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Background In the United States, anal squamous cell carcinoma rates have increased rapidly, particularly among women 50 or older than 66 years of age. As immunosuppression is associated with increased risk, autoimmune conditions may be associated with greater risk of anal squamous cell carcinoma. Methods We conducted a population-based, case-control study using Surveillance, Epidemiology, and End Results–Medicare data (2000-2017). Anal squamous cell carcinoma cases (n = 4505) were matched to 200 000 cancer-free controls. Using multivariable logistic regression, we calculated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between 47 autoimmune conditions diagnosed before selection, identified using Medicare claims, and anal squamous cell carcinoma. The Bonferroni threshold was used to correct for multiple comparisons. Population attributable fractions were calculated for conditions nominally associated with anal squamous cell carcinoma. Results In total, 18% of anal squamous cell carcinoma cases and 15% of cancer-free controls had a diagnosed autoimmune condition. Any autoimmune condition was associated with an increased risk of anal squamous cell carcinoma (OR = 1.11, 95% CI = 1.02 to 1.21; population attributable fraction = 1.8%). Anal squamous cell carcinoma was associated with systemic lupus erythematosus (OR = 1.79, 95% CI = 1.32 to 2.42; population attributable fraction = 0.4%) and nominally associated (P  < .05) with sarcoidosis (OR = 2.09, 95% CI = 1.30 to 3.37; population-attributable fraction = 0.2%) and psoriasis (OR = 1.28, 95% CI = 1.06 to 1.56; population attributable fraction = 0.5%). Stratified by sex, only women showed statistically significant associations for systemic lupus erythematosus (OR = 1.97, 95% CI = 1.46 to 2.68). Statistically significant interaction was observed by sex for psoriasis (men vs women: OR = 1.68 [95% CI = 1.03 to 4.28] vs OR = 1.12 [95% CI = 0.88 to 1.43]) and polymyalgia rheumatica (OR = 0.33 [95% CI = 0.12 to 0.89] vs OR = 0.99 [95% CI = 0.75 to 1.30]). Conclusion Systemic lupus erythematosus, sarcoidosis, and psoriasis were associated with a moderately increased risk of anal squamous cell carcinoma. Given these conditions' rarity and moderate associations with anal squamous cell carcinoma, autoimmune diseases cannot explain the rising trend in this disease. [ABSTRACT FROM AUTHOR]

Background Anal intraepithelial neoplasia grade III is a precursor to squamous cell carcinoma of the anus for which rates are nearly 20-fold higher in people with HIV than in the general population in the United States. We describe trends in anal intraepithelial neoplasia grade III diagnosis and risk of squamous cell carcinoma of the anus following anal intraepithelial neoplasia grade III by HIV status and sex. Methods We used data from a population-based linkage between cancer and HIV registries in 11 US states; Puerto Rico; and Washington, DC, during 1996-2019. We identified all individuals with a diagnosis of anal intraepithelial neoplasia grade III and determined their HIV status. We estimated the average annual percentage change of anal intraepithelial neoplasia grade III using Poisson regression stratified by HIV status and sex. We estimated the 5-year cumulative incidence of squamous cell carcinoma of the anus following an anal intraepithelial neoplasia grade III diagnosis stratified by sex, HIV status, and prior AIDS diagnosis. Results Among people with HIV, average annual percentage changes for anal intraepithelial neoplasia grade III were 15% (95% confidence interval [CI] = 12% to 17%) per year among females and 12% (95% CI = 11% to 14%) among males. Average annual percentage changes for those without HIV were 8% (95% CI = 7% to 8%) for females and 8% (95% CI = 6% to 9%) for males. Among people with HIV, a prior AIDS diagnosis was associated with a 2.7-fold (95% CI = 2.23 to 3.40) and 1.9-fold (95% CI = 1.72 to 2.02) increased risk of anal intraepithelial neoplasia grade III diagnosis for females and males, respectively. Five-year cumulative incidence of squamous cell carcinoma of the anus following anal intraepithelial neoplasia grade III for people with HIV with a prior AIDS diagnosis were 3.4% and 3.7% for females and males, respectively. Conclusions Rates of anal intraepithelial neoplasia grade III diagnoses have increased since 1996, particularly for people with HIV, likely influenced by increased screening. A prior AIDS diagnosis was strongly associated with risk of anal intraepithelial neoplasia grade III diagnosis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: In the United States, incidence and mortality rates of hepatocellular carcinoma (HCC) are increasing in older individuals. Chronic infection with hepatitis C virus (HCV) and hepatitis B virus (HBV) are important causes of HCC; however, the contribution of viral hepatitis to recent trends in HCC incidence among older Americans is unclear.Methods: Data from the Surveillance, Epidemiology, and End Results-Medicare linkage (SEER-Medicare) for the years 2001 through 2013 were used to identify HCC cases among individuals aged ≥66 years and Medicare files were used to assess the HCV and HBV status of these HCC cases. Age-standardized incidence rates of HCV-attributable, HBV-attributable, and HCV/HBV-unrelated HCC were estimated overall and by age group, sex, and race/ethnicity. The authors also calculated annual percent changes (APCs) in HCC incidence.Results: Between 2001 and 2013, a total of 15,300 HCC cases occurred in this population. Overall HCC rates increased 43% from 16.3 to 23.3 per 100,000 population (APC, 3.40% per year), whereas HCV-attributable HCC rates nearly doubled from 4.2 to 8.2 per 100,000 population (APC, 5.62% per year). HCC rates increased more slowly for HBV-attributable HCC (1.3 to 1.8 per 100,000 population; APC, 3.17% per year) and HCV/HBV-unrelated HCC (11.3 to 14.1 per 100,000 population; APC, 2.35% per year). The percentage of HCC cases with evidence of HCV infection increased from 25.7% in 2001 through 2004 to 32.3% in 2011 through 2013, whereas the percentage with HBV remained stable at 8%. In 2013, higher rates for both HCV-attributable and HBV-attributable HCC were noted among individuals aged 66 to 75 years, men, and individuals of Asian ancestry.Conclusions: Among Americans aged ≥66 years, HCC rates increased rapidly between 2001 and 2013. Although HCV-attributable cases contributed substantially to this increase, rates of HBV-attributable and HCV/HBV-unrelated HCC also rose during this period. [ABSTRACT FROM AUTHOR]

The article discusses the cancer risk following post-transplant lymphoproliferative disorders in solid organ transplant recipients. Topics include how post-transplant lymphoproliferative disorders (PTLDs) are associated with immunosuppressive therapy administered to prevent graft rejection, leading to uncontrolled replication of Epstein–Barr virus (EBV).

