Epidemiology of Cervical Adenocarcinoma and Squamous Cell Carcinoma Among Women Living With Human Immunodeficiency Virus Compared With the General Population in the United States.

BACKGROUND: Although cervical cancer risk overall is elevated among women living with human immunodeficiency virus (HIV; WLH), it is unclear whether risks are similarly elevated across histologic subtypes. METHODS: Data from the HIV/AIDS Cancer Match Study, a linkage of 12 US HIV and cancer registries during 1996 -2016, were used. Cervical cancers were categorized as adenocarcinoma (AC), squamous cell carcinoma (SCC), or other histologic subtype. Standardized incidence ratios compared rates of AC and SCC in WLH to those in general population. For WLH, risk factors for AC and SCC were evaluated using Poisson regression. Five-year survival was estimated by HIV status and histology. RESULTS: Overall, 62 615 cervical cancers were identified, including 609 in WLH. Compared with the general population, incidence of AC was 1.47 times higher (95% confidence interval [CI]: 1.03-2.05) and SCC was 3.62 times higher among WLH (95% CI: 3.31-3.94). Among WLH, there was no difference in AC rates by race/ethnicity or HIV transmission group, although SCC rates were lower among White women (vs Black) and higher among women who inject drugs (vs heterosexual transmission). Among WLH, 5-year overall survival was similar for AC (46.2%) and SCC (43.8%) but notably lower than for women not living with HIV. CONCLUSIONS: Among WLH, AC rates were modestly elevated, whereas SCC rates were greatly elevated compared with the general population. These findings suggest there may be differences in the impact of immunosuppression and HIV in the development of AC versus SCC, given their common etiology in human papillomavirus infection.

Age-specific burden of cervical cancer associated with HIV: A global analysis with a focus on sub-Saharan Africa.

HIV substantially worsens human papillomavirus (HPV) carcinogenicity and contributes to an important population excess of cervical cancer, particularly in sub-Saharan Africa (SSA). We estimated HIV- and age-stratified cervical cancer burden at a country, regional and global level in 2020. Proportions of cervical cancer (a) diagnosed in women living with HIV (WLHIV), and (b) attributable to HIV, were calculated using age-specific estimates of HIV prevalence (UNAIDS) and relative risk. These proportions were validated against empirical data and applied to age-specific cervical cancer incidence (GLOBOCAN 2020). HIV was most important in SSA, where 24.9% of cervical cancers were diagnosed in WLHIV, and 20.4% were attributable to HIV (vs 1.3% and 1.1%, respectively, in the rest of the world). In all world regions, contribution of HIV to cervical cancer was far higher in younger women (as seen also in empirical series). For example, in Southern Africa, where more than half of cervical cancers were diagnosed in WLHIV, the HIV-attributable fraction decreased from 86% in women ≤34 years to only 12% in women ≥55 years. The absolute burden of HIV-attributable cervical cancer (approximately 28 000 cases globally) also shifted toward younger women: in Southern Africa, 63% of 5341 HIV-attributable cervical cancer occurred in women <45 years old, compared to only 17% of 6901 non-HIV-attributable cervical cancer. Improved quantification of cervical cancer burden by age and HIV status can inform cervical cancer prevention efforts in SSA, including prediction of the impact of WLHIV-targeted vs general population approaches to cervical screening, and impact of HIV prevention.

Deaths Attributable to Cancer in the US Human Immunodeficiency Virus Population During 2001-2015.

