cell count of 397 cells/μL(interquartile range, 264-555). Following an adjusted analysis, HIV infection was significantly associated with an increased risk of death among all patients(hazard ratio[HR], 1.95; 95%CI, 1.20-3.17) and among the subset of those who received guideline-concordant curative therapy(HR, 2.63; 95% CI, 1.05-6.55). These results suggest that HIV infection has an adverse effect on cervical

cancer survival. That this effect was greater for those with a lower CD4+T-cell count(P=.036) suggests that immune suppression plays a significant role. Of note, the study was conducted in a resource-limited environment, and survival of these patients, regardless of their HIV status, was lower than would be expected in the United States. Another study in Botswana included 143 patients with and without HIV who were treated with radiation therapy for cervical cancer.247 No differences were seen in 2-year overall survival or on acute toxicities between the participants with and without HIV. Other African studies have also shown that chemoradiation therapy is safe in PWH who have cervical cancer.248,249

Based on these limited data, the NCCN Panel recommends that PWH be treated for cervical cancer as per the NCCN Guidelines for Cervical Cancer (available at www.NCCN.org), and that modifications to cancer treatment should not be made solely on the basis of HIV status. The NCCN Panel also notes that non-malignant causes for lymphadenopathy should be considered in PWH who have cervical cancer, with referral for an infectious disease workup if suspicious/PET-avid nodes are seen (also see Cancer Workup in PWH, above). Poor performance status in PWH who have cervical cancer may be from HIV,cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions. ART is recommended for all PWH and may improve performance status.

Hodgkin Lymphoma in PWH

PWH are 5 to 14 times more likely to be diagnosed with Hodgkin lymphoma than individuals without HIV.9,10,18,19 The incidence of Hodgkin lymphoma in PWH increased through 2002,8,9 but studies that assessed the trends of incidence from 1996 through 2010 or 2012 found it to be decreasing.11,19 Evidence regarding the role of

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immunosuppression in the development of lymphoma are conflicting.3,18,250,251

Hodgkin lymphoma is classified into nodular lymphocyte-predominant Hodgkin lymphoma and classical Hodgkin lymphoma. Only classical Hodgkin lymphoma has been linked to HIV infection. Classical Hodgkin lymphoma is further subclassified as nodular sclerosis, lymphocyte-rich,mixed cellularity, and lymphocyte-depleted.252 PWH who develop Hodgkin lymphoma typically present with mixed cellularity or, less commonly, nodular sclerosis or lymphocyte-depleted histologies of classical disease.253-257

In contrast to individuals without HIV, nearly 90% of cases of Hodgkin lymphoma in PWH are EBV-associated.252.258 PWH often present with more advanced disease, including extranodal disease and bone marrow involvement.253,254,258,259 Bone-marrow-only presentations sometimes occur,260 whereas CNS involvement is rare.261 PWH with Hodgkin lymphoma have also been shown to present with more aggressive disease and worse performance status. However, they have similar response rates and short-term survival as patients without HIV when they receive standard cancer treatment.254,262,263

Recommendations for the management of Hodgkin lymphoma are presented in the NCCN Guidelines for Hodgkin Lymphoma(available at www.NCCN.org) and the NCCN Guidelines for Hodgkin Lymphoma:Sub-Saharan Africa(available at www.NCCN.org/international-adaptations).

Workup for Hodgkin Lymphoma in PWH

Approximately 4% of 22,355 patients with Hodgkin lymphoma in the SEER database from 2000 to 2010 were living with HIV at the time of diagnosis.264 The NCCN Panel recommends that all patients with Hodgkin lymphoma be tested for HIV if not already known to have a

documented HIV infection. PWH should be referred to an HIV specialist(see HIV Management During Cancer Therapy, above). Use of effective ART has been associated with increased cancer-specific survival and overall survival in PWH with Hodgkin lymphoma.61,265

Diagnosis and staging workup for Hodgkin lymphoma in PWH should be performed as described in the NCCN Guidelines for Hodgkin Lymphoma(available at www.NCCN.org). However, it should be noted that both opportunistic infection and HIV itself can lead to FDG-avid lymadenopathy and organ lesions(see Cancer Workup in PWH,above). Non-malignant causes for lymphadenopathy and organ lesions should be considered, with referral for an infectious disease evaluation as indicated.

Management of Hodgkin Lymphoma in PWH

Cancer mortality can be similar between PWH and those without HIV who have Hodgkin lymphoma.30,32,254 However, disparities in treatment received results in increased mortality in PWH whose cancer is not treated.41,42,266 In a population-based study of 2090 PWH, unadjusted 5-year overall survival was decreased in PWH compared to those without HIV(66% vs.80%), whereas the difference disappeared in those who received chemotherapy.266 One large database study, however, found that overall survival was decreased in PWH who have Hodgkin lymphoma(HR,1.47;95% CI,1.25-1.74), even though the population was matched by treatment characteristics.267 Cancer-specific survival was not assessed in this study.

Treatment with ABVD(doxorubicin, bleomycin, vinblastine, and dacarbazine) has been shown to be safe and effective in PWH who have Hodgkin lymphoma, with oncologic outcomes similar to those without HIV.254,256,259,263 Favorable results have also been seen with Stanford V (doxorubicin, vinblastine, mechlorethamine, vincristine,bleomycin, etoposide, and prednisone).268 BEACOPP(bleomycin,

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etoposide, doxorubicin,cyclophosphamide, vincristine, procarbazine,and prednisone) is also active but associated with more toxicity and treatment-related mortality than Stanford V and ABVD. 269,270 Recent data demonstrate that combining treuximab vedotin with AVD is highly active and safe in PWH.271

When using these regimens, ART with overlapping toxicities or direct interactions with chemotherapy should be avoided (see Systemic Therapy and Drug-Drug Interactions, above). DDIs are common in patients with Hodgkin lymphoma and HIV. For example, a clinically significant interaction between vinblastine and antivirtes ronavir and lopinavir has been associated with neurotoxicity and hematologic toxicity.272 Similarly, bentrumab vedotin and ronavitar or cobicistat are associated with excess hematologic toxicity.116 These ARVs should therefore be avoided whenever possible; ISTI-based regimens are preferred. When possible, an HIV pharmacist and an oncology pharmacist should be consulted regarding chemotherapy in PWH who have Hodgkin lymphoma. Also see Principles of Systemic Therapy and Drug-Drug Interactions in the algorithm and Systemic Therapy and Drug-Drug Interactions, above.

Autologous hematopoietic cell transplantation (HCT) also appears to be safe and effective in PWH who have recurrent/relapsed Hodgkin lymphoma. The AIDS Malignancy Consortium study 020 found that dose-reduced high-dose busulfan, cyclophosphamide, and autologous HCT were effective and well-tolerated in a selected group of PWH with Hodgkin lymphoma. ${}^{273}$ In addition, a retrospective matched cohort analysis showed that relapse, overall survival, and PFS were similar in patients with Hodgkin lymphoma who received autologous HCT,regardless of their HIV status. ${}^{255}$ A retrospective, multicenter, registry-based study in Europe also found autologous HCT to be a beneficial option in this population. ${}^{274}$ Most recently, autologous transplant was

established as a standard of care for PWH who have relapsed/refractory HIV-associated lymphomas in a study run jointly by the AMC and Blood& Marrow Transplant Clinical Trials Network(the BMT CTN 0803/AMC 071 trial) that included 15 patients with Hodgkin lymphoma and 25 patients with diffuse large B-cell lymphoma.275 Allogeneic HCT also appears to be safe in this population based on results of the phase II, prospective, multicenter BMT CTN-0903/AMC-080 trial, which included 17 PWH with acute leukemia, myelodysplasia,or lymphoma.63

Limited experience with PET/CT-guided therapy, based on interim or final post-treatment restaging in HIV-associated Hodgkin lymphoma,indicates that it is feasible, despite potential confounding factors (ie,non-malignant causes for PET-avid regions).276,277

Based on these data, the NCCN Panel recommends that PWH should be treated for Hodgkin lymphoma as per the NCCN Guidelines for Hodgkin Lymphoma(available at www.NCCN.org), and that modifications to cancer treatment should not be made solely on the basis of HIV status. Poor performance status in PWH who have Hodgkin lymphoma may be from HIV, cancer, or other causes. The reason for poor performance status should be considered when making treatment decisions. ART is recommended for all PWH and may improve performance status. ABVD is less toxic than Stanford V or BEACOPP and therefore may be preferred in PWH. Extrapolating from randomized data in the general Hodgkin lymphoma population,bleomycin can be discontinued after 2 cycles in PWH who have advanced-stage Hodgkin lymphoma and a PET/CT scan showing response.278 It is also reasonable to discontinue bleomycin in patients who have symptoms of pulmonary compromise or fall in diffusing capacity of the lungs for carbon monoxide(DLCO). Whereas the routine use of growth factors is not recommended during ABVD treatment

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because of concerns about possible adverse interactions/lung toxicity with bleomycin in the NCCN Guidelines for Hodgkin Lymphoma(available at www.NCCN.org), growth factors may be required in PWH especially if CD4+ T-cell counts are low and in the setting of prolonged severe neutropenia or neutropenic fever. Similarly, whereas dose reduction is not recommended for leukopenia with ABVD in the NCCN Guidelines for Hodgkin Lymphoma(available at www.NCCN.org), dose reductions in early cycles may be appropriate in PWH with advanced immunosuppression(CD4+ T-cell counts<200). Prophylaxis against pneumocystis pneumonia is necessary for all patients and herpes simplex virus(HSV)/varicella-zoster virus(VZV) prophylaxis should be strongly considered. Gram-negative prophylaxis with quinolones should be considered for those with neutropenia or CD4+ T-cell counts<100.

B symptoms, which include fever, drenching night sweats, and/or weight loss of>10% body weight, are common in PWH who have Hodgkin lymphoma.279 B symptoms may also indicate a concurrent opportunistic infection if CD4 counts are low.

Kaposi Sarcoma in PWH

The risk for Kaposi sarcoma in the setting of HIV has been as high as a 3640-fold increase over the general population,8-10,18,280 but this risk has declined in the ART era.8,11,19,226,281 Still, estimates indicate that the risk of Kaposi sarcoma in PWH between the years 2009 and 2012 was elevated approximately 498-fold compared with the general U.S.population.19 In 2010, Kaposi sarcoma accounted for approximately 12% of cancers diagnosed in PWH, with an estimated 765 to 910 cases diagnosed per year in the United States.229,282

Recommendations for the management of Kaposi sarcoma in PWH are presented in the NCCN Guidelines for Kaposi Sarcoma(available at www.NCCN.org).For recommendations for patients in sub-Saharan

Africa, please see the NCCN Guidelines for Kaposi Sarcoma: Sub-Saharan Africa(available at www.NCCN.org/international-adaptations).

Lung Cancer in PWH

Lung cancer rates among PWH declined 6% annually from 2001 to 2016.283 However, it is projected to become one of the most common cancers due to increased life expectancy in this population. ${ }^{15}$ The risk of lung cancer is about 2 to 5 times higher in PWH than in those without HIV. ${ }^{9,10,19,284}$ Some data suggest that the incidence of lung cancer in PWH has been declining since the beginning of the ART era, ${ }^{8,19}$ but other studies demonstrate an increase. ${ }^{12}$ Mortality is also increased in people with lung cancer who also have HIV, compared to those without HIV. ${ }^{285-287}$

Smoking is a well-known risk factor for lung cancer, and smoking prevalence is higher in PWH than in those without HIV. ${ }^{21,24,288}$ Thus,smoking likely contributes to the increased risk of lung cancer in PWH.However, immunosuppression also likely plays a role. ${ }^{3,289,290}$ Overall,PWH who smoke and are on ART are 6 to 13 times more likely to die of lung cancer than of HIV-associated causes.291

Recommendations for the management of lung cancer can be found in the NCCN Guidelines for Non-Small Cell Lung Cancer(available at www.NCCN.org), the NCCN Guidelines for Non-Small Cell Lung Cancer: Sub-Saharan Africa(available at www.NCCN.org/international-adaptations) and the NCCN Framework" for Non-Small Cell Lung Cancer (available at www.NCCN.org/framework).