Background: Human papillomavirus (HPV) causes 10% of cancers among human immunodeficiency virus (HIV)-infected people in the United States. Because Hispanics are disproportionally affected by the HIV epidemic and by infection-related cancers, this study compared incidence rates for HPV-related cancers and survival between Hispanics and non-Hispanic whites (NHWs) and non-Hispanic blacks (NHBs) in the HIV-infected US population.Methods: Based on data from the HIV/AIDS Cancer Match Study, standardized incidence ratios (SIRs) were used to estimate cancer risk in HIV-infected Hispanics and the general US Hispanic population. Among HIV-infected people, cancer rates were compared with incidence rate ratios (IRRs), and survival was compared with hazard ratios between Hispanics and NHWs and NHBs.Results: Five hundred two HPV-related cancers occurred in 864,067 person-years of follow-up among HIV-infected Hispanics. Except for oropharyngeal cancer, the risk of HPV-related cancers was higher among HIV-infected Hispanics than in the general population (SIR range, 3.59 [cervical cancer] to 18.7 [anal cancer in men]). Among HIV-infected females, Hispanics had higher cervical cancer rates than NHWs (IRR, 1.70; 95% confidence interval [CI], 1.19-2.43) but lower vulvar cancer rates than NHWs (IRR, 0.40; 95% CI, 0.24-0.67) and NHBs (IRR, 0.62; 95% CI, 0.41-0.95). Among HIV-infected males, Hispanics had higher penile cancer rates than NHWs (IRR, 2.60; 95% CI, 1.36-4.96) but lower anal cancer rates than NHWs (IRR, 0.54; 95% CI, 0.46-0.63) and NHBs (IRR, 0.65; 95% CI, 0.56-0.77). Among HIV-infected Hispanics, 5-year survival was greater than 50% across HPV-related cancer types, with no major differences by racial/ethnic group.Conclusions: HIV-infected Hispanics have an elevated risk for HPV-related cancers. Similarly to the general population, HIV-infected Hispanics have higher rates of cervical and penile cancer than NHWs and NHBs. HPV vaccination should be promoted among HIV-infected individuals to reduce the burden of HPV-related cancers. [ABSTRACT FROM AUTHOR]

Background: Although people living with HIV or AIDS (PLWHA) are at higher risk for many cancers, breast, prostate, and colorectal cancer rates are lower in this patient population. Because these tumors are often screen-detected, these inverse associations could be driven by HIV-related differences in utilization of cancer screening.Methods: We ascertained incident breast, prostate, and colorectal cancer in PLWHA using data from the HIV/AIDS Cancer Match Study (1996-2012). Comparisons with general population cancer rates were made using standardized incidence ratios (SIRs), overall and stratified by tumor stage/size, breast cancer estrogen receptor status, and colorectal site. We also examined the potential effect of study design and unmeasured confounding on inverse standardized incidence ratios.Results: Compared with the general population, PLWHA had lower rates of invasive breast (SIR = 0.63, 95% confidence interval [CI] = 0.58 to 0.68), prostate (SIR = 0.48, 95% CI = 0.46 to 0.51), proximal colon (SIR = 0.67, 95% CI = 0.59 to 0.75), distal colon (SIR = 0.51, 95% CI = 0.43 to 0.59), and rectal cancers (SIR = 0.69, 95% CI = 0.61 to 0.77). Reduced risk persisted across tumor stage/size for prostate and colorectal cancers. Although distant-stage breast cancer rates were not reduced (SIR = 0.94, 95% CI = 0.73 to 1.20), HIV-infected women had lower rates of large (>5 cm) breast tumors (SIR = 0.65, 95% CI = 0.50 to 0.83). The magnitude of these inverse standardized incidence ratios could not plausibly be attributed to case underascertainment, out-migration, or unmeasured confounding.Conclusions: Breast, prostate, and colorectal cancer rates are markedly lower among PLWHA, including rates of distant-stage/large tumors that are not generally screen-detected. This set of inverse HIV-cancer associations is therefore unlikely to be due primarily to differential screening and may instead represent biological relationships requiring future investigation. [ABSTRACT FROM AUTHOR]

Background. Cancer risk is increased in persons living with human immunodeficiency virus (HIV) (PLWH). Improved survival has led to an aging of PLWH. We evaluated the cancer risk in older PLWH (age ≥50 years). Methods. We included data from the HIV/AIDS Cancer Match Study (1996--2012) and evaluated risks of Kaposi sarcoma (KS), non-Hodgkin lymphoma (NHL), Hodgkin lymphoma, and cervical, anal, lung, liver, oral cavity/pharyngeal, breast, prostate, and colon cancers in older PLWH with risk in the general population by calculating standardized incidence ratios (SIRs) and excess absolute risks (EARs). Cancer risk by time since HIV diagnosis was estimated using Poisson regression. Results. We identified 10 371 cancers among 183 542 older PLWH. Risk was significantly increased for KS (SIR, 103.34), NHL (3.05), Hodgkin lymphoma (7.61), and cervical (2.02), anal (14.00), lung (1.71), liver (2.91), and oral cavity/pharyngeal (1.66) cancers, and reduced for breast (0.61), prostate (0.47), and colon (0.63) cancers. SIRs declined with age for all cancers; however, EARs increased with age for anal, lung, liver, and oral cavity/pharyngeal cancers. Cancer risk was highest for most cancers within 5 years after HIV diagnosis; risk decreased with increasing time since HIV diagnosis for KS, NHL, lung cancer, and Hodgkin lymphoma. Conclusions. Cancer risk is elevated among older PLWH. Although SIRs decrease with age, EARs are higher for some cancers, reflecting a greater absolute excess in cancer incidence among older PLWH. High risk in the first 5 years after HIV diagnosis for some cancers highlights the need for early HIV diagnosis and rapid treatment initiation. [ABSTRACT FROM AUTHOR]