BACKGROUND: Antiretroviral therapy (ART) has reduced mortality among people living with human immunodeficiency virus (HIV), but cancer remains an important cause of death. We characterized cancer-attributable mortality in the HIV population during 2001-2015. METHODS: We used data from population-based HIV and cancer registries in the United States (US). Cox proportional hazards regression models were used to estimate adjusted hazard ratios (HRs) associating cancer diagnoses with overall mortality, we could perhaps cut these words to accommodate the word limit. However readers will probably want to know what statistical adjustments were made to the model. Population-attributable fractions (PAFs) were calculated using these HRs and the proportion of deaths preceded by cancer. Cancer-specific PAFs and cancer-attributable mortality rates were calculated for demographic subgroups, AIDS-defining cancers (Kaposi sarcoma [KS], non-Hodgkin lymphoma [NHL], cervical cancer), and non-AIDS-defining cancers. RESULTS: Cancer-attributable mortality was 386.9 per 100 000 person-years, with 9.2% and 5.0% of deaths attributed to non-AIDS-defining and AIDS-defining cancers, respectively. Leading cancer-attributable deaths were from NHL (3.5%), lung cancer (2.4%), KS (1.3%), liver cancer (1.1%), and anal cancer (0.6%). Overall, cancer-attributable mortality declined from 484.0 per 100 000 person-years during 2001-2005 to 313.6 per 100 000 person-years during 2011-2015, while the PAF increased from 12.6% to 17.1%; the PAF for non-AIDS-defining cancers increased from 7.2% to 11.8% during 2011-2015. Cancer-attributable mortality was highest among those aged ≥60 years (952.2 per 100 000 person-years), with 19.0% of deaths attributed to non-AIDS-defining cancers. CONCLUSIONS: Although cancer-attributable mortality has declined over time, it remains high and represents a growing fraction of deaths in the US HIV population. Mortality from non-AIDS-defining cancers may rise as the HIV population ages. ART access, early cancer detection, and improved cancer treatment are priorities for reducing cancer-attributable mortality.

High Cancer Burden Among Antiretroviral Therapy Users in Malawi: A Record Linkage Study of Observational Human Immunodeficiency Virus Cohorts and Cancer Registry Data.

BACKGROUND: With antiretroviral therapy (ART), AIDS-defining cancer incidence has declined and non-AIDS-defining cancers (NADCs) are now more frequent among human immunodeficiency virus (HIV)-infected populations in high-income countries. In sub-Saharan Africa, limited epidemiological data describe cancer burden among ART users. METHODS: We used probabilistic algorithms to link cases from the population-based cancer registry with electronic medical records supporting ART delivery in Malawi's 2 largest HIV cohorts from 2000-2010. Age-adjusted cancer incidence rates (IRs) and 95% confidence intervals were estimated by cancer site, early vs late incidence periods (4-24 and >24 months after ART start), and World Health Organization (WHO) stage among naive ART initiators enrolled for at least 90 days. RESULTS: We identified 4346 cancers among 28 576 persons. Most people initiated ART at advanced WHO stages 3 or 4 (60%); 12% of patients had prevalent malignancies at ART initiation, which were predominantly AIDS-defining eligibility criteria for initiating ART. Kaposi sarcoma (KS) had the highest IR (634.7 per 100 000 person-years) followed by cervical cancer (36.6). KS incidence was highest during the early period 4-24 months after ART initiation. NADCs accounted for 6% of new cancers. CONCLUSIONS: Under historical ART guidelines, NADCs were observed at low rates and were eclipsed by high KS and cervical cancer burden. Cancer burden among Malawian ART users does not yet mirror that in high-income countries. Integrated cancer screening and management in HIV clinics, especially for KS and cervical cancer, remain important priorities in the current Malawi context.

Socioeconomic disparities in colorectal cancer mortality in the United States, 1990-2007.

United States colorectal cancer mortality rates have declined; however, disparities by socioeconomic status and race/ethnicity persist. The objective of this study was to describe the temporal association between colorectal cancer mortality and socioeconomic status by sex and race/ethnicity. Cancer mortality rates in the United States from 1990 to 2007, which were generated by the National Center for Health Statistics, and county-level socioeconomic status, which was estimated as the proportion of county residents living below the national poverty line based on 1990 US Census Bureau data, were obtained from the Surveillance, Epidemiology, and End Results program. The Kunst-Mackenbach relative index of inequality, which considers data across all poverty levels when comparing risks in the poorest (≥ 20%) and richest counties (<10%), was calculated as the measure of association. The study found that colorectal cancer mortality rates were significantly lower in the poorest counties than the richest counties during 1990-1992 among non-Hispanic whites, non-Hispanic black women and non-Hispanic API men. Over time though the tendency was for the poorest counties to have higher mortality rates. By 2003-2007 colorectal cancer mortality rates were significantly higher in the poorest than the richest counties among all sex-race/ethnicity groups. This disparity was most noticeable and appeared to be increasing most among Hispanic men. This suggests that socioeconomic disparities in colorectal cancer mortality were apparent after stratifying by sex and race/ethnicity and reversed over time. Further studies into the causes of these disparities would provide a basis for targeted cancer control interventions and allocation of public health resources.