Screening for Lung Cancer in PWH

Because of the increased risk for the development of lung cancer in PWH, lung cancer screening has the potential to play an important role in early detection in this population. In the National Lung Screening Trial(NLST), annual low-dose helical chest CT screening in patients at high

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risk who smoke was associated with a reduction in lung cancer-specific mortality. ${ }^{292,293}$ However, data informing the potential role of lung cancer screening in PWH are limited. ${ }^{294-296}$ One study assessed annual CT-based lung cancer screening (≤4 scans) in 224 PWH who actively and formerly smoked with a $\geq 20$ pack-year history. ${ }^{294}$ Screening between 2006 and 2013 identified 1 case of lung cancer in 678 patient-years.Another study assessed a single CT scan to screen for lung cancer in 442 PWH who smoke with a≥20 pack-year history and a CD4+ T-cell nadir count of<350 cells/μL.295 Lung cancer was diagnosed by CT scan in 9 patients (2.0%; 95% CI, 0.9-3.8). Longer follow-up of these trials should be informative.

At this time, the Panel recommends that screening for lung cancer should be performed in PWH based on the same criteria used in the general population (see the NCCN Guidelines for Lung Cancer Screening, available at www.NCCN.org).

Workup for Lung Cancer in PWH

The NCCN Panel recommends that all patients with NSCLC should be tested for HIV if not already known to have a documented HIV infection.PWH should be referred to an HIV specialist if they do not already have HIV care established(see HIV Management During Cancer Therapy,above).

PWH may be more likely to have alternative causes of lung nodules(see Cancer Workup in PWH, above). Infectious granuloma or TB are possible differential diagnoses as is Kaposi sarcoma or lymphoma.Consideration of alternative causes of lung lesions may warrant an infectious disease workup. The differential diagnosis should be considered before biopsy to inform studies to be performed on biopsy(ie, cultured for bacteria, fungi, and mycobacteria acid-fast bacilli[AFB]when relevant) and for consideration of biopsy risks. For example, if

<EndOfPara>pulmonary Kaposi sarcoma is strongly suspected, the risk of bleeding complications needs to be considered.

Non-malignant causes for lymphadenopathy should be considered.Suspicious PET-avid lymphadenopathy should be biopsied to differentiate between nodal metastasis or infectious etiology(consult with an HIV specialist). If negative for cancer, refer for an infectious disease workup. Similarly, workup of brain lesions in patients with NSCLC and advanced HIV-associated immunosuppression should include consideration of consultation with an HIV specialist and an infectious disease evaluation to rule out infectious processes(eg,toxoplasmosis) and other malignancies such as lymphoma (also see Cancer Workup in PWH, above). 98.99 Consideration of relative risks based on viral load and CD4+ T-cell count may further inform these assessments. Treatment for possible non-malignant diagnoses can be considered before biopsy.

Additional workup for NSCLC in PWH should be performed as described in the NCCN Guidelines for Non-Small Cell Lung Cancer(available at www.NCCN.org).

Management of Lung Cancer in PWH Some studies have shown that patients with lung cancer show similar outcomes regardless of their HIV status.297,298 Other studies, however,have found disparities in receipt of cancer treatment and/or survival.299,300 For example, a registry-based analysis found that PWH diagnosed with lung cancer between 1995 and 2009 were less likely to receive cancer treatment and had higher lung cancer-specific mortality.300 The effect of HIV on lung cancer-specific mortality was partially reduced in those who received cancer treatment. A phase II trial evaluated CaP(carboplatin plus pemetrezed) in patients with non-squamous NSCLC(NS-NSCLC) and HIV.301 Half the patients achieved a disease control rate(DCR)≥30%, which can be compared to 57%

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found in the general population with NS-NSCLC.302 Overall survival was shorter at 7.6 months compared to 13.4 months in the general population with NS-NSCLC.303 Furthermore, a single-center,retrospective cohort study that compared outcomes following resection in 22 PWH who have lung cancer with outcomes following resection in 2430 patients with lung cancer and unknown HIV status from 1985 to 2009 showed that the PWH group had more postoperative pulmonary and infectious complications (P=.001 and P<.001, respectively),faster disease progression (P=.061), and shorter survival (P=.001).304 In contrast, another study found that PWH who had lung cancer resections between 2000 and 2016 experienced similar short-term complications as patients without HIV.305

Overall, the NCCN Panel recommends that PWH should be treated for NSCLC as per the NCCN Guidelines for Non-Small Cell Lung Cancer(available at www.NCCN.org). In those guidelines, performance status is taken into consideration when making treatment decisions in patients with NSCLC. In PWH who have NSCLC, poor performance status may result from HIV, lung cancer, or other causes. ART is recommended for all PWH and may improve performance status. The Panel recommends that the reason for poor performance status should be considered when making treatment decisions. If poor performance status is the result of cancer-related symptoms that may be reversed with cancer therapy,treatment initiation should be strongly considered. As in other cancers,modifications to cancer therapy should not be made solely on the basis of HIV status.

As for all PWH who smoke, smoking cessation support should be offered to PWH with lung cancer as clinically indicated (see the NCCN Guidelines for Smoking Cessation, available at www.NCCN.org, and see Smoking Cessation in PWH Who Have Cancer, above).

DDIs can occur in patients with NSCLC and HIV. When possible, an HIV pharmacist and an oncology pharmacist should be consulted. Also see Principles of Systemic Therapy and Drug-Drug Interactions in the algorithm and Systemic Therapy and Drug-Drug Interactions above.

NHL in PWH

The risk of NHL is elevated 7- to 23-fold in PWH, with the risk being even higher for PWH with certain disease subtypes such as primary CNS lymphoma.8,9,18,19 The development of NHL in PWH is associated with recent immunosuppression and prolonged HIV viremia. ${ }^{306}$ In the ART era, the incidence of NHL has declined. 11,19 One study showed that the increased risk of NHL in PWH compared with the general population declined from 28-fold in 1996 to 1999 to 8-fold in 2009 to 2012.19 In 2010, NHL accounted for about 21% of cancers diagnosed in PWH. 229

For recommendations regarding the management of NHL in PWH, see the NCCN Guidelines for B-Cell Lymphomas(available at www.NCCN.org), the NCCN Guidelines for B-Cell Lymphomas: Sub-Saharan Africa(available at www.NCCN.org/international-adaptations),and, for other lower-resource regions, the NCCN FrameworkTM for B-Cell Lymphomas(available at www.NCCN.org/framework).

Management of Cancer in PWH in Lower Resource Settings

LMIC have been disproportionately affected by HIV. In fact, there were>20 million PWH in East and Southern Africa and almost 5 million in West and Central Africa in 2022, together accounting for 67% of global HIV incidence.307 As ART has become more accessible in LMIC, PWH have a decreased risk of AIDS development, improved survival, a decline in HIV-defining cancers, and an increase in non-AIDS-defining cancers, much like higher-resource regions experienced previously.308 Despite these declines, the burden of cervical cancer and Kaposi sarcoma has remained high in LMIC.308-310

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Cancer treatment in LMIC, however, is constrained by limited resources.311 In fact, cancer mortality is higher in Africa than in high-income countries.312 Research into effective cancer treatments that are more cost-effective and readily available in lower-resource regions are needed, but conducting clinical trials in these areas can be challenging.313

Overall, the Panel believes that most PWH who develop cancer in LMIC should be offered the same cancer therapies as individuals without HIV,and modifications to cancer treatment should not be made solely on the basis of HIV status. NCCN Guidelines that have been adapted for specific regions(eg, Latin America, the Middle East/North Africa, and Sub-Saharan Africa) and the NCCN Framework(TM(all available at www.NCCN.org) are resources that can help PWH worldwide who have cancer to receive the best care available.

Summary

Cancer treatment is generally as safe and effective for PWH as it is for patients without HIV, and the NCCN Panel recommends that most PWH who develop cancer should be offered the same cancer therapies as individuals without HIV. Modifications to cancer treatment should not be made solely based on HIV status. However, PWH who have cancer require special considerations, including the possible need to modify ART or cancer therapy based on the potential for DDIs, potential modifications to supportive care, the need for an infectious disease workup for possible non-malignant imaging findings, and the need for more intensive monitoring for toxicities. Furthermore, performance status is taken into consideration when making treatment decisions in patients with cancer. In PWH who have cancer, poor performance status may result from HIV, cancer, or other causes. The Panel recommends that the reason for poor performance status should be considered when making treatment decisions and notes that ART is

recommended for all PWH and may improve performance status.The Panel strongly recommends that an HIV specialist be involved in the care of PWH during cancer treatment.

Unfortunately, data on the treatment of PWH who have cancer are relatively limited. Increased accrual of this population to clinical trials should be a goal of the oncology community. Based on recommendations from the American Society of Clinical Oncology(ASCO) and Friends of Cancer Research HIV Working Group, PWH should not be excluded from cancer clinical trials if they meet specified criteria.314 Clinicians who work with PWH who have cancer should encourage participation in clinical trials(see www.clinicaltrials.gov).

As more evidence becomes available, the Panel will update these guidelines accordingly.

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25. Rentsch C,Tate JP,Akgun KM,et al.Alcohol-related diagnoses and all-cause hospitalization among HIV-infected and uninfected patients: a longitudinal analysis of United States veterans from 1997 to 2011. AIDS Behav 2016;20:555-564. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25711299.

26.Horner MJ, Shiels MS, Pfeiffer RM, Engels EA. Deaths as attributable to cancer in the US human immunodeficiency virus population during 2001-2015. Clin Infect Dis 2021;72:e224-e231. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32710777.

27. PubMed Overview. U.S. National Library of Medicine; 2023.Available at:https://pubmed.ncbi.nlm.nih.gov/about/. Accessed March 6,2025.

28. Freedman-Cass DA, Fischer T, Alpert AB, et al. The value and process of inclusion: Using sensitive, respectful, and inclusive language and images in NCCN content. J Natl Compr Canc Netw 2023;21:434-441. Available at: https://www.ncbi.nlm.nih.gov/pubmed/37156485.

29. Biggar RJ,Engels EA, Ly S,et al. Survival after cancer diagnosis in persons with AIDS. J Acquir Immune Defic Syndr 2005;39:293-299.

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30.Coghill AE, Shiels MS, Suneja G, Engels EA. Elevated cancer-specific mortality among HIV-infected patients in the United States. J Clin Oncol 2015;33:2376-2383. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26077242.

31. Coghill AE, Pfeiffer RM, Shiels MS, Engels EA. Excess mortality among HIV-infected individuals with cancer in the United States. Cancer

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

Epidemi Biomarkers Prev 2017;26:1027-1033. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28619832.

32. Marcus JL, Chao C, Leyden WA, et al. Survival among HIV-infected and HIV-uninfected individuals with common non-AIDS-defining cancers. Cancer Epidemiol Biomarkers Prev 2015;24:1167-1173.Available at: https://www.ncbi.nlm.nih.gov/pubmed/25713023.

33. Coghill AE, Suneja G, Rositch AF, et al. HIV infection, cancer treatment regimens, and cancer outcomes among elderly adults in the United States. JAMA Oncol 2019;5. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31369037.

34. Brandao M, Bruzzone M, Franzoi MA, et al. Impact of HIV infection on baseline characteristics and survival of women with breast cancer AIDS 2021;35:605-618. Available at:https://www.ncbi.nlm.nih.gov/pubmed/3394680.

35. Brock MV, Hooker CM, Engels EA, et al. Delayed diagnosis and elevated mortality in an urban population with HIV and lung cancer:implications for patient care. J Acquir Immune Defic Syndr 2006;43:47-55. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16936558.

36. Ferreira MP, Coghill AE, Chaves CB, et al. Outcomes of cervical cancer among HIV-infected and HIV-uninfected women treated at the Brazilian National Institute of Cancer. AIDS 2017;31:523-531. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28060014.

37.Dryden-Peterson S,Bvoochora-Nsingo M,Suneja G,et al.HIV infection and survival among women with cervical cancer. J Clin Oncol 2016;34:3749-3757.Available at:https://www.ncbi.nlm.nih.gov/pubmed/27573661.

38.Coghill AE,Han X,Suneja G,et al.Advanced stage at diagnosis and elevated mortality among US patients with cancer infected with HIV in the National Cancer Data Base. Cancer 2019;125:2868-2876.Available at:https://www.ncbi.nlm.nih.gov/pubmed/31050361.

39. Marcus JL, Leyden WA, Alexeeff SE, et al. Comparison of overall and comorbidity-free life expectancy between insured adults with and without HIV infection, 2000-2016. JAMA Netw Open 2020;3:e207954.Available at: https://www.ncbi.nlm.nih.gov/pubmed/32539152.