Background: Oral tongue cancer incidence has increased among whites in the United States; however, the cause remains unknown. If an infectious agent is implicated, then elevated risk would be expected among immunosuppressed individuals.Methods: By using population-based registry linkage information from the US Transplant Cancer Match and human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) Cancer Match studies, the authors examined the risk of oral tongue squamous cell carcinoma (SCC) among immunocompromised transplantation recipients and HIV-infected individuals. In addition, the risks of oropharyngeal SCC (strongly related to human papillomavirus infection; modestly affected by immunosuppression), other tobacco/alcohol-related oral cavity SCCs (not thought to be infection/immunosuppression-related), and non-Hodgkin lymphoma of oral cavity/pharynx (strongly related to Epstein-Barr virus; profoundly affected by immunosuppression) were evaluated.Results: Compared with the general population, the risk of non-Hodgkin lymphoma was strongly increased (standardized incidence ratio [SIR] > 8.0). The risk of all SCCs was modestly and similarly elevated among transplantation recipients (SIR range, 2.2-2.7; Pheterogeneity  = .2); whereas, among HIV-infected individuals, the risk of oral tongue SCC was higher compared with the risk of other SCCs (SIR, 3.0 vs 1.7 [for oropharyngeal SCCs] and 2.3 [for other oral cavity SCCs]; Pheterogeneity  < .001). The risk of SCCs was significantly higher among men, older individuals, and whites; and risk increased with the time since transplantation/AIDS onset. The risk of oral tongue SCC was significantly higher among HIV-infected men who have sex with men compared with the average risk in HIV-infected individuals (adjusted incidence rate ratio = 2.0).Conclusions: Similar modest increases in the risk of oral tongue and other oral cavity SCCs do not suggest that an infectious agent or exposure profoundly affected by immunosuppression underlies the increase in oral tongue cancer. Cancer 2018;124:2515-22. © 2018 American Cancer Society. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background. Cancer remains an important cause of morbidity and mortality in people with human immunodeficiency virus (PWHIV) on effective antiretroviral therapy (ART). Estimates of cancer-attributable mortality can inform public health efforts. Methods. We evaluated 46 956 PWHIV receiving ART in North American HIV cohorts (1995-2009). Using information on incident cancers and deaths, we calculated population-attributable fractions (PAFs), estimating the proportion of deaths due to cancer. Calculations were based on proportional hazards models adjusted for age, sex, race, HIV risk group, calendar year, cohort, CD4 count, and viral load. Results. There were 1997 incident cancers and 8956 deaths during 267 145 person-years of follow-up, and 11.9% of decedents had a prior cancer. An estimated 9.8% of deaths were attributable to cancer (cancer-attributable mortality rate 327 per 100 000 person-years). PAFs were 2.6% for AIDS-defining cancers (ADCs, including non-Hodgkin lymphoma, 2.0% of deaths) and 7.1% for non-AIDS-defining cancers (NADCs: lung cancer, 2.3%; liver cancer, 0.9%). PAFs for NADCs were higher in males and increased strongly with age, reaching 12.5% in PWHIV aged 55+ years. Mortality rates attributable to ADCs and NADCs were highest for PWHIV with CD4 counts <100 cells/mm³. PAFs for NADCs increased during 1995-2009, reaching 10.1% in 2006-2009. Conclusions. Approximately 10% of deaths in PWHIV prescribed ART during 1995-2009 were attributable to cancer, but this fraction increased over time. A large proportion of cancer-attributable deaths were associated with non-Hodgkin lymphoma, lung cancer, and liver cancer. Deaths due to NADCs will likely grow in importance as AIDS mortality declines and PWHIV age. [ABSTRACT FROM AUTHOR]

The acquired immune deficiency syndrome (AIDS) epidemic was first recognized in 1981, and it quickly became a public health emergency. In a 1987 paper in the American Journal of Epidemiology (Am J Epidemiol. 1987;126(2): 310-318), Richard Kaslow et al. described the launch of the Multicenter AIDS Cohort Study (MACS), a cohort study of homosexual men in 4 US cities, the purpose of which was to better understand the natural history of AIDS and its determinants. The MACS enrolled participants through a range of community contacts. These efforts facilitated rapid recruitment, but given the targeted approaches, participants tended to comprise high-risk social networks. At baseline, 4%-26% of participants at the 4 sites reported having a sexual partner who had developed AIDS. Kaslow et al. also described baseline testing for the causative agent of AIDS, the human immunodeficiency virus (HIV). HIV sero- prevalence was remarkably high, ranging from 11 %-26% across age groups in Pittsburgh to 38%-53% in Los Angeles. The major turning point in the epidemic occurred in 1995-1996 when combination antiretroviral therapy was introduced, effectively blocking HIV replication and markedly reducing AIDS morbidity and mortality. The MACS cohort continues to be followed actively 3 decades after its launch and has proven to be an important resource for information on HIV infection and AIDS. [ABSTRACT FROM AUTHOR]

Background: Although ultraviolet radiation (UVR) is established as both an inducer of herpes simplex virus reactivation and as the primary risk factor for many common skin cancers, its relationship with human herpes virus 8 (HHV8) infection or risk of Kaposi sarcoma (KS) is unknown.Methods: Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for the association between ambient UVR, history of nonmelanoma skin cancer (NMSC; as a biomarker of personal cumulative UVR dose), and incidence of first primary KS in a nationwide US cohort of white and African American male veterans infected with HIV between 1986 and 1996 (prior to the widespread availability of treatment) using Cox regression. All statistical tests were two-sided.Results: Based on discharge records, there were 422 newly diagnosed KS cases among 17 597 HIV-infected veterans. Cohort members with prior NMSC had a statistically significantly increased risk of KS (HR = 8.64, 95% CI = 6.23 to 11.96) in the total population. Risk of KS was higher for quartile 4 vs 1 among the total population (HR = 1.49, 95% CI = 1.02 to 2.16, Ptrend UVR quartile [coded 1 to 4] = .02) and among whites (HR = 1.75, 95% CI = 1.11 to 2.78, Ptrend = .009), but not among African Americans (HR = 1.23, 95% CI = 0.71 to 2.15, Ptrend = .23).Conclusions: KS risk was elevated among HIV-infected men with NMSC diagnosis and in those living in locations with high ambient UVR at time of HIV diagnosis. Our novel findings suggesting that UVR exposure may increase KS risk warrant further investigation. [ABSTRACT FROM AUTHOR]