Fine Particulate Matter, Noise Pollution, and Greenspace and Prostate Cancer Risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial Cohort.

BACKGROUND: Greenspace is hypothesized as being protective against cancer, whereas noise pollution and fine particulate matter (<2.5 µm in diameter, PM2.5) are both potential risk factors. Findings from recent studies of greenspace and PM2.5 with prostate cancer are not conclusive and the association between noise exposure and cancer has not been evaluated in a U.S. study. METHODS: We assessed PM2.5, noise, and greenspace exposure using spatiotemporal models and satellite-based estimates at enrollment addresses for N = 43,184 male participants of the prospective Prostate, Lung, Colorectal, and Ovarian Cancer (PLCO) Screening Trial cohort (enrolled 1994-2001). We used Cox regression models adjusted for age, race and ethnicity, study center, family history of prostate cancer, and Area Deprivation Index to estimate associations between ambient PM2.5 (µg/m3), greenspace (index range from -1 to 1), and noise pollution (loudest 10% of total existing sound, decibels) and incident prostate cancer risk through December 2017. RESULTS: A total of 6,327 cases of prostate cancer were diagnosed among male participants during follow-up. PM2.5 and noise exposures were moderately positively correlated (Spearman ρ = 0.46), and PM2.5 and greenspace were not correlated (ρ = 0.10); greenspace and noise were inversely correlated (ρ = -0.32). In single-pollutant and multipollutant models mutually adjusted for coexposures, we found no associations with prostate cancer risk. CONCLUSIONS: We did not find evidence that PM2.5, greenspace, and noise pollution were associated with prostate cancer risk in this large, geographically spread cohort. IMPACT: This study contributes to a small body of existing literature investigating these biologically plausible associations.

Risk of hepatocellular carcinoma in people with HIV in the United States, 2001-2019.

BACKGROUND: People with HIV have higher risk of hepatocellular carcinoma than the general population, partly because of higher prevalence of coinfection with hepatitis B virus (HBV) or hepatitis C virus (HCV). METHODS: We calculated standardized incidence ratios for hepatocellular carcinoma in people with HIV by comparing rates from people with HIV in the HIV/AIDS Cancer Match Study, a population-based HIV and cancer registry linkage, to those in the general population. We used multivariable Poisson regression to estimate adjusted incidence rate ratios among people with HIV and linked the Texas HIV registry with medical claims data to estimate adjusted odds ratios (AORs) of HBV and HCV in hepatocellular carcinoma patients with logistic regression. RESULTS: Compared with the general population, hepatocellular carcinoma rates in people with HIV were elevated 2.79-fold (n = 1736; 95% confidence interval [CI] = 2.66 to 2.92). Hepatocellular carcinoma rates decreased statistically significantly from 2001-2004 to 2015-2019 (P < .001). Compared with men who have sex with men, hepatocellular carcinoma risk was elevated 4.28-fold among men who injected drugs (95% CI = 3.72 to 4.93) and 1.83-fold among women who injected drugs (95% CI = 1.49 to 2.26). In Texas, 146 hepatocellular carcinoma cases among people with HIV were linked to claims data: 25% HBV positive, 59% HCV positive, and 13% coinfected with HBV and HCV. Compared with men who had sex with men, people who inject drugs had 82% decreased odds of HBV (AOR = 0.18, 95% CI = 0.05 to 0.63) and 2 times the odds of HCV (AOR = 20.4, 95% CI = 3.32 to 125.3). CONCLUSIONS: During 2001-2019, hepatocellular carcinoma risk declined among people with HIV, though rates remain statistically significantly elevated compared with the general population, particularly among people who inject drugs. Prevention and treatment of HBV/HCV are needed to reduce hepatocellular carcinoma risk among people with HIV.