40. Islam JY, Nogueira L, Suneja G, et al. Palliative care use among people living with HIV and cancer: An analysis of the National Cancer Database(2004-2018). JCO Oncol Pract 2022;18:e1683-e1693.Available at:https://www.ncbi.nlm.nih.gov/pubmed/35867956.

41. Suneja G,Lin CC,Simard EP,et al.Disparities in cancer treatment among patients infected with the human immunodeficiency virus.Cancer 2016;122:2399-2407.Available at:https://www.ncbi.nlm.nih.gov/pubmed/27187086.

42.Suneja G,Shiels MS,Angulo R,et al.Cancer treatment disparities in HIV-infected individuals in the United States. J Clin Oncol 2014;32:2344-2350. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24982448.

43. Rositch AF, Jiang S, Coghill AE, et al. Disparities and determinants of cancer treatment in elderly Americans living with human immunodeficiency virus/AIDS. Clin Infect Dis 2018;67:1904-1911.

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44. Levinson KL, Riedel DJ, Ojalvo LS, et al. Gynecologic cancer in HIV-infected women: treatment and outcomes in a multi-institutional cohort. AIDS 2018;32:171-177. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29028665.

45.Suneja G,Boyer M,Yehia BR,et al.Cancer treatment in patients with HIV infection and non-AIDS-defining cancers: a survey of US oncologists. J Oncol Pract 2015;11:e380-387. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25873060.

46.McGee-Avila JK,Suneja G,Engels EA,et al.Cancer Treatment Disparities in People With HIV in the United States, 2001-2019. J Clin Oncol 2024;42:1810-1820. Available at:https://www.ncbi.nlm.nih.gov/pubmed/38513161.

![NCCN\n](2/aj0YEe4oUhYkBdfpda0fYP/figure749646d2cd18417198e4cecce0c86784_0_1.png)

National Comprehensive Cancer Network®

NCCN Guidelines Version 1.2026 Cancer in People with HIV

47. Marks G, Repacz N, Senterfitt JW, Janssen RS. Meta-analysis of high-risk sexual behavior in persons aware and unaware they are infected with HIV in the United States: implications for HIV prevention programs. J Acquir Immune Defic Syndr 2005;39:446-453. Available at:https://www.ncbi.nlm.nih.gov/pubmed/16010168.

48.HIV Testing.CDC.gov;2023.Available at:https://www.cdc.gov/hiv/testing/index.html. Accessed March 6,2025.

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49.Chiao EY, Dezube BJ, Krown SE, et al. Time for oncologists to opt in for routine opt-out HIV testing? JAMA 2010;304:334-339. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20639567.

50. Ramsey SD, Unger JM, Baker LH, et al. Prevalence of hepatitis B Virus, hepatitis C Virus, and HIV infection among patients with newly diagnosed cancer from academic and community oncology practices.JAMA Oncol 2019;5:497-505. Available at:https://www.ncbi.nlm.nih.gov/pubmed/30653226.

51. Hwang JP, Granwehr BP, Torres HA, et al. HIV testing in patients with cancer at the initiation of therapy at a large US comprehensive cancer center. J Oncol Pract 2015;11:384-390. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26243649.

52.Li J,Thompson TD,Tai E,et al. Testing for human immunodeficiency virus among cancer survivors under age 65 in the United States. Prev Chronic Dis 2014;11:E200. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25393748.

53. HIV Care Continuum.HIV.gov;2022.Available at:https://www.hiv.gov/federal-response/policies-issues/hiv-aids-care-continuum.Accessed March 6,2025.

54. Flash CA, Pasalar S, Hemmige V, et al. Benefits of a routine opt-out HIV testing and linkage to care program for previously diagnosed patients in publicly funded emergency departments in Houston, TX.J Acquir Immune Defic Syndr 2015;69 Suppl 1:S8-15. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25867782.

55. Irvine MK, Chamberlin SA, Robbins RS, et al. Improvements in HIV care engagement and viral load suppression following enrollment in a comprehensive HIV care coordination program. Clin Infect Dis 2015;60:298-310. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25301208.

56. Kitahata MM, Gange SJ, Abraham AG, et al. Effect of early versus deferred antiretroviral therapy for HIV on survival. N Engl J Med 2009;360:1815-1826. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19339714.

57. Silverberg MJ, Neuhaus J, Bower M, et al. Risk of cancers during interrupted antiretroviral therapy in the SMART study. AIDS 2007;21:1957-1963. Available at:https://www.ncbi.nlm.nih.gov/pubmed/1721103.

58. Silverberg MJ, Leyden W, Hernandez-Ramirez RU, et al. Timing of antiretroviral therapy initiation and risk of cancer among persons living with human immunodeficiency virus. Clin Infect Dis 2021;72:1900-1909.Available at:https://www.ncbi.nlm.nih.gov/pubmed/32785640.

59. Chammartin F,Lodi S,Logan R,et al.Risk for non-AIDS-defining and AIDS-defining cancer of early versus delayed initiation of antiretroviral therapy: A multinational prospective cohort study. Ann Intern Med 2021:174:768-776. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33721519.

60. El-Sadr WM, Lundgren J, Neaton JD, et al. CD4+ count-guided interruption of antiretroviral treatment. N Engl J Med 2006;355:2283-2296. Available at:https://www.ncbi.nlm.nih.gov/pubmed/17135583.

61. Hessol NA, Pipkin S, Schwarcz S, et al. The impact of highly active antiretroviral therapy on non-AIDS-defining cancers among adults with AIDS. Am J Epidemiol 2007;165:1143-1153. Available at:https://www.ncbi.nlm.nih.gov/pubmed/17344204.

62.Gerard L,Galicier L, Maillard A, et al. Systemic non-Hodgkin lymphoma in HIV-infected patients with effective suppression of HIV replication: persistent occurrence but improved survival. J Acquir

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

Immune Defic Syndr 2002;30:478-484. Available at:https://www.ncbi.nlm.nih.gov/pubmed/12154338.

63.Ambinder RF,Wu J,Logan B,et al.Allogeneic hematopoietic cell transplant for HIV patients with hematologic malignancies: The BMT CTN-0903/AMC-080 Trial.Biol Blood Marrow Transplant 2019;25:2160-2166. Available at: https://www.ncbi.nlm.nih.gov/pubmed/31279752.

64. Calkins KL,Chander G,Joshu CE,et al.Immune status and associated mortality after cancer treatment among individuals with HIV in the antiretroviral therapy era. JAMA Oncol 2020;6:227-235. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31804663.

65. Sparano JA, Hu X, Wiernik PH, et al. Opportunistic infection and immunologic function in patients with human immunodeficiency virus-associated non-Hodgkin's lymphoma treated with chemotherapy. J Natl Cancer Inst 1997;89:301-307. Available at:https://www.ncbi.nlm.nih.gov/pubmed/9048834.

66. Buchacz K, Baker RK, Palella FJ, Jr.,et al. AIDS-defining opportunistic illnesses in US patients, 1994-2007: a cohort study. AIDS 2010;24:1549-1559. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20502317

67. Ledgerber B, Egger M, Erard V, et al. AIDS-related opportunistic illnesses occurring after initiation of potent antiretroviral therapy: the Swiss HIV Cohort Study. JAMA 1999;282:2220-2226. Available at:https://www.ncbi.nlm.nih.gov/pubmed/10605973.

68. Schwarcz L, Chen MJ, Vittinghoff E,et al. Declining incidence of AIDS-defining opportunistic illnesses: results from 16 years of population-based AIDS surveillance. AIDS 2013;27:597-605. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23079812.

69.Djawe K, Buchacz K, Hsu L, et al. Mortality risk after AIDS-defining opportunistic illness among HIV-infected persons--San Francisco, 1981-2012. J Infect Dis 2015;212:1366-1375. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26044289.

70. Borg C, Ray-Coquard I, Philip I, et al. CD4 lymphopenia as a risk factor for febrile neutropenia and early death after cytotoxic chemotherapy in adult patients with cancer. Cancer 2004;101:2675-2680. Available at:https://www.ncbi.nlm.nih.gov/pubmed/15503313.

71.Dale DC, McCarter GC, Crawford J., Lyman GH. Myelotoxicity and dose intensity of chemotherapy: reporting practices from randomized clinical trials. J Natl Compr Canc Netw 2003;1:440-454. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19761076.

72.Seropian S,Nadkarni R,Jilella AP,et al.Neutropenic infections in 100 patients with non-Hodgkin's lymphoma or Hodgkin's disease treated with high-dose BEAM chemotherapy and peripheral blood progenitor cell transplant: out-patient treatment is a viable option. Bone Marow Transplant 1999;23:599-605. Available at:https://www.ncbi.nlm.nih.gov/pubmed/10217191.

73. Savage DG, Lindenbaum J, Garrett TJ. Biphasic pattern of bacterial infection in multiple myeloma. Ann Intern Med 1982;96:47-50. Available at:https://www.ncbi.nlm.nih.gov/pubmed/6976144.

74.Griffiths H, Lea J, Bunch C, et al. Predictors of infection in chronic lymphocytic leukaemia(CLL). Clin Exp Immunol 1992;89:374-377.Available at:https://www.ncbi.nlm.nih.gov/pubmed/1516254.

75. Bodey GP, Buckley M, Sathe YS, Freireich EJ. Quantitative relationships between circulating leukocytes and infection in patients with acute leukemia. Ann Intern Med 1966;64:328-340. Available at:http://www.ncbi.nlm.nih.gov/pubmed/5216294.

76. Schimpff SC.Empiric antibiotic therapy for granulocytopenic cancer patients. Am J Med 1986;80:13-20. Available at:http://www.ncbi.nlm.nih.gov/pubmed/3521270.

77. Morrison VA. Immunosuppression associated with novel chemotherapy agents and monoclonal antibodies. Clin Infect Dis 2014;59 Suppl 5:S360-364. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25352632.

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

78. Ngidi S, Magula N, Sartorius B, et al. Incidence of chemotherapy-induced neutropenia in HIV-infected and uninfected patients with breast cancer receiving neoadjuvant chemotherapy. S Afr Med J 2017;107:595-601. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29025449.

79. Park J, Kim TM, Hwang JH, et al. Risk factors for febrile neutropenia during chemotherapy for HIV-related lymphoma. J Korean Med Sci 2012;27:1468-1471. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23255844.

80. Wang ES, Straus DJ, Teruya-Feldstein J, et al. Intensive chemotherapy with cyclophosphamide, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine(CDOX-M/IVAC) for human immunodeficiency virus-associated Burkitt lymphoma. Cancer 2003;98:1196-1205. Available at:https://www.ncbi.nlm.nih.gov/pubmed/12973843.

81. Reddy KP, Kruse GR, Lee S, et al. Tobacco use and treatment of tobacco dependence among people with human immunodeficiency virus: A practical guide for clinicians. Clin Infect Dis 2022;75:525-533.Available at:https://www.ncbi.nlm.nih.gov/pubmed/34979543.

82. Baser S, Shannon VR, Eapen GA, et al. Smoking cessation after diagnosis of lung cancer is associated with a beneficial effect on performance status. Chest 2006;130:1784-1790. Available at:https://www.ncbi.nlm.nih.gov/pubmed/17166997.

83. Parsons A, Daley A, Begh R, Aveyard P. Influence of smoking cessation after diagnosis of early stage lung cancer on prognosis:systematic review of observational studies with meta-analysis. BMJ 2010;340:b5569. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20093278.

84. Mason DP, Subramanian S, Nowicki ER, et al. Impact of smoking cessation before resection of lung cancer: a Society of Thoracic Surgeons General Thoracic Surgery Database study. Ann Thorac Surg 2009;88:362-370; discussion 370-361. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19632374.

85.Khuri FR,Kim ES,Lee JJ,et al.The impact of smoking status,disease stage, and index tumor site on second primary tumor incidence and tumor recurrence in the head and neck retinoid chemoprevention trial.Cancer Epidemiol Biomarkers Prev 2001;10:823-829. Available at:https://www.ncbi.nlm.nih.gov/pubmed/11489748.

86. Roach MC, Rehman S, DeWees TA, et al. It's never too late:smoking cessation after stereotactic body radiation therapy for non-small cell lung carcinoma improves overall survival. Pract Radiat Oncol 2016;6:12-18. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26598909.

87.Dobson Amato KA, Hyland A, Reed R, et al. Tobacco cessation may improve lung cancer patient survival. J Thorac Oncol 2015;10:1014-1019. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26102442.