We did not examine autoimmune pancreatitis (AIP) in our study, but Liu and Zhou highlight the potential role of this condition as a cause of gastric cancer, especially in Eastern Asia. We thank Liu and Zhou for their comments ([1]) regarding our recent publication investigating associations between autoimmune diseases and gastric cancer in older adults in the United States ([2]). However, other studies of AIP and gastric cancer did not report measures of association, including the 3 studies ([[3], [6]]), Liu and Zhou referenced in their letter ([1]). [Extracted from the article]

Transplant recipients have elevated cancer risk, perhaps partly due to direct carcinogenic effects of immunosuppressive medications. Experimental evidence indicates that calcineurin inhibitors given to transplant recipients increase cellular expression of transforming growth factor β1 ( TGF- β1) and vascular endothelial growth factor ( VEGF), which could promote cancer. To assess the potential role of these pathways in the transplantation setting, we conducted a case-control study nested in a cohort of liver recipients. Cases had nonmelanoma skin cancer ( N = 84), cancer of the lung ( N = 29), kidney ( N = 20), or colorectum ( N = 17), or melanoma ( N = 3). We selected N = 463 recipients without cancer as controls. TGF- β1 and VEGF levels were measured in sera obtained, on average, approximately 3 years before case diagnosis/control selection. We also measured platelet factor 4 ( PF4), a marker of ex vivo platelet degranulation, because TGF- β1 and VEGF can be released from platelets, and we developed a statistical model to isolate the platelet-derived fraction from the remaining circulating component. Compared with controls, lung cancer cases had higher levels of TGF- β1 (median 22.8 vs. 19.4 ng/mL, P = 0.02) and VEGF (277 vs. 186 pg/mL, P = 0.02). However, lung cancer cases also had higher platelet counts ( P = 0.08) and PF4 levels ( P = 0.02), while residual serum levels of TGF- β1 and VEGF, after accounting for PF4, were unassociated with lung cancer ( P = 0.40 and P = 0.15, respectively). Associations were not seen for other cancers. In conclusion, TGF- β1 and VEGF levels were increased in association with lung cancer among transplant recipients, which may be explained by increased platelet counts and platelet degranulation in lung cancer cases. [ABSTRACT FROM AUTHOR]

Background: Younger ages at diagnosis for blacks compared with whites have been reported for several cancer types. However, the US black population is younger than the white population, which may bias age comparisons that do not account for the populations at risk. Methods: We analyzed Surveillance, Epidemiology, and End Results data for non-Hispanic blacks and non-Hispanic whites from 18 regions for the year 2010. We calculated crude mean ages at diagnosis among cases of 29 cancer types for whites and blacks. Separately, we calculated adjusted means that corrected for differences in population structure, which we obtained by itting linear regression models to the ages at diagnosis with statistical weights speciic to age and sex. Negative differences indicate younger ages in blacks, while positive differences indicate older ages in blacks. All statistical tests were two-sided. Results: Based on crude means, blacks were diagnosed at younger ages than whites for nearly every cancer type. However, adjustment for population structure shifted the comparisons toward older ages among blacks, and only six statistically signiicant differences of three or more years remained. Blacks were younger than whites at diagnosis for Kaposi sarcoma (-10.2 years), male soft tissue cancer (-5.6), male anal cancer (-5.5), and non-Hodgkin's lymphoma (-3.7), but older for cervical cancer (+4.7 years) and female thyroid cancer (+3.3). Smaller differences (<3 years) were present for female breast, female colon, lung, pancreas, prostate, and uterine corpus cancers (all P = .001). Conclusions: Most differences between blacks and whites in the age at cancer diagnosis are small. Large differences for a few cancer types may be driven by etiologic and subtype heterogeneity as well as disparities in access to care. [ABSTRACT FROM AUTHOR]

Background Blood transfusions are common in older adults and also may modulate the immune system. However, the impact of transfusion on cancer risk in the elderly has not been studied. Study Design and Methods Cancer risk after blood transfusion was evaluated in a US population-based case-control study using 552,951 elderly cases identified from cancer registries and 100,000 frequency-matched controls. Transfusions received 0 to 12, 13 to 30, and 31 to 48 months before cancer diagnosis or selection date were identified using Medicare claims. Odds ratios ( ORs) and 95% confidence intervals ( CIs) were calculated using logistic regression models. A Bonferroni correction adjusted for multiple testing. Results Transfusions received 0 to 12 months before cancer diagnosis and/or selection were associated with significantly elevated risk of cancer overall ( OR, 2.05; 95% CI, 1.95-2.16) and cancer of the stomach; cancer of the colon; cancer of the liver, kidney, renal pelvis, and/or ureter; lymphoma; myeloma; and leukemia. No significant associations for cancer overall were observed for the two earlier intervals. No site was associated with transfusions received 13 to 30 or 31 to 48 months before diagnosis and/or selection. Nonetheless, overall cancer risk increased with the number of transfused periods (p-trend < 0.0001). Conclusion Risk of overall cancer and specific sites was elevated 0 to 12 months after blood transfusion and associated with multiple transfusions, possibly due to reverse causation, that is, incipient cancers or cancer precursors causing anemia. [ABSTRACT FROM AUTHOR]