Real-world use of antiretroviral therapy and risk of cancer among people with HIV in Texas.

BACKGROUND: Combination antiretroviral therapy (cART) may reduce cancer risk among people with HIV (PWH), but cancer-specific associations are incompletely understood. METHODS: We linked HIV and cancer registries in Texas to a national prescription claims database. cART use was quantified as the proportion of days covered (PDC). Cox proportional hazards models assessed associations of cancer risk with cART usage, adjusting for demographic characteristics, AIDS status, and time since HIV report. RESULTS: We evaluated 63 694 PWH followed for 276 804 person-years. The median cART PDC was 21.4% (interquartile range: 0.0-59.8%). cART use was associated with reduced risk of Kaposi sarcoma [adjusted hazard ratio (aHR) 0.48, 95% confidence interval (CI) 0.34-0.68 relative to unexposed status] and non-Hodgkin lymphoma (aHR 0.41, 95% CI 0.31-0.53), liver cancer (aHR 0.61, 95% CI 0.39-0.96), anal cancer (aHR 0.65, 95% CI 0.46-0.92), and a miscellaneous group of 'other' cancers (aHR 0.80, 95% CI 0.66-0.98). In contrast, cART-exposed status was not associated with risk for cervical, lung, colorectal, prostate or breast cancers. CONCLUSION: In a large HIV cohort incorporating data from prescription claims, cART was associated with greatly reduced risks of Kaposi sarcoma and non-Hodgkin lymphoma, and to a lesser degree, reduced risks of liver and anal cancers. These associations likely reflect the beneficial effects of HIV suppression and improved immune control of oncogenic viruses. Efforts to increase cART use and adherence may further decrease cancer incidence among PWH.

Cancer Treatment Disparities in People With HIV in the United States, 2001-2019.

PURPOSE: People with HIV (PWH) have worse cancer outcomes, partially because of inequities in cancer treatment. We evaluated cancer treatment disparities among PWH, including an assessment of changes in disparities over time. METHODS: We used data from the HIV/AIDS Cancer Match Study, a population-based HIV and cancer registry linkage to examine diffuse large B-cell lymphoma (DLBCL), Hodgkin lymphoma (HL), and cancers of the cervix, lung, anus, prostate, colon, and female breast. Outcomes included receipt of (1) any cancer treatment and (2) standard therapy among patients with local-stage cancer. We assessed associations between HIV and each outcome by estimating adjusted prevalence odds ratios (aORs) with 95% CI and trends over time. We identified predictors of nonreceipt of cancer treatment in PWH. RESULTS: From 2001 to 2019, compared with people with cancer without HIV (n = 2,880,955), PWH (n = 16,334) were more likely to not receive cancer treatment for cervical cancer (aOR, 2.03 [95% CI, 1.52 to 2.70]), DLBCL (aOR, 1.53 [95% CI, 1.38 to 1.70]), HL (aOR, 1.39 [95% CI, 1.19 to 1.63]), lung cancer (aOR, 1.79 [95% CI, 1.65 to 1.93]), prostate cancer (aOR, 1.32 [95% CI, 1.21 to 1.44]), colon cancer (aOR, 1.73 [95% CI, 1.43 to 2.08]), and breast cancer (aOR, 1.38 [95% CI, 1.07 to 1.77]). Similar associations were observed in PWH with local-stage cancers although no difference was observed for anal cancers. The association between HIV and nonreceipt of cancer treatment significantly decreased over time for breast, colon, and prostate cancers (all P trend <.0001), but PWH remained less likely to receive treatment in 2014-2019 for DLBCL, cervix, and lung cancers. Among PWH, Black individuals, people who inject drugs, and those 65 years and older were less likely to receive cancer treatment. CONCLUSION: Disparities in receipt of cancer treatment persist for PWH in the United States in contemporary time periods. Solutions to address inequitable receipt of cancer treatment among PWH are urgently needed.