88. Richardson GE, Tucker MA, Venzon DJ, et al. Smoking cessation after successful treatment of small-cell lung cancer is associated with fewer smoking-related second primary cancers. Ann Intern Med 1993;119:383-390. Available at:https://www.ncbi.nlm.nih.gov/pubmed/8393311.

89.Kuri M, Nakagawa M, Tanaka H, et al. Determination of the duration of preoperative smoking cessation to improve wound healing after head and neck surgery. Anesthesiology 2005;102:892-896. Available at:https://www.ncbi.nlm.nih.gov/pubmed/15851873.

90.Ashare RL,Bernstein SL,Schnoll R,et al.The United States National Cancer Institute's coordinated research effort on tobacco use as a major cause of morbidity and mortality among people with HIV.Nicotine Tob Res 2021;23:407-410. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32803251.

91. Davison JM, Subramaniam RM, Surasi DS, et al. FDG PET/CT in patients with HIV.AJR Am J Roentgenol 2011;197:284-294.Available at:https://www.ncbi.nlm.nih.gov/pubmed/21785073.

![NCCN\n](2/aj0YEe4oUhYkBdfpda0fYP/figuref946f700e9964d1f8186da4d0dbd853f_0_1.png) ![National\nNCCN\nComprehensive\nNCCN\nNetwork®\n](2/aj0YEe4oUhYkBdfpda0fYP/figure27c2db81fc8c4417b039dd974febccfd_0_2.png)

NCCN Guidelines Version 1.2026 Cancer in People with HIV

92. Goodman PC. Radiographic assessment of HIV-associated diseases. HIV InSite 2006. Available at:

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93. Scharko AM, Perlman SB, Pyzalski RW, et al. Whole-body positron emission tomography in patients with HIV-1 infection. Lancet 2003;362:959-961. Available at:

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94. Brust D, Polis M, Davey R, et al. Fluorodeoxyglucose imaging in healthy subjects with HIV infection: impact of disease stage and therapy on pattern of nodal activation. AIDS 2006;20:985-993. Available at:https://www.ncbi.nlm.nih.gov/pubmed/16603850.

95. Goshen E, Davidson T, Vavigador A, et al. PET/CT in the evaluation of lymphoma in patients with HIV-1 with suppressed viral loads. Clin Nucl Med 2008;33:610-614. Available at:

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96. Allen CM, Al-Jahdali HH, Irion KL,et al. Imaging lung manifestations of HIV/AIDS. Ann Thorac Med 2010;5:201-216. Available at:

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97.Gingo MR, Morris A. Pathogenesis of HIV and the lung. Curr HIV/AIDS Rep 2013;10:42-50. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23079728.

98. Langford TD, Letendre SL, Larrea GJ, Masliah E. Changing patterns in the neuropathogenesis of HIV during the HAART era. Brain Pathol 2003;13:195-210. Available at:

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99.Gottumukkala RV, Romero JM, Riascos RF, et al. Imaging of the brain in patients with human immunodeficiency virus infection. Top Magn Reson Imaging 2014;23:275-291. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25296273.

100. Acosta MC, Kundro M, Viloria G, et al. The role of brain biopsy in the clinical management of HIV-related focal brain lesions. HIV Med

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101. Sathege M, Maes A, Van de Wiele C. FDG-PET imaging in HIV infection and tuberculosis. Semin Nucl Med 2013;43:349-366. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23905617.

102. Restrepo CS, Lemos DF, Gordillo H, et al. Imaging findings in musculoskeletal complications of AIDS. Radiographics 2004;24:1029-1049. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15256627.

103. Mangioni D, Bandera A, Muscatello A, et al. Focal bone lesions in HIV-positive patient treated with tenofovir. BMC Infect Dis 2014;14:131.Available at:https://www.ncbi.nlm.nih.gov/pubmed/24602357.

104. Yee J, Wall SD. Gastrointestinal manifestations of AIDS.Gastroenterol Clin North Am 1995;24:413-434. Available at:https://www.ncbi.nlm.nih.gov/pubmed/7642250.

105. Lefkowitch JH. Pathology of AIDS-related liver disease. Dig Dis 1994;12:321-330. Available at:https://www.ncbi.nlm.nih.gov/pubmed/7712615.

106. Sparano JA, Wiernik PH, Hu X, et al. Saquinavir enhances the mucosal toxicity of infusional cyclophosphamide, doxorubicin, and etoposide in patients with HIV-associated non-Hodgkin's lymphoma.Med Oncol 1998;15:50-57. Available at:https://www.ncbi.nlm.nih.gov/pubmed/9643531.

107.Rudek MA,Flexner C,Ambinder RF. Use of antineoplastic agents in patients with cancer who have HIV/AIDS. Lancet Oncol 2011;12:905-912. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24602357.

108.Torres HA, Mulanovich V. Management of HIV infection in patients with cancer receiving chemotherapy. Clin Infect Dis 2014;59:106-114.Available at:https://www.ncbi.nlm.nih.gov/pubmed/24642555.

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

109. Larson KB, Wang K, Delille C, et al. Pharmacokinetic enhancers in HIV therapeutics. Clin Pharmacokinet 2014;53:865-872. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25164142.

110.Deeken JF,Beumer JH,Anders NM,et al.Preclinical assessment of the interactions between the antiretroviral drugs, ritonavir and efavirenz, and the tyrosine kinase inhibitor erlotinib. Cancer Chemother Pharmacol 2015;76:813-819. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26330331.

111.Rudek MA, Chang CY, Steadman K, et al. Combination antiretroviral therapy (cART) component ritonavir significantly alters docetaxel exposure. Cancer Chemother Pharmacol 2014;73:729-736.Available at:https://www.ncbi.nlm.nih.gov/pubmed/24488374.

112. Boosman RJ, de Gooijer CJ, Groenland SL, et al. Ritonavir-boosted exposure of kinase inhibitors: An open label, cross-over pharmacokinetic proof-of-concept trial with erlotinib. Pharm Res 2022;39:669-676. Available at:https://www.ncbi.nlm.nih.gov/pubmed/35352280.

113. Rudek MA, Moore PC, Mitsuyasu RT, et al. A phase 1/pharmacokinetic study of unitinib in combination with highly active antiretroviral therapy in human immunodeficiency virus-positive patients with cancer: AIDS Malignancy Consortium trial AMC 061. Cancer 2014;120:1194-1202. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24474568.

114. Rubinstein PG, Braik T, Jain S,et al. Ritonavir based highly active retroviral therapy(HAART) correlates with early neurotoxicity when combined with ABVD treated HIV associated Hodgkin lymphoma but not non-Hodgkin lymphoma. A retrospective study[abstract]. Blood 2010;116:2807. Available at:http://www.bloodjournal.org/content/116/21/2807.

115. Cingolani A, Torti L, Pinnetti C,et al. Detrimental clinical interaction between ritonavir-boostate protease inhibitors and vinblastine in HIV-infected patients with Hodgkin's lymphoma. AIDS 2010;24:2408-2412.Available at:https://www.ncbi.nlm.nih.gov/pubmed/20671541.

116. Rubinstein PG, Moore PC, Rudek MA, et al. Brentuximab vedotin with AVD shows safety, in the absence of strong CYP3A4 inhibitors, in newly diagnosed HIV-associated Hodgkin lymphoma. AIDS 2018;32:605-611. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29280762.

117. Casado JL, Machuca I, Banon S, et al. Raltegravir plus two nucleoside analogues as combination antiretroviral therapy in HIV-infected patients who require cancer chemotherapy. Antivir Ther 2015;20:773-777. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25879675.

118.Torres HA,Rallapalli V,Saxena A,et al.Efficacy and safety of antiretrovirals in HIV-infected patients with cancer. Clin Microbiol Infect 2014;20:0672-679. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24529214.

119.Moyle GJ, Sadler M. Peripheral neuropathy with nucleoside antiretrovirals: risk factors, incidence and management. Drug Saf 1998;19:481-494. Available at:https://www.ncbi.nlm.nih.gov/pubmed/9880091.

120.Bower M, McCall-Peat N, Ryan N, et al. Protease inhibitors potentiate chemotherapy-induced neutropenia. Blood 2004;104:2943-2946. Available at:https://www.ncbi.nlm.nih.gov/pubmed/15238428.

121. Bower M, Powles T, Stebbing J, Thirlwell C. Potential antiretroviral drug interactions with cyclophosphamide, doxorubicin, and etoposide.J Clin Oncol 2005;23:1328-1329; author reply 1329-1330. Available at:https://www.ncbi.nlm.nih.gov/pubmed/15718342.

122. Hughes CA, Robinson L, Tseng A, MacArthur RD. New antiretroviral drugs: a review of the efficacy, safety, pharmacokinetics,and resistance profile of tipranavir, darunavir, etravirine, rilipivirine, maraviroc, and raltegravir. Expert Opin Pharmacother 2009;10:2445-2466. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19678794.

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123. Ly T, Ruiz ME. Prolonged QT interval and torsades de points associated with atazanavir therapy. Clin Infect Dis 2007;44:e67-68.Available at:https://www.ncbi.nlm.nih.gov/pubmed/17304444.

124. Behrens G, Dejam A, Schmidt H, et al. Impaired glucose tolerance,beta cell function and lipid metabolism in HIV patients under treatment with protease inhibitors. AIDS 1999;13:F63-70. Available at:https://www.ncbi.nlm.nih.gov/pubmed/10416516.

125. Shah NJ, Al-Shbool G, Blackburn M, et al. Safety and efficacy of immune checkpoint inhibitors (ICIs) in cancer patients with HIV,hepatitis B, or hepatitis C viral infection. J Immunother Cancer 2019;7:353. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31847881.

126. Polizzotto MN, Uldrick TS, Wyvill KM, et al. Clinical features and outcomes of patients with symptomatic Kaposi sarcoma herpesvirus(KSHV)-associated inflammation: Prospective characterization of KSHV inflammatory cytokine syndrome(KICS). Clin Infect Dis 2016;62:730-738. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26658701.

127. Cook MR, Kim C. Safety and efficacy of immune checkpoint inhibitor therapy in patients with HIV infection and advanced-stage cancer: A systematic review. JAMA Oncol 2019;5:1049-1054. Available at:at:https://www.ncbi.nlm.nih.gov/pubmed/30730549.

128.Tio M,Rai R,Ezeoke OM,et al. Anti-PD-1/PD-L1 immunotherapy in patients with solid organ transplant, HIV or hepatitis B/C infection. Eur J Cancer 2018;104:137-144. Available at:https://www.ncbi.nlm.nih.gov/pubmed/30347289.

129. Ostios-Garcia L, Faig J, Leonardi GC, et al. Safety and efficacy of PD-1 inhibitors among HIV-positive patients with non-small cell lung cancer. J Thorac Oncol 2018;13:1037-1042. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29631035.

130.Chang E,Sabichi AL,Kramer JR,et al. Nivolumab treatment for cancers in the HIV-infected population. J Immunother 2018;41:379-383.Available at:https://www.ncbi.nlm.nih.gov/pubmed/30020193.

131.Galanina N, Goodman A, Goodman AM, Cohen PR, et al. Successful treatment of HIV-associated Kaposari sarcoma with immune checkpoint blockade.Cancer Immunol Res 2018;6:1129-1135. Available at:https://www.ncbi.nlm.nih.gov/pubmed/30194084.

132.Chang E, Rivero G, Patel NR, et al. HIV-related refractory Hodgkin lymphoma: A case report of complete response to nivolumab. Clin Lymphoma Myeloma Leuk 2018;18:e143-e146. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29342442.

133. Gonzalez-Cao M, Moran T, Dalmau J, et al. Assessment of the feasibility and safety of durvalumab for treatment of solid tumors in patients with HIV-1 infection: The Phase 2 DURVAST Study. JAMA Oncol 2020;6:1063-1067. Available at:https://www.ncbi.nlm.nih.gov/pubmed/3271353.

134.Spano JP, Veyri M, Gobert A, et al. Immunotherapy for cancer in people living with HIV: safety with an efficacy signal from the series in real life experience. AIDS 2019;33:F13-F19. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31259762.

135. Luo L, Xu Y, Li T. Immune checkpoint inhibitor therapy for cancer patients infected with HIV: A systematic review. Asia Pac J Clin Oncol 2022;18:e17-e22. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32506823.

136. Lavole A, Mazieres J, Schneider S, et al. Assessment of nivolumab in HIV-Infected patients with advanced non-small cell lung cancer after prior chemotherapy. The IFCT-1602 CHIVA2 phase 2 clinical trial. Lung Cancer 2021;158:146-150. Available at:https://www.ncbi.nlm.nih.gov/pubmed/34217967.