BACKGROUND: Pulmonary inflammation may contribute to lung cancer etiology. The authors conducted a broad evaluation of the association of single nucleotide polymorphisms (SNPs) in innate immunity and inflammation pathways with lung cancer risk and conducted comparisons with a lung cancer genome-wide association study (GWAS). METHODS: In total, 378 patients with lung cancer (cases) and a group of 450 controls from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial were included. A proprietary oligonucleotide pool assay was used to genotype 1429 SNPs. Odds ratios and 95% confidence intervals were estimated for each SNP, and P values for trend ( Ptrend) were calculated. For statistically significant SNPs ( Ptrend < .05), the results were replicated with genotyped or imputed SNPs in the GWAS, and P values were adjusted for multiple testing. RESULTS: In the PLCO analysis, a significant association was observed between lung cancer and 81 SNPs located in 44 genes ( Ptrend < .05). Of these 81 SNPS, there was evidence for confirmation in the GWAS for 10 SNPs. However, after adjusting for multiple comparisons, the only SNP that retained a significant association with lung cancer in the replication phase was reference SNP rs4648127 (nuclear factor of kappa light polypeptide gene enhancer of B-cells 1 [NFKB1]) (multiple testing-adjusted Ptrend = .02). The cytosine-thymine (CT)/TT genotype of NFKB1 was associated with reduced odds of lung cancer in the PLCO study (odds ratio, 0.56; 95% confidence interval, 0.37-0.86) and the in the GWAS (odds ratio, 0.79; 95% confidence interval, 0.69-0.90). CONCLUSIONS: A significant association was observed between a variant in the NFKB1 gene and the risk of lung cancer. The current findings add to evidence implicating inflammation and immunity in lung cancer etiology. Cancer 2012. Published 2012 by the American Cancer Society. [ABSTRACT FROM AUTHOR]

BACKGROUND: Malignancies that occur in excess among human immunodeficiency virus (HIV)-infected individuals may be caused by immunosuppression or infections. Because histologically defined cancer subtypes have not been systematically evaluated, their risk was assessed among people with acquired immunodeficiency syndrome (AIDS). METHODS: Analyses included 569,268 people with AIDS from the HIV/AIDS Cancer Match Study, a linkage of 15 US population-based HIV/AIDS and cancer registries during 1980 to 2007. Standardized incidence ratios (SIRs) were estimated to compare cancer risk in people with AIDS to the general population overall, and stratified by age, calendar period (a proxy of changing HIV therapies), and time since onset of AIDS (a proxy of immunosuppression). RESULTS: Sixteen individual cancer histologies or histology groupings manifested significantly elevated SIRs. Risks were most elevated for adult T cell leukemia/lymphoma (SIR = 11.3), neoplasms of histiocytes and accessory lymphoid cells (SIR = 10.7), giant cell carcinoma (SIR = 7.51), and leukemia not otherwise specified (SIR = 6.69). SIRs ranged from 1.4 to 4.6 for spindle cell carcinoma, bronchioloalveolar adenocarcinoma, adnexal and skin appendage neoplasms, sarcoma not otherwise specified, spindle cell sarcoma, leiomyosarcoma, mesothelioma, germ cell tumors, plasma cell tumors, immunoproliferative diseases, acute lymphocytic leukemia, and myeloid leukemias. For several of these cancer subtypes, significant declines in SIRs were observed across calendar periods (consistent with decreasing risk with improved HIV therapies) or increase in SIRs with time since onset of AIDS (ie, prolonged immunosuppression). CONCLUSIONS: The elevated risk of certain cancer subtypes in people with AIDS may point to an etiologic role of immunosuppression or infection. Future studies are needed to further investigate these associations and evaluate candidate infectious agents. Cancer 2012. © 2012 American Cancer Society. [ABSTRACT FROM AUTHOR]

The article discusses a cohort study of the overall pattern of cancer after solid organ (SO) transplantation in the U.S. The authors used linked data on 175,732 SO transplant recipients (TR) from the Scientific Registry of TR, from 1987 to 2008, and 13 state and regional cancer registries. They performed a comparison of the relative and absolute cancer risk in TR with the general population. They found that non-Hodgkin lymphoma was the most common malignancies with increased risk. They also observed that some cancers arise from the loss of immunologic control of oncogenic viruses.

Cancer is an important cause of morbidity in the elderly, and many medical conditions and treatments influence cancer risk. The Surveillance, Epidemiology, and End Results (SEER)-Medicare database can be used to conduct population-based case-control studies that elucidate the etiology of cancer among the US elderly. SEER-Medicare links data on malignancies ascertained through SEER cancer registries to claims from Medicare, the US government insurance program for people over age 65 years. Under one approach described herein, elderly cancer cases are ascertained from SEER data (1987–2005). Matched controls are selected from a 5% random sample of Medicare beneficiaries. Risk factors of interest, including medical conditions and procedures, are identified by using linked Medicare claims. Strengths of this design include the ready availability of data, representative sampling from the US elderly population, and large sample size (e.g., under one scenario: 1,176,950 cases, including 221,389 prostate cancers, 185,853 lung cancers, 138,041 breast cancers, and 124,442 colorectal cancers; and 100,000 control subjects). Limitations reflect challenges in exposure assessment related to Medicare claims: restricted range of evaluable risk factors, short time before diagnosis/selection for ascertainment, and inaccuracies in claims. With awareness of limitations, investigators have in SEER-Medicare data a valuable resource for epidemiologic research on cancer etiology. [ABSTRACT FROM PUBLISHER]

The article presents a study which discusses the pulmonary infections and risk of lung cancer among patients with AIDS. It mentions that the researchers evaluate lung cancer hazard ratios (HRs) using Cox regression and investigate whether AIDS-defeining pulmonary infections affected the risk of subsequent lung cancer. The authors concluded that increased lung cancer associated with pneumonia supports that chronic pulmonary inflammation contributes to lung carcinogenesis.