Survival by sex and HIV status in patients with anal cancer in the USA between 2001 and 2019: a retrospective cohort study.

BACKGROUND: The risk of anal cancer is increased among people with HIV, particularly men who have sex with men. Estimating survival by HIV status and sex and identifying groups at high risk is crucial for documenting prognostic differences between populations. We aimed to compare all-cause and anal cancer-specific survival in patients with anal cancer with and without HIV, stratified by sex, and to identify predictors of survival, stratified by HIV status. METHODS: In this retrospective cohort study, we used data from the HIV/AIDS Cancer Match Study of 13 population-based HIV and cancer registries throughout the USA. We included individuals aged 20-79 years diagnosed with invasive anal cancer between 2001 and 2019. To estimate associations between HIV status and both all-cause and anal cancer-specific mortality overall, we used Cox proportional hazards models, adjusting for year of and age at diagnosis, sex, race and ethnicity, histology, cancer stage, region, and treatment. We also calculated sex-specific adjusted hazard ratios (HRs). By HIV status, we identified characteristics associated with mortality. Models among people with HIV were further adjusted for AIDS status and HIV transmission risk group. FINDINGS: Between Jan 1, 2001, and Dec 31, 2019, 1161 (43·6%) of 2662 patients with anal cancer and HIV and 7722 (35·4%) of 21 824 patients without HIV died. HIV was associated with a 1·35 times (95% CI 1·24-1·47) increase in all-cause mortality among male patients and a 2·47 times (2·10-2·90) increase among female patients. Among patients with HIV, all-cause mortality was increased among non-Hispanic Black individuals (adjusted HR 1·19, 95% CI 1·04-1·38), people with AIDS (1·36, 1·10-1·68), people who inject drugs (PWID; 1·49, 1·17-1·90), patients with adenocarcinoma (2·74, 1·82-4·13), and those with no or unknown surgery treatment (1·34, 1·18-1·53). HIV was associated with anal cancer-specific mortality among female patients only (1·52, 1·18-1·97). Among patients with HIV, anal cancer-specific mortality was increased among patients with adenocarcinoma (3·29, 1·89-5·72), those with no or unknown treatment (1·59, 1·17-2·17), and PWID (1·60, 1·05-2·44). INTERPRETATION: HIV was associated with all-cause mortality among patients with anal cancer, especially women. Anal cancer-specific mortality was elevated among female patients with HIV. As screening for anal cancer becomes more widespread, examining the effects of screening on survival by HIV status and sex is crucial. FUNDING: US National Cancer Institute Intramural Research Program.

Cancer risk among HIV-exposed uninfected children in the United States.

In utero exposure to didanosine was associated with increased risk of brain cancer in a French study. We used United States health department records to assess cancer risk among 13 617 children exposed to HIV in utero , who remained HIV-uninfected after birth (1990-2017). Risk of brain tumors was borderline elevated among these children (standardized incidence ratio 2.2, 95% confidence interval 0.8-4.8, P  = 0.12, based on six cases). Risk was not significantly increased for leukemia or other cancers.

Risk of Nonkeratinocyte Skin Cancers in People Living with HIV during the Era of Antiretroviral Therapy.