137.Uldrick TS, Goncalves PH, Abdul-Hay M,et al.Assessment of the safety of pembrolizumab in patients with HIV and advanced cancer-A phase 1 study.JAMA Oncol 2019;5:1332-1339. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31154457.

138.Fujita K,Yamamoto Y, Kanai O, et al. Development of Mycobacterium Avium Complex Lung Disease in Patients With Lung

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Cancer on Immune Checkpoint Inhibitors. Open Forum Infect Dis 2020;7:ofaa067. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32190712.

139. Bae S, Kim YJ, Kim MJ, et al. Risk of tuberculosis in patients with cancer treated with immune checkpoint inhibitors: a nationwide observational study. J Immunother Cancer 2021;9. Available at:https://www.ncbi.nlm.nih.gov/pubmed/34521732.

140.Zaemes J, Kim C. Immune checkpoint inhibitor use and tuberculosis: a systematic review of the literature. Eur J Cancer 2020;132:168-175. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32375103.

141.Suliman AM, Bek SA, Elkhatim MS,et al. Tuberculosis following programmed cell death receptor-1(PD-1) inhibitor in a patient with non-small cell lung cancer. Case report and literature review. Cancer Immunol Immunol 2021;70:935-944. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33070259.

142. AnidiU, Sakai S, Brooks K, et al. Exacerbation of CMV and nontuberculous mycobacterial infections following PD-1 blockade for HIV-associated Kaposi Sarcoma. Open Forum Infect Dis 2024;11:ofae183. Available at:https://www.ncbi.nlm.nih.gov/pubmed/38680611

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143. Alongi F, Giaj-Levra N, Sciascia S, et al. Radiotherapy in patients with HIV: current issues and review of the literature. Lancet Oncol 2017;18:e379-e393. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28677574.

144.Chiao EY,Giordano TP,Richardson P,El-Serag HB.Human immunodeficiency virus-associated squamous cell cancer of the anus:epidemiology and outcomes in the highly active antiretroviral therapy era.J Clin Oncol 2008;26:474-479. Available at:http://www.ncbi.nlm.nih.gov/pubmed/18202423.

145.Seo Y,Kinsella MT, Reynolds HL,et al. Outcomes of chemoradiotherapy with 5-Fluorouracil and mitomycin C for anal cancer in immunocompetent versus immunodeficient patients. Int J Radiat Oncol Biol Phys 2009;75:143-149. Available at:http://www.ncbi.nlm.nih.gov/pubmed/19203845.

146. Lord RV. Anorectal surgery in patients infected with human immunodeficiency virus: factors associated with delayed wound healing.Ann Surg 1997;226:92-99. Available at:https://www.ncbi.nlm.nih.gov/pubmed/9242343.

147. Burke EC, Orloff SL, Freise CE, et al. Wound healing after anorectal surgery in human immunodeficiency virus-infected patients.Arch Surg 1991;126:1267-1270; discussion 1270-1261. Available at:https://www.ncbi.nlm.nih.gov/pubmed/1929828.

148. Buehr JL, Weber DJ, Meyer AA, et al. Wound infection rates after invasive procedures in HIV-1 seropositive versus HIV-1 seronegative hemophiliacs. Ann Surg 1990;21:492-498. Available at:https://www.ncbi.nlm.nih.gov/pubmed/2322041.

149. Horberg MA, Hurley LB, Klein DB, et al. Surgical outcomes in human immunodeficiency virus-infected patients in the era of highly active antiretroviral therapy. Arch Surg 2006;141:1238-1245. Available at:https://www.ncbi.nlm.nih.gov/pubmed/1718967.

150. Chi A, Adams BE, Sesti J, et al. Outcomes following major oncologic operations for non-AIDS-defining cancers in the HIV population: A matched comparison to the general population. World J Surg 2019;43:3019-3026. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31493193.

151. Alfa-Wali M, Dalla Pria A, Nelson M, et al. Surgical excision alone for stage T1 anal verge cancers in people living with HIV. Eur J Surg Oncol 2016;42:813-816. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27012999.

152. Leeds IL, Alturki H, Canner JK, et al. Outcomes of abdominoperineal resection for management of anal cancer in HIV-

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positive patients: a national case review. World J Surg Oncol 2016;14:208. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27495294.

153. Lefevre JH, Corte H, Tiret E, et al. Abdominoprenaline resection for squamous cell anal carcinoma: survival and risk factors for recurrence.Ann Surg Oncol 2012;19:4186-4192. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22825769.

154. Izadmehr S, Leapman M, Hobbs AR, et al. Clinical characteristics and outcomes of HIV-seropositive men treated with surgery for prostate cancer. Int Urol Nephrol 2016;48:1639-1645. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27318820.

155.Silberstein JL, Parsons JK, Palazzi-Churas K, et al. Robot-assisted laparoscopic radical prostatectomy in men with human immunodeficiency virus. Prostate Cancer Prostatic Dis 2010;13:328-332. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20877308.

156. Sigel C, Cavalcanti MS, Daniel T, et al. Clinicopathologic features of colorectal carcinoma in HIV-positive patients. Cancer Epidemiol Biomarkers Prev 2016;25:1098-1104. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27197294.

157. Di Benedetto F, Tarantino G, Ercolani G, et al. Multicenter Italian experience in liver transplantation for hepatocellular carcinoma in HIV-infected patients. Oncologist 2013;18:592-599. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23666950.

158.Bizer LS,Pettorino R,Ashikari A.Emergency abdominal operations in the patient with acquired immunodeficiency syndrome.J Am Coll Surg 1995;180:205-209. Available at:https://www.ncbi.nlm.nih.gov/pubmed/7850056.

159. Cacala SR, Mafana E, Thomson SR, Smith A. Prevalence of HIV status and CD4 counts in a surgical cohort: their relationship to clinical outcome. Ann R Coll Surg Engl 2006;88:46-51. Available at:https://www.ncbi.nlm.nih.gov/pubmed/16460640.

160.Harris HW, Schercter WP. Surgical risk assessment and management in patients with HIV disease. Gastroenterol Clin Clin Am 1997;26:377-391.Available at:https://www.ncbi.nlm.nih.gov/pubmed/9187930.

161.Madiba TE,Muckart DJ,Thomson SR.Human immunodeficiency disease: how should it affect surgical decision making? World J Surg 2009;33:899-909. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19280251.

162. Yii MK, Saunders A, Scott DF. Abdominal surgery in HIV/AIDS patients: indications, operative management, pathology and outcome.Aust Z J Surg 1995;65:320-326. Available at:https://www.ncbi.nlm.nih.gov/pubmed/7741674.

163.Fausto JA, Jr., Selwyn PA. Palliative care in the management of advanced HIV/AIDS. Prim Care 2011;38:311-326, ix. Available at:https://www.ncbi.nlm.nih.gov/pubmed/21628041.

164. Coghill AE, Brownstein NC, Sinha S, et al. Patient-reported outcomes in cancer patients with HIV. Cancers(Basel) 2022;14.Available at:https://www.ncbi.nlm.nih.gov/pubmed/36497369.

165. Corrigan KL, Knettel BA, Ho N, et al.Improving access to cancer care in the HIV population: Qualitative research to identify barriers to care. Health Equity 2020;4:468-475. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33269330.

166.Knettel B, Corrigan K, Cherenack E, et al. HIV, cancer, and coping:The cumulative burden of a cancer diagnosis among people living with HIV. J Psychosoc Oncol 2021;39:734-748. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33407058.

167.Hwang JP,Feld JJ, Hammond SP,et al.Hepatitis b virus screening and management for patients with cancer prior to therapy:ASCO provisional clinician update. J Clin Oncol 2020;38:3698-3715. Available at: https://www.ncbi.nlm.nih.gov/pubmed/32716741.

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168. Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents With HIV. U.S. Department of Health and Human Services, NIH Office of AIDS Research; 2024.Available at:https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/human?view=full. Accessed March 6,2025.

169. Palefsky JM, Holly EA, Ralston ML, Jay N. Prevalence and risk factors for human papillomavirus infection of the anal canal in human immunodeficiency virus(HIV)-positive and HIV-negative homosexual men.J Infect Dis 1998;177:361-367. Available at:http://www.ncbi.nlm.nih.gov/pubmed/9466522.

170.Clifford GM, Georges D, Shiels MS, et al. A meta-analysis of anal cancer incidence by risk group: Toward a unified anal cancer risk scale.Int J Cancer 2021;148:38-47. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32621759.

171. Piketty C, Selinger-Leneman H, Bouvier AM, et al. Incidence of HIV-related anal cancer remains increased despite long-term combined antiretroviral treatment: results from the french hospital database on HIV.J Clin Oncol 2012;30:4360-4366. Available at:http://www.ncbi.nlm.nih.gov/pubmed/23091098.

172.Colon-Lopez V, Shiels MS, Machin M, et al. Anal cancer risk among people with HIV infection in the United States. J Clin Oncol 2018;36:68-75. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29140774.

173. Pesut E, Dukic A, Lilic L, et al. Human papillomaviruses-associated cancers: An update of current knowledge. Viruses 2021;13:2234. Available at:https://www.ncbi.nlm.nih.gov/pubmed/34835040.

174. Duncan KC, Chan KJ, Chiu CG, et al. HAART slows progression to anal cancer in HIV-infected MSM. AIDS 2015;29:305-311. Available at:http://www.ncbi.nlm.nih.gov/pubmed/25686679.

175. Libois A, Feoli F, Nkuize M, et al. Prolonged antiretroviral therapy is associated with fewer anal high-grade squamous intraepithelial lesions in HIV-positive MSM in a cross-sectional study. Sex Transm Infect 2017;93:15-17. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27030607.

176. Kelly H, Chikandiwa A, Alemany Vilches L, et al. Association of antiretroviral therapy with anal high-risk human papillomavirus, anal intraepithelial neoplasia, and anal cancer in people living with HIV: a systematic review and meta-analysis. Lancet HIV 2020;7:e262-e278.Available at:https://www.ncbi.nlm.nih.gov/pubmed/32109408.

177.Gaisa M,Sigel K, Hand J, Goldstone S. High rates of anal dysplasia in HIV-infected men who have sex with men, women, and heterosexual men. AIDS 2014;28:215-222. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24072194.

178.Berry JM,Jay N,Cranston RD,et al. Progression of anal high-grade squamous intraepithelial lesions to invasive anal cancer among HIV-infected men who have sex with men. Int J Cancer 2014;134:1147-1155.Available at: http://www.ncbi.nlm.nih.gov/pubmed/23934991.

179.Scholefield JH,Castle MT,Watson NF.Malignant transformation of high-grade anal intraepithelial neoplasia. Br J Surg 2005;92:1133-1136. Available at: http://www.ncbi.nlm.nih.gov/pubmed/16044425.

180.Tinmouth J, Peeva V, Amare H, et al. Progression from perianal high-grade anal intraepithelial neoplasia to anal cancer in HIV-positive men who have sex with men. Dis Colon Rectum 2016;59:836-842.Available at:https://www.ncbi.nlm.nih.gov/pubmed/27505112.

181.Watson AJ,Smith BB,Whitehead MR,et al.Malignant progression of anal intra-epithelial neoplasia.ANZ J Surg 2006;76:715-717.Available at: http://www.ncbi.nlm.nih.gov/pubmed/16916390.

182.Gautier M, Brochard C, Lion A, et al. High-grade anal intraepithelial neoplasia: progression to invasive cancer is not a certainty. Dig Liver Dis 2016;48:806-811. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27103359.

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183.Stier EA, Clarke MA, Deshmukh AA, et al. International Anal Neoplasia Society's consensus guidelines for anal cancer screening.Int J Cancer 2024;154:1694-1702. Available at:https://www.ncbi.nlm.nih.gov/pubmed/38297406.

184. Gaisa MM, Sigel KM, Deshmukh AA, et al. Comparing anal cancer screening algorithms using cytology and human papillomavirus DNA testing in 3 high-risk populations. J Infect Dis 2021;224:881-888.Available at:https://www.ncbi.nlm.nih.gov/pubmed/33388757.

185. Alam NN, White DA, Narang SK, et al. Systematic review of guidelines for the assessment and management of high-grade anal intraepithelial neoplasia(AIN I/III). Colorectal Dis 2016;18:135-146.Available at: http://www.ncbi.nlm.nih.gov/pubmed/26559167.