Background. People with human immunodeficiency virus (HIV) infection and AIDS have an elevated risk for cancer. Highly active antiretroviral therapy (HAART), which has been widely available since 1996, has resulted in dramatic decreases in AIDS-related deaths. Methods. We evaluated cancer as a cause of death in a US registry-based cohort of 83,282 people with AIDS (1980-2006). Causes of death due to AIDS-defining cancers (ADCs) and non-ADCs (NADCs) were assessed. We evaluated mortality rates and the fraction of deaths due to cancer. Poisson regression assessed rates according to calendar year of AIDS onset. Results. Overall mortality decreased from 302 deaths per 1000 person-years in 1980-1989, to 140 deaths per 1000 person-years in 1990-1995, and to 29 deaths per 1000 person-years in 1996-2006. ADC-related mortality decreased from 2.95 deaths per 1000 person-years in 1980-1989 to 0.65 deaths per 1000 person-years in 1996-2006 (P<.01), but the fraction of ADC-related deaths increased from 1.05% to 2.47% in association with decreases in other AIDS-related deaths. Non-Hodgkin lymphoma was the most common cancer-related cause of death (36% of deaths during 1996-2006). Likewise, NADC-related mortality decreased from 2.21 to 0.84 deaths per 1000 person-years from the period 1980-1989 to the period 1996-2006 (P<.05), but the fraction of NADC-deaths increased to 3.16% during 1996-2006. Lung cancer was the most common NADC cause of death (21% of cancer-related deaths in 1996-2006). Conclusions. Cancer-related mortality decreased in the HAART era, but because of decreasing mortality due to AIDS, cancers account for a growing fraction of deaths. Improved cancer prevention and treatment, particularly for non-Hodgkin lymphoma and lung cancer, would reduce mortality among people with AIDS. [ABSTRACT FROM AUTHOR]

Summary: Background: Hepatitis B virus (HBV) infection is common throughout Asia and Africa. Whether chronic HBV infection increases risk of non-Hodgkin lymphoma (NHL) is unclear. We aimed to assess the association between chronic HBV infection and subsequent development of NHL in a South Korean cohort. Methods: The Korean Cancer Prevention Study is a cohort study of South Korean workers and their dependants enrolled during 1992–95. From this cohort, we excluded individuals who died before Jan 1, 1993, who had cancer at or before the initial visit, who had missing information about weight, height, alanine aminotransferase or aspartate aminotransferase concentrations, or alcohol use, or who had evidence of HIV or HCV infection. Of 1 284 586 eligible participants, 603 585 had baseline data for serum hepatitis B surface antigen (HBsAg) status and were included in our study. We regarded HBsAg positivity at baseline as evidence of chronic HBV infection. Participants were followed up from baseline until Dec 31, 2006. We used national databases of inpatient and outpatient diagnoses and mortality records to ascertain occurrence of haematological malignancies. We assessed incidence of NHL overall and of NHL subtypes, malignant immunoproliferation, Hodgkin''s lymphoma, multiple myeloma, and various leukaemias. We used Cox regression to evaluate associations with HBsAg status, adjusting for sex, age, and enrolment year. Findings: 53 045 (9%) of 603 585 participants tested positive for HBsAg at baseline. Subsequently, 133 HBsAg-positive and 905 HBsAg-negative individuals developed NHL. HBsAg-positive participants had an increased risk of NHL overall compared with those who were HBsAg-negative (incidence 19·4 vs 12·3 per 100 000 person-years; hazard ratio [HR] 1·74, 95% CI 1·45–2·09, adjusted for sex, age at baseline, and enrolment year). Among NHL subtypes, HBsAg positivity was associated with increased risk of diffuse large B-cell lymphoma (n=325, incidence 6·86 vs 3·79 per 100 000 person-years; adjusted HR 2·01, 1·48–2·75) and other or unknown subtypes (n=591, incidence 10·5 vs 7·07 per 100 000 person-years; adjusted HR 1·65, 1·29–2·11), compared with HBsAg negativity. Increased risk was also recorded for malignant immunoproliferation (n=14, incidence 0·44 vs 0·15 per 100 000 person-years; adjusted HR 3·79, 1·05–13·7). Risk of these malignancies was consistently raised in HBsAg-positive participants throughout 14 years of follow-up. HBsAg positivity was not associated with follicular or T-cell NHL, Hodgkin''s lymphoma, multiple myeloma, or various leukaemias. Interpretation: During extended follow-up, HBsAg-positive individuals had an increased risk of NHL, suggesting that chronic HBV infection promotes lymphomagenesis. Funding: Korean Seoul City Research and the National Research and Development Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea; US National Cancer Institute. [Copyright &y& Elsevier]

The article presents a retrospective cohort study on non-Hodgkin lymphoma (NHL) of HIV-infected patients who were treated with highly active antiretroviral therapy (HAART) at urban HIV clinic. The study had included patients in Johns Hopkins Hospital Moor Clinic have received a baseline evaluation composed of demographic and clinical data. It shows the importance of immunosuppression in the development of NHL in HIV-infected persons during highly active antiretroviral therapy (HAART) era.

Background: Case reports suggest that hairy cell leukemia (HCL) may be associated with autoimmune conditions, however no systematic investigations in this area have been undertaken. Methods: Using the United States Surveillance, Epidemiology, and End Results Medicare linked database, we conducted an exploratory study comparing autoimmune conditions in 418 HCL cases (aged ≥65 years) and 160,086 controls. Results: Overall, the proportion with autoimmune conditions was similar between HCL cases and controls (n = 79 (18.9%) and n = 29,284 (18.3%), respectively). Before diagnosis/selection, there was no overall difference in the prevalence of autoimmune conditions in HCL cases (n = 37, 8.9%) compared with controls (n = 14,085, 8.8%), p = 0.969. However, compared with controls, HCL cases more frequently had sarcoidosis (OR 9.6, 95%CI 2.4-39.5), Sjögren syndrome (OR 6.1, 95%CI 2.0-19.3) and erythema nodosum (OR 37, 95%CI 4.9-284) before diagnosis. Autoimmune conditions were also more common in HCL cases than controls around the time of diagnosis/ selection (p < 0.001) but not subsequently. Conclusions: The findings do not support an overall relationship between autoimmune conditions and HCL, although the association with some autoimmune conditions prior to HCL diagnosis may warrant further investigation. Our findings also suggest that autoimmune conditions in HCL patients may be detected around the time of diagnosis. [ABSTRACT FROM AUTHOR]

The article features the study conducted by Elizabeth Y. Chiao and colleagues regarding the vital role played by hepatitis C virus (HCV) infection in the etiology of immune thrombocytopenia purpura (ITP) and autoimmune hemolytic anemia (AIHA) in the U.S. It mentions that HCV is a chronic viral infection affecting 3% of the world's population and most common chronic blood-borne infection found in the country. Researchers analyzed incidence rates of ITP and AIHA in 120,691 HCV infected and 454.905 matched HCV-uninfected veterans diagnosed during 1997 to 2004. Results reveal that among the HCV-infected vs. HCV-uninfected persons, the overall incidence rates of ITP are 30.2 and 18.5 per 100,000 person-years. They concluded that those infected with HCV are at increased risk for ITP.