Antiretroviral therapy may alter susceptibility to nonkeratinocyte skin cancers (NKSCs) by improving immunity in people living with HIV. Using linked data from HIV and cancer registries in 12 states/regions in the United States during the antiretroviral therapy era (1996‒2018), we calculated standardized incidence ratios for 27 NKSCs, comparing incidence with that of the general population. Risk factors for NKSCs were evaluated using Poisson regression. There were 2,743 NKSCs diagnosed in 585,706 people living with HIV followed for 4,575,794 person-years. Kaposi sarcoma was the most common cancer (82%), followed by melanoma (12%) and cutaneous lymphoma (2.6%). Incidence was elevated for virus-related NKSCs: Kaposi sarcoma (standardized incidence ratio = 147, 95% confidence interval = 141‒153), diffuse large B-cell lymphoma (standardized incidence ratio = 5.19, 95% confidence interval = 3.13‒8.11), and Merkel cell carcinoma (standardized incidence ratio = 3.15, 95% confidence interval = 1.93‒4.87); elevated incidence for diffuse large B-cell lymphoma and Merkel cell carcinoma was observed only among people living with HIV with a previously acquired immunodeficiency syndrome diagnosis. Kaposi sarcoma risk was highest among men who have sex with men. Incidence was not increased for melanoma, adnexal carcinomas, and sarcomas. Melanoma and Merkel cell carcinoma arose disproportionately on sun-exposed skin, supporting a role for UVR in their development. In conclusion, risk for most NKSCs was similar to that of the general population during the antiretroviral therapy era, suggesting that people living with HIV without NKSC risk factors may not require intensive skin surveillance.

Cumulative incidence of anal cancer since HIV or AIDS diagnosis in the United States.

Treatment of screen-detected anal high-grade squamous intraepithelial lesions has been shown to effectively reduce the incidence of invasive anal cancer in people with HIV. We provide population-based estimates of cumulative incidence of anal cancer by risk group and age at HIV or AIDS diagnosis. The 0- to 10-year cumulative incidence of anal cancer for men who have sex with men and are younger than 30 years of age at HIV diagnosis was 0.17% (95% confidence interval [CI] = 0.13% to 0.20%) compared with 0.04% (95% CI = 0.02% to 0.06%) in other men and 0.03% (95% CI = 0.01% to 0.04%) in women. For men who have sex with men and have a diagnosis of AIDS and are younger than 30 years of age, the 0- to 10-year cumulative incidence was 0.35% (95% CI = 0.28% to 0.41%). Among people with HIV, men who have sex with men are at the greatest risk of anal cancer, and those with a diagnosis of AIDS had higher risk than those without AIDS. These estimates may inform recommendations for priority populations that could benefit most from anal cancer screening and treatment.

Fine mapping of 14q24.1 breast cancer susceptibility locus.

In the National Cancer Institute Cancer Genetic Markers of Susceptibility (CGEMS) genome-wide association study of breast cancer, a single nucleotide polymorphism (SNP) marker, rs999737, in the 14q24.1 interval, was associated with breast cancer risk. In order to fine map this region, we imputed a 3.93 MB region flanking rs999737 for Stages 1 and 2 of the CGEMS study (5,692 cases, 5,576 controls) using the combined reference panels of the HapMap 3 and the 1000 Genomes Project. Single-marker association testing and variable-sized sliding-window haplotype analysis were performed, and for both analyses the initial tagging SNP rs999737 retained the strongest association with breast cancer risk. Investigation of contiguous regions did not reveal evidence for an additional independent signal. Therefore, we conclude that rs999737 is an optimal tag SNP for common variants in the 14q24.1 region and thus narrow the candidate variants that should be investigated in follow-up laboratory evaluation.

Socioeconomic disparities and breast cancer hormone receptor status.

PURPOSE: Recent research, although inconsistent, indicates that socioeconomic status (SES) may be associated with hormone receptor (HR) status. This study aims to examine the association between SES and breast cancer HR status within and across racial/ethnic groups stratified by age at diagnosis and tumor stage. METHODS: The study subjects were 184,602 women with incident breast cancer diagnosed during 2004-2007 and identified from the National Cancer Institute's Surveillance, Epidemiology and End Results program. Log-binomial regression assessed the risk of having breast tumors that were (1) HR-negative versus HR-positive and (2) HR-unknown versus HR-known between women who, at the time of diagnosis, were residing in high or medium poverty areas compared to low poverty areas. RESULTS: High poverty areas tended to have a greater prevalence of HR-negative tumors compared to more affluent areas. Although not always significant, this was observed among non-Hispanic white and Hispanic women regardless of age-tumor stage category, and only among young, non-Hispanic black women and non-Hispanic Asian/Pacific Islander women with regional and distant stage. High poverty areas also tended to have a greater prevalence of HR-unknown tumors compared to more affluent areas. Furthermore, significant trends between HR status and poverty level varied by race/ethnicity, age, and tumor stage. CONCLUSIONS: Poverty may be related to breast cancer negative and unknown HR status. These findings suggest the effects of non-genetic factors on biochemical features of breast cancer, as well as imply a clinical importance to improve HR measurement or recording for low socioeconomic breast cancer patients.