186. Hartschuh W, Breitkopf C, Lenhard B, et al. S1 guideline: anal intraepithelial neoplasia(AIN) and perianial intraepithelial neoplasia(PAIN). J Dtsch Dermatol Ges 2011;9:256-258. Available at:http://www.ncbi.nlm.nih.gov/pubmed/21208377.

187. Scholefield JH, Harris D, Radcliffe A. Guidelines for management of anal intraepithelial neoplasia. Colorectal Dis 2011;13 Suppl 1:3-10.Available at: http://www.ncbi.nlm.nih.gov/pubmed/21251167.

188. Steele SR, Varma MG, Melton GB, et al. Practice parameters for anal squamous neoplasms. Dis Colon Rectum 2012;55:735-749.

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189. Johnstone AA, Silvera R, Goldstone SE. Targeted ablation of perianal high-grade dysplasia in men who have sex with men: an alternative to mapping and wide local excision. Dis Colon Rectum 2015;58:45-52. Available at:

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190. Smulian AG, Moore DM, Robertson JC, Kralovic SM. Phase I study demonstrates safety and tolerability of radiofrequency ablation(RFA) of the anal mucosa. HIV Clin Trials 2014;15:36-44. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24525427.

191. Willems N, Libois A, Nkuize M, et al. Treatment of anal dysplasia in HIV-positive men who have sex with men in a large AIDS reference centre. Acta Clin Belg 2017;72:29-35. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27320416.

192. Palefsky JM, Lee JY, Jay N, et al. Treatment of anal high-grade squamous intraepithelial lesions to prevent anal cancer. N Engl J Med 2022;386:2273-2282.Available at:https://www.ncbi.nlm.nih.gov/pubmed/335704479.

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193. Goldstone SE, Johnstone AA, Moshier EL. Long-term outcome of ablation of anal high-grade squamous intraepithelial lesions: recurrence and incidence of cancer. Dis Colon Rectum 2014;57:316-323. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24509453.

194. Gosens KCM, van der Zee RP, van Heukelom MLS, et al. HPV vaccination to prevent recurrence of anal intraepithelial neoplasia in HIV+ MSM.AIDS 2021;35:1753-1764. Available at:https://www.ncbi.nlm.nih.gov/pubmed/21208377.

195. Richel O, de Vries HJ, van Nosel CJ, et al. Comparison of imiquimod, topical fluorouracil, and electrocautery for the treatment of anal intraepithelial neoplasia in HIV-positive men who have sex with men: an open-label, randomised controlled trial. Lancet Oncol 2013;14:346-353. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23499546.

196. Goldstone SE, Lensing SY, Stier EA, et al. A randomized clinical trial of infrared coagulation ablation versus active monitoring of intra-anal high-grade dysplasia in HIV-infected adults: An AIDS Malignancy Consortium Clin Infect Dis 2019;68:1204-1212. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24509468

197. Palefsky JM, Lensing SY, Belzer M, et al. High prevalence of anal high-grade squamous intraepithelial lesions, and prevention through human papillomavirus vaccination, in young men who have sex with men living with human immunodeficiency virus. Clin Infect Dis 2021;73:1388-1396. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33991185.

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198. Palefsky JM, Giuliano AR, Goldstone S, et al. HPV vaccine against anal HPV infection and anal intraepithelial neoplasia. N Engl J Med 2011;365:1576-1585. Available at:

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199. Bryant AK, Mudgway R, Huynh-Le M-P, et al. Effect of CD4 count on treatment toxicity and tumor recurrence in HIV positive patients with anal cancer. Intl J Rad Oncol Phys 2018;100:478-485. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29102276.

200. Bryant AK, Huynh-Le MP, Simpson DR, et al. Association of HIV status with outcomes of anal squamous cell carcinoma in the era of highly active antiretroviral therapy. JAMA Oncol 2018;4:120-122.

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201. Grew D, Bitterman D, Leichman CG, et al. HIV infection is associated with poor outcomes for patients with anal cancer in the highly active antiretroviral therapy era. Dis Colon Rectum 2015;58:1130-1136. Available at:http://www.ncbi.nlm.nih.gov/pubmed/26544809.

2022. Oehler-Janne C, Huguet F, Provencher S, et al. HIV-specific differences in outcome of squamous cell carcinoma of the anal canal: a multicentric cohort study of HIV-positive patients receiving highly active antiretroviral therapy. J Clin Oncol 2008;26:2550-2557. Available at:http://www.ncbi.nlm.nih.gov/pubmed/18427149.

203.Susko M, Wang CJ, Lazar AA, et al. Factors impacting differential outcomes in the definitive radiation treatment of anal cancer between HIV-positive and HIV-negative patients. Oncologist 2020;25:772-779.Available at: https://www.ncbi.nlm.nih.gov/pubmed/32390297.

204. Camandaroba MPG, Iseas S, Oliveira C, et al. Disease-free survival and time to complete response after definitive chemoradiotherapy for squamous-cell carcinoma of the anus according to HIV infection. Clin Colorectal Cancer 2020;19:e129-e136. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32389596.

205.White EC,Khodayari B,Erickson KT,et al. Comparison of toxicity and treatment outcomes in HIV-positive versus HIV-negative patients with squamous cell carcinoma of the anal canal. Am J Clin Oncol 2014;40:386-392. Available at:

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206. Martin D,Balermpas P,Fokas E,et al.Are there HIV-specific differences for anal cancer patients treated with standard chemoradiotherapy in the era of combined antiretroviral therapy? Clin Oncol(R Coll Radiol) 2017;29:248-255. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28049602.

207.Pappou EP, Magruder JT,Fu T,et al. Prognostic and predictive clinicopathologic factors of squamous anal canal cancer in HIV-positive and HIV-negative patients: does HAART influence outcomes? World J Surg 2018;42:876-883. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28948325.

208. Leiker AJ, Wang CJ, Sanford NN, et al. Feasibility and outcome of routine use of concurrent chemoradiation in HIV-positive patients with squamous cell anal cancer. Am J Clin Oncol 2020;43:701-708.

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209. Oliveira SC, Moniz CM, Riechelmann R, et al. Phase II study of capecitabine in substitution of 5-FU in the chemoradiotherapy regimen for patients with localized squamous cell carcinoma of the anal canal. J Gastrointest Cancer 2016;47:75-81. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26691173.

210. Morris VK, Salem ME, Nimeir I, et al. Nivolumab for previously treated unresectable metastatic anal cancer(NCI9673): a multicentre,single-arm, phase 2 study. Lancet Oncol 2017;18:446-453. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28223062.

211. Garg M, Lee JY, Kachnic LA, et al. Phase II trials of cetuximab(CX) plus cisplatin(CDDP), 5-fluorouracil (5-FU) and radiation (RT) in immunocompetent (ECOG 3205) and HIV-positive (AMC045) patients with squamous cell carcinoma of the anal canal (SCAC): Safety and preliminary efficacy results [abstract]. ASCO Meeting Abstracts

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2012;30:4030.Available at:http://meetinglibrary.asco.org/content/95820-114.

212. Garg MK,Zhao F,Sparano JA,et al. Cetuximab plus chemoradiotherapy in immunocompetent patients with anal carcinoma:a phase II Eastern Cooperative Oncology Group-American College of Radiology Imaging Network Cancer Research Group trial(E3205). J Clin Oncol 2017;35:718-726. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28068178.

213.Sparano JA, Lee JY, Palefsky J, et al. Cetuximab plus chemoradiotherapy for HIV-associated anal carcinoma: a phase II AIDS Malignor Consortium trial.J Clin Oncol 2017;35:727-733. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27937092.

214. Walboomers JM, Jacobs MV, Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol 1999;189:12-19. Available at:https://www.ncbi.nlm.nih.gov/pubmed/10451482.

215. Adebamowo SN, Olawande O, Famoto A, et al. Persistent low-risk and high-risk human papillomavirus infections of the uterine cervix in HIV-negative and HIV-positive women. Front Public Health 2017;5:178. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28785554.

216. McDonald AC, Tergas Al, Kuhn L, et al. Distribution of human papillomavirus genotypes among HIV-positive and HIV-negative women in Cape Town, South Africa. Front Oncol 2014;4:48. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24672770.

217. Abraham AG, D'Souza G, Jing Y,et al. Invasive cervical cancer risk among HIV-infected women: a North American multicohort collaboration prospective study. J Acquir Immune Defic Syndr 2013;62:405-413. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23254153.

218. Chen YC, Li CY, Liu HY, et al. Effect of antiretroviral therapy on the incidence of cervical neoplasia among HIV-infected women: a

population-based cohort study in Taiwan. AIDS 2014;28:709-715.Available at:https://www.ncbi.nlm.nih.gov/pubmed/24326354.

219. Stelzle D,Tanaka LF,Lee KK,et al.Estimates of the global burden of cervical cancer associated with HIV. Lancet Glob Health 2021;9:e161-e169. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33212031.

220.Adler DH, Kakinami L, Modisenyane T, et al. Increased regression and decreased incidence of human papillomavirus-related cervical lesions among HIV-infected women on HAART. AIDS 2012;26:1645-1652. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22555167.

221. Heard I, Potard V, Costagliola D. Limited impact of immunosuppression and HAART on the incidence of cervical intraepithelial lesions in HIV-positive women. Antivir Ther 2006;11:1091-1096. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17302379.

222. Menon S, Rossi R, Zdraveska N, et al. Associations between highly active antiretroviral therapy and the presence of HPV,premalignant and malignant cervical lesions in sub-Saharan Africa, a systematic review: current evidence and directions for future research.BMJ Open 2017;7:e015123. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28780541.

223.Kelly H, Weiss HA, Benavente Y, et al. Association of antiretroviral therapy with high-risk human papillomavirus, cervical intraepithelial neoplasia, and invasive cervical cancer in women living with HIV: a systematic review and meta-analysis. Lancet HIV 2018;5:e45-e58.Available at:https://www.ncbi.nlm.nih.gov/pubmed/29107561.

224. Atemnkeng N,Aji AD, de Sanjose S,et al. Antiretroviral therapy and detection of high-grade cervical intraepithelial neoplasia (CIN2+) at post-CIN management follow-up among women living with human immunodeficiency virus: A systematic review and meta-analysis.Clin Infect Dis 2020;71:e540-e548. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32162657.

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

225.Gupta R, Mariano LC, Singh S, Gupta S. Highly active antiretroviral therapy (HAART) and outcome of cervical lesions and high-risk HPV in women living with HIV (WLHIV): A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol 2022;278:153-158. Available at: https://www.ncbi.nlm.nih.gov/pubmed/36194939.

226. Shiels MS,Pfeiffer RM,Hall HI,et al. Proportions of Kaposarcoma, selected non-Hodgkin lymphomas, and cervical cancer in the United States occurring in persons with AIDS, 1980-2007. JAMA 2011;305:1450-1459. Available at:https://www.ncbi.nlm.nih.gov/pubmed/21486978.

227.International Collaboration on HIV, Cancer. Highly active antiretroviral therapy and incidence of cancer in human immunodeficiency virus-infected adults. J Natl Cancer Inst 2000;92:1823-1830. Available at:https://www.ncbi.nlm.nih.gov/pubmed/11078759.

228. Grabar S, Hleyhel M, Belot A, et al. Invasive cervical cancer in HIV-infected women: risk and survival relative to those of the general population in France. Results from the French Hospital Database on HIV(FHDH)-Agence Nationale de Recherches sur le SIDA et les Hepatites Virales (ANRS) CO4 cohort study. HIV Med 2019;20:222-229.Available at: https://www.ncbi.nlm.nih.gov/pubmed/30693646.

229.Robbins HA, Pfeiffer RM, Shiels MS,et al. Excess cancers among HIV-infected people in the United States. J Natl Cancer Inst 1507.Available at:https://www.ncbi.nlm.nih.gov/pubmed/25663691.

230. Santesso N, Mustafa RA, Schunemann HJ, et al. World Health Organization Guidelines for treatment of cervical intraepithelial neoplasia 2-3 and screen-and-treat strategies to prevent cervical cancer. Int J Gynaecol Obstet 2016;132:252-258. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26868062.

231.Firnhaber C, Swarts A, Goeieman B, et al. Cryotherapy reduces progression of cervical intraepithelial neoplasia grade 1 in South African HIV-infected women: A rRandomized, controlled trial. J Acquir Immune

Defic Syndr 2017;76:532-538. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28902073.