Background Given the extended survival of patients diagnosed with cervical cancer, the large number of these women treated with radiotherapy, and the presence in this population of established cancer risk factors such as human papillomavirus (HPV) infection and cigarette smoking, it is important to clarify long-term trends in second cancer risk. Methods Using data from 104 760 one-year survivors of cervical cancer reported to 13 population-based cancer registries in Denmark, Finland, Norway, Sweden, and the United States, we calculated standardized incidence ratios (SIRS) for second cancers overall and cancers at particular sites among women with cervical cancer, including cervical cancer patients who were treated or not treated with radiation, over more than 40 years of follow-up. Cox regression models were used to assess the time-varying association of radiotherapy with risk of second cancers and to assess the interaction of radiation treatment with age at diagnosis. All statistical tests were two-sided. Results Among 104760 one-year survivors of cervical cancer, the risk of all second cancers taken together was increased to a statistically significant extent (n = 12496; SIR = 1.30; 95% confidence interval [CI] = 1.28 to 1.33). Compared with the general population, in both radiotherapy (N = 52 613) and no-radiotherapy groups (N = 27 382), risks for HPV-related cancers (of the pharynx, genital sites, and rectumlanus) and smoking-related cancers (of the pharynx, trachealbronchusllung, pancreas, and urinary bladder) were elevated to a statistically significant extent. Cervical cancer patients treated with radiotherapy, but not those who did not receive radiotherapy, were at increased risk for all second cancers and cancers at heavily irradiated sites (colon, rectumlanus, urinary bladder, ovary, and genital sites) beyond 40 years of follow-up compared with women in the general population. The association of radiotherapy with second cancer risk was modified by age at cervical cancer diagnosis for rectumlanus, genital sites, and urinary bladder, with higher hazard ratios for second cancer at younger ages of cervical cancer. After adjustment for competing mortality, the 40-year cumulative risk of any second cancer was higher among women diagnosed with cervical cancer before age 50 (22.2%; 95% CI = 21.5% to 22.8%) than among women diagnosed after age 50 (16.4%; 95% CI = 16.1% to 16.9%). Conclusion Cervical cancer patients treated with radiotherapy are at increased risk of second cancers at sites in close proximity to the cervix beyond 40 years of follow-up. [ABSTRACT FROM AUTHOR]

Background. Human herpesvirus 8 (HHV-8) causes Kaposi sarcoma. In the United States, transmission routes for HHV-8 are uncertain. Methods. The National Health and Nutrition Examination Survey III sampled individuals from the US general population (1988-1994). We used enzyme immunoassays (EIAs) to measure HHV-8 antibodies (K8.1 and open reading frame [ORF] 73 antigens) in 13,894 surveyed adults. HHV-8 seroprevalence was examined according to sexual history and viral coinfection markers. Results. Overall, seroprevalence was low when a highly specific cutoff was used (K8.1, 1.6%; ORF73, 1.5%) but was higher when a less-specific cutoff was used (K8.1, 7.1%; ORF73, 7.4%). When the more-specific approach was used, K8.1 seroprevalence was similar in men and women. Men who have sex with men (MSM) had a higher K8.1 seroprevalence (8.2%). Among other men, K8.1 seroprevalence was marginally associated with duration of heterosexual activity (P = .1) and was positively associated with the lifetime number of sex partners (P = .04) and with coinfections with hepatitis B virus (6.1% vs. 1.2% without coinfection; P < .001) and herpes simplex virus 2 (2.7% vs. 1.0%; P = .1). Among women, K8.1 seroprevalence was not significantly related to duration of sexual activity, the lifetime number of sex partners, or viral coinfections. The ORF73 EIA revealed similar but less clear-cut patterns. Conclusions. Among men, HHV-8 transmission may occur through sexual activity, particularly sex with other men. No evidence was observed for heterosexual transmission to women. [ABSTRACT FROM AUTHOR]

Background: Personal history of autoimmune diseases is consistently associated with increased risk of non-Hodgkin lymphoma. In contrast, there are limited data on risk of Hodgkin lymphoma following autoimmune diseases and almost no data addressing whether there is a familial association between the conditions. Methods: Using population-based linked registry data from Sweden and Denmark, 32 separate autoimmune and related conditions were identified from hospital diagnoses in 7476 case subjects with Hodgkin lymphoma, 18 573 matched control subjects, and more than 86 000 first-degree relatives of case and control subjects. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) as measures of relative risks for each condition using logistic regression and also applied multivariable hierarchical regression models. All P values are two-sided. Results: We found statistically significantly increased risks of Hodgkin lymphoma associated with personal histories of several autoimmune conditions, including rheumatoid arthritis (OR = 2.7, 95% CI = 1.9 to 4.0), systemic lupus erythematosus (OR = 5.8, 95% CI = 2.2 to 15.1), sarcoidosis (OR = 14.1, 95% CI = 5.4 to 36.8), and immune thrombocytopenic purpura (OR = ∞, P = .002). A statistically significant increase in risk of Hodgkin lymphoma was associated with family histories of sarcoidosis (OR = 1.8, 95% C! = 1.01 to 3.1) and ulcerative colitis (OR = 1.6, 95% CI = 1.02 to 2.6). Conclusions: Personal or family history of certain autoimmune conditions was strongly associated with increased risk of Hodgkin lymphoma. The association between both personal and family histories of sarcoidosis and a statistically significantly increased risk of Hodgkin lymphoma suggests shared susceptibility for these conditions. [ABSTRACT FROM AUTHOR]