Years of life lost to cancer among the United States HIV population, 2006-2015.

OBJECTIVES: We estimated years of life lost (YLLs) to all causes of death and YLL lost to cancer among persons with HIV (PWH) in the United States. DESIGN: Linked HIV and cancer registry data from the HIV/AIDS Cancer Match Study were used to identify incident cancers and deaths among PWH in 11 regions of the United States during 2006-2015. METHODS: Mean YLL (MYLL) to all causes of death and MYLL to cancer during 2006-2015 were derived from the restricted mean survival estimated from Cox proportional hazards regression models. MYLLs were then upweighted to the national population of PWH to obtain all-cause total YLL (TYLL) and cancer-related TYLL in the United Staets during 2006-2015. RESULTS: Among 466 234 PWH in the study population, 25 772 (5.5%) developed cancer during 2006-2015. Nationally, an estimated 134 986 years of life were lost to cancer of all types during 2006-2015 among PWH, representing 9.6% of TYLL to all causes. Non-Hodgkin lymphoma (NHL), Kaposi sarcoma, anal cancer, and lung cancer were the four largest cancer contributors (45% of TYLL to cancer). The largest fraction of TYLL occurred among back PWH, MSM, and PWH aged 40-59 years old. CONCLUSION: PWH have higher mortality rates after developing cancer. NHL, Kaposi sarcoma and anal and lung cancers were large contributors to YLL to cancer in the United States population of PWH, highlighting opportunities to reduce cancer mortality through improved access to antiretroviral treatment, prevention, and screening.

Impact of HIV on Anal Squamous Cell Carcinoma Rates in the United States, 2001-2015.

BACKGROUND: Incidence of anal squamous cell carcinoma (SCC) has increased in the United States. People living with HIV (PLWH) have an elevated risk of anal SCC, and changes in the number of anal SCCs among PLWH may have influenced general population trends. METHODS: Data were obtained from a linkage of HIV and cancer registries in 12 US regions. The proportion of anal SCCs occurring among PLWH was estimated by sex, age group, and race and ethnicity. To assess the impact of anal SCCs among PLWH on general population trends, annual percent changes (APCs) in incidence rates including and excluding anal SCCs among PLWH were estimated. RESULTS: Between 2001 and 2015, 14.5% of 16 110 anal SCC diagnoses occurred in PLWH. In 2013-2015, 35% of anal SCCs among men occurred in PLWH, but only 2% among women. The proportion of anal SCCs among PLWH was highest among 20- to 49-year-olds and Black and Hispanic individuals. General population anal SCC trends among men were strongly influenced by anal SCCs among PLWH: rates increased 4.6%/y (95% confidence interval [CI] = 1.4% to 8.0%) from 2001 to 2009 followed by a statistically non-significant decline (APC = -2.7%/y, 95% CI = -7.1% to 2.0%) from 2009 to 2015, but without anal SCCs among PLWH, rates were stable (APC = 0.7%/y, 95% CI = -0.8% to 2.3%). Anal SCC rates among women increased 3.8%/y (95% CI = 3.2% to 4.4%) during 2001-2012 and then declined statistically non-significantly (APC = -3.8%/y, 95% CI = -6.9% to -0.6%), and anal SCCs among PLWH had little impact on these trends. CONCLUSIONS: During 2001-2015, anal SCCs among PLWH contributed strongly to changes in incidence trends in the general US population among men, but not women.

Trends and risk of lung cancer among people living with HIV in the USA: a population-based registry linkage study.