232.Forhan SE,Godfrey CC, Watts DH, Langley CL. A systematic review of the effects of visual inspection with acetic acid, cryotherapy,and loop electrosurgical excision procedures for cervical dysplasia in HIV-infected women in low- and middle-income countries. J Acquir Immune Defic Syndr 2015;68 Suppl 3:S350-356. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25768874.

233. Hank E, Hoque ME, Zungu L. Cervical precancerous lesions and cancer among patients in the gynaecology outpatient department at a tertiary hospital in South Africa. Asian Pac J Cancer Prev 2013;14:4903-4906. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24083765.

234.Heard I, Potard V,Foulot H,et al. High rate of recurrence of cervical intraepithelial neoplasia after surgery in HIV-positive women.J Acquir Immune Defic Syndr 2005;39:412-418. Available at:https://www.ncbi.nlm.nih.gov/pubmed/16010162.

235. Kreitchmann R, Bajotto H, da Silva DA, Fuchs SC. Squamous intraepithelial lesions in HIV-infected women: prevalence, incidence,progression and regression. Arch Gynecol Obstet 2013;288:1107-1113.Available at:https://www.ncbi.nlm.nih.gov/pubmed/23644923.

236.McClung EC,Blumenthal PD.Efficacy,safety,acceptability and affordability of cryotherapy: a review of current literature. Minerva Ginecol 2012;64:149-171. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22481625.

237.Reimers LL,Sotardi S,Daniel D,et al. Outcomes after an excisional procedure for cervical intraepithelial neoplasia in HIV-infected women. Gynecol Oncol 2010;119:92-97. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20605046.

238.Foulot H, Heard I, Potard V, et al. Surgical management of cervical intraepithelial neoplasia in HIV-infected women. Eur J Obstet Gynecol

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NCCN Guidelines Versation 1.2026 Cancer in People with HIV

Reprod Biol 2008;141:153-157. Available at:https://www.ncbi.nlm.nih.gov/pubmed/18760524.

239. Bambury I, Mullings A, Fletcher H, et al. Cervical intraepithelial neoplasia in a cohort of HIV-positive women at the University Hospital of the West Indies: management and outcome. West Indian Med J 2013;62:313-317. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24756591.

240. Cejtin HE, Zimmerman L, Mathews M, Patel A. Predictors of persistent or recurrent disease after loop electrosurgical excision procedure. J Low Genit Tract Dis 2017;21:59-63. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27824789.

241.Smith JS, Sanusi B, Swats A, et al. A randomized clinical trial comparing cervical dysplasia treatment with cryotherapy vs loop electrosurgical excision procedure in HIV-seropositive women from Johannesburg, South Africa. Am J Obstet Gynecol 2017;217:183 e181-183 e111. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28366730.

242. Greene SA, De Vuyst H, John-Stewart GC, et al. Effect of cryotherapy vs loop electrosurgical excision procedure on cervical disease recurrence among women with HIV and high-grade cervical lesions in kenya: A randomized clinical trial. JAMA 2019;322:1570-1579. Available at:https://www.ncbi.nlm.nih.gov/pubmed/31638680.

243.Chung MH,De Vuyst H,Greene SA,et al.Human papillomavirus persistence and association with recurrent cervical intraepithelial neoplasia after cryotherapy vs loop electrosurgical excision procedure among hiv-positive women: A secondary analysis of a randomized clinical trial. JAMA Oncol 2021;7:1514-1520. Available at:https://www.ncbi.nlm.nih.gov/pubmed/34351377.

244.Finhaber C, Swarts A, Jezile V, et al. Human papillomavirus vaccination prior to loop electroexcision procedure does not prevent recurrent cervical high-grade squamous intraepithelial lesions in women living with human immunodeficiency virus: A randomized, double-blind,

placebo-controlled trial. Clin Infect Dis 2021;73:e2211-e2216. Available at:https://www.ncbi.nlm.nih.gov/pubmed/3297556

245.Ntekim A,Campbell O, Rothenbacher D. Optimal management of cervical cancer in HIV-positive patients: a systematic review. Cancer Med 2015;4:1381-1393. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26136407.

246.Simonds HM,Neugut Al,Jacobson JS.HIV status and acute hematologic toxicity among patients with cervix cancer undergoing radical chemoradiation. Int J Gynecol Cancer 2015;25:884-890.Available at:https://www.ncbi.nlm.nih.gov/pubmed/25853380.

247.Grover S,Bvochora-Nsingo M,Yeager A,et al.Impact of human immunodeficiency virus infection on survival and acute toxicities from chemoradiation therapy for cervical cancer patients in a limited-resource setting. Int J Radiat Oncol Biol Phys 2018;101:201-210. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29619965.

248.Simonds HM,Botha MH,Neugut Al,et al.Five-year overall survival following chemoradiation among HIV-positive and HIV-negative patients with locally advanced cervical carcinoma in a South African cohort. Gynecol Oncol 2018;151:215-220.Available at:https://www.ncbi.nlm.nih.gov/pubmed/30194006.

249.Einstein MH,Ndlovu N,Lee J,et al.Cisplatin and radiation therapy in HIV-positive women with locally advanced cervical cancer in sub-Saharan Africa: A phase II study of the AIDS malignancy consortium.com.Gynecol Oncol 2019;153:20-25. Available at:https://www.ncbi.nlm.nih.gov/pubmed/30773222.

250.Biggar RJ,Jaffe ES, Goedert JJ, et al. Hodgkin lymphoma and immunodeficiency in persons with HIV/AIDS. Blood 2006;108:3786-3791. Available at:https://www.ncbi.nlm.nih.gov/pubmed/16917006.

251. Kowalkowski MA, Mims MP, Amiran ES, et al. Effect of immune reconstitution on the incidence of HIV-related Hodgkin lymphoma. PLoS One 2013;8:e77409. Available at:

https://www.ncbi.nlm.nih.gov/pubmed/24098586.

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252. Mani H, Jaffe ES. Hodgkin lymphoma: an update on its biology with new insights into classification. Clin Lymphoma Myeloma 2009;9:206-216. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19525189.

253. Ruiz M, Parsons C, Cole J. Characterization of HIV-associated Hodgkin's lymphoma in HIV-infected patients: a single-center experience. J Int Assoc Physicians AIDS Care (Chic) 2012;11:234-238. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22302202.

254. Sorigue M, Garcia O, Tapia G, et al. HIV-infection has no prognostic impact on advanced-stage Hodgkin lymphoma. AIDS 2017;31:1445-1449. Available at:

https://www.ncbi.nlm.nih.gov/pubmed/28574963.

255. Diez-Martin JL,Balsalobre P,Re A,et al.Comparable survival between HIV+ and HIV- non-Hodgkin and Hodgkin lymphoma patients undergoing autologous peripheral blood stem cell transplantation. Blood 2009;113:6011-6014. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19307667.

256. Xicoy B, Ribera JM, Miralles P, et al. Results of treatment with doxorubicin, bleomycin, vinblastine and dacarbazine and highly active antiretroviral therapy in advanced stage, human immunodeficiency virus-related Hodgkin's lymphoma. Haematologica 2007:92:191-198.Available at:https://www.ncbi.nlm.nih.gov/pubmed/17296568.

257.Serraino D,Carbone A,Franceschi S,Tirelli U. Increased frequency of lymphocyte depletion and mixed cellularity subtypes of Hodgkin's disease in HIV-infected patients. Italian Cooperative Group on AIDS and Tumours. Eur J Cancer 1993;29A:1948-1950. Available at:https://www.ncbi.nlm.nih.gov/pubmed/8280487.

258.Tirelli U,Errante D, Dolcetti R,et al.Hodgkin's disease and human immunodeficiency virus infection: clinicopathologic and virologic features of 114 patients from the Italian Cooperative Group on AIDS and Tumors.J Clin Oncol 1995;13:1758-1767. Available at:https://www.ncbi.nlm.nih.gov/pubmed/7541452.

259. Besson C, Lancar R, Prevot S, et al. High risk features contrast with favorable outcomes in HIV-associated Hodgkin lymphoma in the modern cART era, ANRS CO16 LYMPHOVIR cohort. Clin Infect Dis 2015;61:1469-1475. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26223997.

260.Shah BK,Subramaniam S, Peace D, Garcia C. HIV-associated primary bone marrow Hodgkin's lymphoma: a distinct entity? J Clin Oncol 2010;28:e459-460. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20679601.

261.O'Neill A, Mikesch K,Fritsch K,et al. Outcomes for HIV-positive patients with primary central nervous system lymphoma after high-dose chemotherapy and auto-SCT. Bone Marrow Transplant 2015;50:999-1000. Available at:https://www.ncbi.nlm.nih.gov/pubmed/25867650.

262.Glaser SL,Clarke CA,Gulley ML,et al.Population-based patterns of human immunodeficiency virus-related Hodgkin lymphoma in the Greater San Francisco Bay Area, 1988-1998. Cancer 2003;98:300-309.Available at:https://www.ncbi.nlm.nih.gov/pubmed/12872349.

263. Montoto S, Shaw K, Okosun J, et al. HIV status does not influence outcome in patients with classical Hodgkin lymphoma treated with chemotherapy using doxorubicin, bleomycin, vinblastine, and dacarbazine in the highly active antiretroviral therapy era. J Clin Oncol 2012;30:4111-4116. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23045581.

264. Shiels MS, Koritzinsky EH, Clarke CA, et al. Prevalence of HIV Infection among U.S. Hodgkin lymphoma cases. Cancer Epidemiol Biomarkers Prev 2014;23:274-281. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24326629.

265. Hoffmann C, Chow KU, Wolf E, et al. Strong impact of highly active antiretroviral therapy on survival in patients with human immunodeficiency virus-associated Hodgkin's disease. Br J Haematol 2004;125:455-462. Available at:https://www.ncbi.nlm.nih.gov/pubmed/15142115.

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266.Olszewski AJ, Castillo JJ. Outcomes of HIV-associated Hodgkin lymphoma in the era of antiretroviral therapy. AIDS 2016;30:787-796.Available at:https://www.ncbi.nlm.nih.gov/pubmed/26730566.

267. Han X, Jemal A, Hulland E, et al. HIV infection and survival of lymphoma patients in the era of highly active antiretroviral therapy.Cancer Epidemiol Biomarkers Prev 2017;26:303-311. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27756777.

268. Spina M, Gabarre J, Rossi G, et al. Stanford V regimen and concomitant HAART in 59 patients with Hodgkin disease and HIV infection. Blood 2002;100:1984-1988. Available at:https://www.ncbi.nlm.nih.gov/pubmed/12200356.

269. Hartmann P, Rehwald U, Salzberger B, et al. BEACOPP therapeutic regimen for patients with Hodgkin's disease and HIV infection.Ann Oncol 2003;14:1562-1569. Available at:https://www.ncbi.nlm.nih.gov/pubmed/14504059.

270.Hentrich M, Berger M, Wyen C, et al. Stage-adapted treatment of HIV-associated Hodgkin lymphoma: results of a prospective multicenter study.J Clin Oncol 2012;30:4117-4123. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23045592.

271. Rubinstein PG, Moore PC, Bimali M, et al. Brentuximab vedotin with AVD for stage II-IV HIV-related Hodgkin lymphoma(AMC 085):phase 2 results from an open-label, single arm, multicentre phase 1/2 trial. Lancet Haematol 2023;10:e624-e632. Available at:https://www.ncbi.nlm.nih.gov/pubmed/37532416.

272. Ezzat HM, Cheung MC, Hicks LK, et al. Incidence, predictors and significance of severe toxicity in patients with human immunodeficiency virus-associated Hodgkin lymphoma. Leuk Lymphoma 2012;53:2390-2396. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22642935.

273. Spitzer TR, Ambinder RF, Lee JY,et al. Dose-reduced busulfan,cyclophosphamide, and autologous stem cell transplantation for human immunodeficiency virus-associated lymphoma: AIDS Malignancy

Consortium study 020. Biol Blood Marrow Transplant 2008;14:59-66.Available at:https://www.ncbi.nlm.nih.gov/pubmed/18158962.

274. Balsalobre P, Diez-Martin JL, Re A, et al. Autologous transplantation in patients with HIV-related lymphoma. J Clin Oncol 2009;27:2192-2198. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19332732.

275. Alvarnas JC,Le Rademacher J, Wang Y,et al. Autologous hematopoietic cell transplantation for HIV-related lymphoma: results of the BMT CTN 0803/AMC 071 trial. Blood 2016;128:1050-1058.Available at:https://www.ncbi.nlm.nih.gov/pubmed/27297790.