BACKGROUND: Lung cancer is a common cancer in people living with HIV, but the risk of cancer in this group has not been investigated for over a decade. We investigated trends in relative and absolute risk of lung cancer among people living with HIV of various age groups in the USA. METHODS: In this population-based registry linkage study, we used 2001-16 data from the HIV/AIDS Cancer Match study, which links data from HIV and cancer registries from 13 regions in the USA. We included non-Hispanic White, non-Hispanic Black, and Hispanic individuals living with HIV aged 20-89 years in our study population. Average annual percentage changes in lung cancer rates were estimated with multivariable Poisson regression, and standardised incidence ratios (SIRs) and excess absolute risks were estimated comparing people living with HIV with the general US population. We used non-parametric cumulative incidence curves to estimate the 5-year cumulative incidence of lung cancer and two AIDS-defining cancers (non-Hodgkin lymphoma and Kaposi sarcoma). FINDINGS: There were 3426 lung cancers in 4 310 304 person-years of follow-up in our study population. Age-standardised lung cancer incidence rates in people living with HIV declined by 6% per year (95% CI -7 to -5) during 2001-16, with greater declines in the 20-29 age group (-11%, -16 to 6) than in the older age groups (eg, -3% [-6 to 1] in those aged 70-89 years). During 2013-16, the SIR of lung cancer in people living with HIV was 2·01 (95% CI 1·52 to 2·61) in those aged 40-49 years, and 1·31 (1·12 to 1·52) in those aged 60-69 years, whereas the excess absolute risk among people living with HIV was 11·87 (3·95 to 21·89) per 100 000 person-years for those aged 40-49 years and 48·23 (6·88 to 95·47) per 100 000 person-years for those aged 60-69 years. Beginning in 2011, the 5-year cumulative incidence for lung cancer (1·36%, 95% CI 1·17 to 1·53) surpassed that of Kaposi sarcoma (0·12%, 0·06 to 0·17) and non-Hodgkin lymphoma (0·45%, 0·35 to 0·56) for people living with HIV aged 60-69 years. INTERPRETATION: Between 2001 and 2016, the risk of lung cancer decreased for people living with HIV aged 20-69 years, but remained substantially elevated compared with the general population, probably due to a combination of smoking and immunosuppression. For people living with HIV aged 60 years and older, the risk of lung cancer exceeds that of two of the most common AIDS-defining cancers, highlighting the importance of lung cancer among the growing older population of people living with HIV. FUNDING: Intramural Research Program of the US National Cancer Institute.

Kaposi Sarcoma Incidence, Burden, and Prevalence in United States People with HIV, 2000-2015.

BACKGROUND: The introduction of combination antiretroviral therapy (cART) has led to a significant reduction in Kaposi sarcoma (KS) incidence among people with HIV (PWH). However, it is unclear if incidence has declined similarly across key demographic and HIV transmission groups and the annual number of incident and prevalent KS cases remains unquantified. METHODS: Using population-based registry linkage data, we evaluated temporal trends in KS incidence using adjusted Poisson regression. Incidence and prevalence estimates were applied to CDC HIV surveillance data, to obtain the number of incident (2008-2015) and prevalent (2015) cases in the United States. RESULTS: Among PWH, KS rates were elevated 521-fold [95% confidence intervals (CI), 498-536] compared with the general population and declined from 109 per 100,000 person-years in 2000 to 47 per 100,000 person-years in 2015, at an annual percentage change of -6%. Rates declined substantially (P trend < 0.005) across all demographic and HIV transmission groups. Of the 5,306 new cases estimated between 2008 and 2015, 89% occurred among men who have sex with men. At the end of 2015, 1,904 PWH (0.20%) had been diagnosed with KS in the previous 5 years. CONCLUSIONS: A consistent gradual decline in KS incidence has occurred among PWH in the United States during the current cART era. This decrease is uniform across key demographic and HIV transmission groups, though rates remain elevated relative to the general population. IMPACT: Continued efforts to control HIV through early cART initiation and retention in care need to be maintained and possibly expanded to sustain declines.