276. Okosun J, Warbey V, Shaw K, et al. Interim fluoro-2-deoxy-D-glucose-PET predicts response and progression-free survival in patients with Hodgkin lymphoma and HIV infection. AIDS 2012;26:861-865.Available at:https://www.ncbi.nlm.nih.gov/pubmed/22333746.

277. Danilov AV, Li H, Press OW, et al. Fasibility of interim positron emission tomography (PET)-adapted therapy in HIV-positive patients with advanced Hodgkin lymphoma (HL): a sub-analysis of SWOG S0816 Phase 2 trial. Leuk Lymphoma 2017; 58:461-465. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27386786.

278. Johnson P, Federico M, Kirkwood A, et al. Adapted treatment guided by interim PET-CT scan in advanced hodgkin's lymphoma. N Engl J Med 2016;374:2419-2429. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27332902.

279. Andrieu JM, Roithmann S, Tourani JM, et al. Hodgkin's disease during HIV1 infection: the French registry experience. French Registry of HIV-associated Tumors. Ann Oncol 1993;4:635-641. Available at:https://www.ncbi.nlm.nih.gov/pubmed/8240994.

280.Lee JY,Dhakal I,Casper C,et al.Risk of cancer among commercially insured HIV-infected adults on antiretroviral therapy. J Cancer Epidemiol 2016;2016:2138259. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27882054.

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281. Luo Q, Satcher Johnson A, Hall HI, et al. Kaposaric rates among persons living with human immunodeficiency virus in the United States:2008-2016. Clin Infect Dis 2021;73:e2226-e2233. Available at:https://www.ncbi.nlm.nih.gov/pubmed/33140823.

282.Yarchoan R,Uldrick TS.HIV-associated cancers and related diseases.N Engl J Med 2018;378:1029-1041. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29539283.

283. Haas CB, Engels EA, Horner MJ, et al. Trends and risk of lung cancer among people living with HIV in the USA: a population-based registry linkage study. Lancet HIV 2022;9:e700-e708. Available at:https://www.ncbi.nlm.nih.gov/pubmed/36179753.

284.Trepka MJ,Auf F, Fennie KP, et al. Deaths due to screenable cancers among people living with HIV infection, Florida, 2000-2014. Am J Prev Med 2017;53:705-709. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28751055.

285. Wang YH, Shen XD. Human immunodeficiency virus infection and mortality risk among lung cancer patients; A systematic review and meta-analysis. Medicine(Baltimore) 2018;97:e0361. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29642182.

286.Smith DM, Salters KA, Eyowo A, et al. Mortality among people living with HIV/AIDS with non-small-cell lung cancer in the modern HAART Era. AIDS Care 2018;30:936-942. Available at:https://www.ncbi.nlm.nih.gov/pubmed/29411625.

287. Hysell K, Yusuf R, Barakat L, et al. Decreased overall survival in HIV-associated non-small-cell lung cancer. Clin Lung Cancer 2021;22:e498-e505. Available at:https://www.ncbi.nlm.nih.gov/pubmed/3468393.

288. Levine AM, Seaberg EC, Hessol NA, et al. HIV as a risk factor for lung cancer in women: data from the Women's Interagency HIV Study.J Clin Oncol 2010;28:1514-1519. Available at:https://www.ncbi.nlm.nih.gov/pubmed/20177022.

289.Kirk GD, Merlo C, P OD, et al. HIV infection is associated with an increased risk for lung cancer, independent of smoking. Clin Infect Dis 2007;45:103-110. Available at:

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290.Sigel K, Wisnivesky J, Crothers K, et al. Immunological and infectious risk factors for lung cancer in US veterans with HIV: a longitudinal cohort study. Lancet HIV 2017;4:e67-e73. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27916584.

291.Reddy KP,Kong CY,Hyle EP,et al. Lung cancer mortality associated with smoking and smoking cessation among people living with HIV in the United States. JAMA Intern Med 2017;177:1613-1621.Available at:https://www.ncbi.nlm.nih.gov/pubmed/28975270.

292. National Lung Screening Trial Research T, Aberle DR, Adams AM,et al. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med 2011;365:395-409. Available at:https://www.ncbi.nlm.nih.gov/pubmed/21714641.

293. National Lung Screening Trial Research T, Church TR, Black WC,et al. Results of initial low-dose computed tomographic screening for lung cancer. N Engl J Med 2013;368:1980-1991. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23697514.

294. Hulbert A, Hooker CM, Keruly JC, et al. Prospective CT screening for lung cancer in a high-risk population: HIV-positive smokers. J Thorac Oncol 2014;9:752-759. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24828660.

295. Makinson A, Eymard-Duvernay S, Raffi F, et al. Feasibility and efficacy of early lung cancer diagnosis with chest computed tomography in HIV-infected smokers. AIDS 2016;30:573-582. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26829006.

296. Ronit A, Kristensen T, Klitbo DM, et al. Incidental lung cancers and positive computed tomography images in people living with HIV. AIDS 2017;31:1973-1977. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28857778.

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297. Powles T, Thirwell C, Newsom-Davis T, et al. Does HIV adversely influence the outcome in advanced non-small-cell lung cancer in the era of HAART? Br J Cancer 2003;89:457-459. Available at:https://www.ncbi.nlm.nih.gov/pubmed/12888811.

298. Lee JY, Moore PC, Lensing SY. Impact of HIV infection on Medicare beneficiaries with lung cancer. J Cancer Epidemiol 2012;2012:706469. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22548059.

299. Lee JY, Moore PC, Steliga MA. Do HIV-infected non-small cell lung cancer patients receive guidance-concordant care? Med Care 2013;51:1063-1068. Available at:https://www.ncbi.nlm.nih.gov/pubmed/24220684.

300.Suneja G, Shiels MS, Melville SK, et al. Disparities in the treatment and outcomes of lung cancer among HIV-infected individuals. AIDS 2013;27:459-468. Available at:https://www.ncbi.nlm.nih.gov/pubmed/23079809.

301. Lavole A, Greillier L, Mazieres J, et al. First-line carplobin plus pemetrexed with pemetrexed maintenance in HIV-positive patients with advanced non-squamous non-small cell lung cancer: the phase II IFCT-1001 CHIVA trial. Eur Respir J 2020;56:1902066. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32444410.

302. Paz-Ares L,de Marinis F,Dediu M,et al. Maintenance therapy with pemetrexed plus best supportive care versus placebo plus best supportive care after induction therapy with pemetrexed plus cisplatin for advanced non-squamous non-small-cell lung cancer(PARAMOUNT): a double-blind, phase 3, randomised controlled trial.Lancet Oncol 2012;13:247-255. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22341744.

303. Ciuleanu T, Brodowicz T, Zielinski C, et al. Maintenance pemetrexed plus best supportive care versus placebo plus best supportive care for non-small-cell lung cancer: a randomised, double-blind, phase 3 study. Lancet 2009;374:1432-1440. Available at:https://www.ncbi.nlm.nih.gov/pubmed/19767093.

304. Hooker CM, Meguid RA, Hulbert A, et al. Human immunodeficiency virus infection as a prognostic factor in surgical patients with non-small cell lung cancer. Ann Thorac Surg 2012;93:405-412. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22269705.

305.Sigel KM,Stone K,Wisnivesky JP,et al. Short-term outcomes for lung cancer resection surgery in HIV infection. AIDS 2019;33:1353-1360.Available at:https://www.ncbi.nlm.nih.gov/pubmed/30889013.

306. Hernandez-Ramirez RU,Qin L,Lin H,et al.Association of immunosuppression and HIV viriaemia with non-Hodgkin lymphoma risk overall and by subtype in people living with HIV in Canada and the USA: a multicentre cohort study. Lancet HIV 2019;6:e240-e249.Available at:https://www.ncbi.nlm.nih.gov/pubmed/30826282.

307.UNAIDS Data 2022.UNAIDS; 2023. Available at:https://www.unaids.org/en/resources/documents/2023/2022 unaids dat a. Accessed March 6,2025.

308.Chinula L, Moses A, Gopal S. HIV-associated malignancies in sub-Saharan Africa: progress, challenges, and opportunities. Curr Opin HIV AIDS 2017;12:89-95. Available at:https://www.ncbi.nlm.nih.gov/pubmed/27607593.

309.Myamboza KP,Dzamalala C,Mdokwe C,et al.Burden of cancer in Malawi; common types,incidence and trends: national population-based cancer registry.BMC Res Notes 2012;5:149. Available at:https://www.ncbi.nlm.nih.gov/pubmed/22424105.

310.Rogena EA,Simbiri KO,De Falco G,et al.A review of the pattern of AIDS defining, HIV associated neoplasms and premalignant lesions diagnosed from 2000-2011 at Kenyatta National Hospital, Kenya. Infect Agent Cancer 2015;10:28. Available at:https://www.ncbi.nlm.nih.gov/pubmed/26306097.

311.Stefan DC. Cancer care in Africa: An overview of resources. J Glob Oncol 2015;1:30-36. Available at:https://www.ncbi.nlm.nih.gov/pubmed/28804769.

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NCCN Guidelines Version 1.2026 Cancer in People with HIV

312. Youlden DR,Cramb SM,Dunn NA,et al.The descriptive epidemiology of female breast cancer: an international comparison of screening,incidence, survival and mortality.Cancer Epidemiol 2012;36:237-248.Available at:https://www.ncbi.nlm.nih.gov/pubmed/22459198.

313.Strother RM,Gopal S, Wirth M, et al. Challenges of HIV lymphoma clinical trials in Africa: Lessons from the AIDS Malignancy Consortium 068 study. JCO Glob Oncol 2020;6:1034-1040. Available at:https://www.ncbi.nlm.nih.gov/pubmed/32634068.

314. Uldrick TS, lson G, Rudek MA, et al. Modernizing clinical trial eligibility criteria: recommendations of the American Society of Clinical Oncology-Friends of Cancer Research HIV Working Group. J Clin Oncology 2017;35:3774-3780. Available at: https://www.ncbi.nlm.nih.gov/pubmed/28968173.

表 1
	NCCN Categories of Evidence and Consensus
Category 1	Based upon high-level evidence (≥1 randomized phase 3 trials or high-quality, robust meta-analyses), there is uniform NCCN consensus (≥85% support of the Panel) that the intervention is appropriate.
Category 2A	Based upon lower-level evidence, there is uniform NCCN consensus (≥85% support of the Panel) that the intervention is appropriate.
Category 2B	Based upon lower-level evidence, there is uniform NCCN consensus (≥50%, but <85% support of the Panel) that the intervention is appropriate.
Category 3	Based upon any level of evidence, there is major NCCN disagreement that the intervention is appropriate.

表 2
NCCN Categories of Preference
Preferred	Interventions that are based on superior efficacy, safety, and evidence; and, when appropriate, affordability.
Other recommended	Other interventions that may be somewhat less efficacious, more toxic, or based on less mature data; or significantly less affordable for similar outcomes.
Useful in certain circumstances	Other interventions that may be used for selected patient populations (defined with recommendation).

表 3
Overall Statements Update Methodology 3
Literature Search Criteria.
Sensitive /Inclusive Language Usage	MS-3
Disparities in Cancer Care for PWH	MS-3
HIV Management During Cancer Therapy	MS-3
HIV Screening.	MS-4
Linkage to HIV Care.	MS-4
HIV Therapy During Cancer Treatment	MS-4
Opportunistic Infection Prophylaxis	MS-5
Smoking Cessation in PWH Who Have Cancer	MS-6
Recommendations for Cancer Management in PWH	MS-6
Cancer Workup in PWH	MS-6
Systemic Therapy and Drug-Drug Interactions	MS-7
Immune Checkpoint Inhibitors	MS-8
Radiation Therapy in PWH	MS-9
Cancer Surgery in PWH	MS-9
Supportive Care During Cancer Therapy in PWH	MS-10
Recommendations for Specific Cancers in PWH	MS-11
Anal Cancer in PWH	MS-11
Cervical Cancer in PWH	MS-14
Hodgkin Lymphoma in PWH	MS-15
Kaposi Sarcoma in PWH	MS-18
Lung Cancer in PWH	MS-18
NHL in PWH	MS-20
Management of Cancer in PWH in Lower Resource Settings	MS-20
Summary.	MS-21
References.	MS-22

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引用 / 出处

NCCN临床实践指南：HIV感染者癌症（2026.V1）. 2026.