We define the reference interval as the range between the 2.5th and 97.5th percentiles of a random variable. We use reference intervals to compare characteristics of a marker of disease progression between affected populations. We use a tolerance interval to assess uncertainty in the reference interval. Unlike the tolerance interval, the estimated reference interval does not contains the true reference interval with specified confidence (or credibility). The tolerance interval is easy to understand, communicate and visualize. We derive estimates of the reference interval and its tolerance interval for markers defined by features of a linear mixed model. Examples considered are reference intervals for time trends in HIV viral load, and CD4 per cent, in HIV-infected haemophiliac children and homosexual men. We estimate the intervals with likelihood methods and also develop a Bayesian model in which the parameters are estimated via Markov-chain Monte Carlo. The Bayesian formulation naturally overcomes some important limitations of the likelihood model. Published in 2005 by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Recently, several studies have reported the detection of DNA from simian virus 40 (SV40), a macaque polyomavirus, in tumor tissues obtained from non-Hodgkin lymphoma (NHL) patients. SV40 accidentally contaminated poliovirus vaccines administered to millions of individuals in 1955–1962. A link between SV40 and NHL is biologically plausible because SV40 causes hematological malignancies in laboratory rodents. However, detection of SV40 DNA in human NHL tumors has not been confirmed by other laboratories. Casting doubt on an association between SV40 and NHL, follow-up studies of recipients of SV40-contaminated poliovirus vaccines have not revealed these individuals to be at increased risk of NHL. Furthermore, 2 recent case-control studies of NHL documented only infrequent SV40 antibody reactivity among NHL cases, and the prevalence of SV40 antibodies was similar in cases and controls. This review summarizes recent laboratory and epidemiological studies bearing on the question of whether SV40 is a cause of NHL in humans. The strengths and weaknesses of these data are discussed, and a framework for considering the collected evidence is presented. Many of the considerations raised in this review apply to the evaluation of data regarding other cancers, such as mesothelioma, brain tumors, and various sarcomas, for which an etiologic link with SV40 also has been proposed. [ABSTRACT FROM AUTHOR]

Presents a study that compared cancer survival in adults with and without AIDS using data from New York City, New York from 1980 through 2000. Kaposi's sarcoma; Non-Hodgkin's lymphoma; Cervical cancer; Non-AIDS-related cancers of the lung, larynx, colorectum, anus, breast, prostate, and testis; Hodgkin's lymphona; Death hazard ratios.

Some laboratories have detected DNA from the macaque polyomavirus simian virus 40 (SV4O) in human tumors, but possible routes of infection remain unknown. In the present study, an enzyme immunoassay using viruslike particles (VLPs) was used to test 254 zoo workers for antibodies to SV40; 25 zoo workers with direct contact with nonhuman primates and 15 other zoo workers (23% vs. 10%, respectively P = .01) were seropositive for 5V40. Additionally, 5V40 seroreactivity confirmed by competitive-inhibition experiments (i.e., blocked by addition of 5V40 VLPs but not by VLPs for BK virus or JC virus, which are related human polyomaviruses) was increased in zoo workers with direct contact with nonhuman primates (10% vs. 3%, respectively; P = .04). 5V40 seroreactivity therefore may reflect zoonotic exposure. [ABSTRACT FROM AUTHOR]

Background: Recent studies have reported detection of simian virus 40 (SV40) DNA in tumor tissues from 15%-43% of U.S. non-Hodgkin lymphoma (NHL) patients. SV40 accidentally contaminated U.S. poliovirus vaccines that were widely administered from 1955 through 1962. However, epidemiologic data linking SV40 with NHL are lacking. Methods: We obtained serum samples from 724 incident NHL case patients and 622 control subjects from a population-based U.S. case-control study. SV40 serostatus was analyzed by two independent laboratories (designated A and B) using similar virus-like particle (VLP) enzyme immunoassays. Associations with serostatus were assessed with logistic regression, adjusting for sex, race, birth year, and study site. VLPs for the human polyomaviruses BK and JC were used in competitive inhibition experiments to assess the specificity of SV40 reactivity. Statistical tests were two-sided. Results: SV40 antibody results from the two laboratories were correlated (R = 0.59; P<.001). Laboratories A and B detected SV40 seropositivity in 7.2% and 9.8% of NHL case patients, respectively, and in 10.5% and 9.6% of control subjects, respectively. SV40 seropositivity was not associated with increased NHL risk (laboratory A: adjusted odds ratio [OR] = 0.68, 95% confidence interval [CI] = 0.46 to 1.00; laboratory B: adjusted OR = 1.02, 95% CI = 0.71 to 1.47). SV40 seropositivity was not associated with NHLs of any specific histology or site. Among subjects born before 1963, 1.0%1.6% showed SV40-specific reactivity, i.e., SV40 reactivity confirmed in competitive inhibition experiments, whereas (based on limited data) none born subsequently demonstrated SV40-specific reactivity. Conclusions: In persons born before 1963, the presence of SV40-specific antibodies, although rare, could reflect exposure to SV40-contaminated vaccines. Nevertheless, NHL risk was unrelated to serologic evidence of SV40 exposure or infection. [ABSTRACT FROM AUTHOR]

Background: Early poliovirus vaccines were accidentally contaminated with simian virus 40 (SV40). In Denmark, poliovirus vaccine was administered to most children from 1955 through 1961. SV40 DNA sequences have been detected in several human malignancies, including mesothelioma, ependymoma, choroid plexus tumors, and non-Hodgkin's lymphoma. To clarify whether SV40 infection increases risk of these cancers or of cancers arising in children, we examined cancer incidence in three Danish birth cohorts.Methods: Population-based cancer incidence data from 1943 through 1997 were obtained from the Danish Cancer Registry. The relationship between exposure to SV40-contaminated vaccine and cancer incidence was evaluated by examining incidence in birth cohorts that differed in exposure to SV40-contaminated vaccine. In addition, cancer incidence was examined in children who were 0-4 years of age before, during, and after the period of vaccine contamination. Incidence was compared using Poisson regression, adjusting for age differences. All statistical tests were two-sided.Results: After 69.5 million person-years of follow-up, individuals exposed to SV40-contaminated poliovirus vaccine as infants (i.e., born 1955-1961) or children (i.e., born 1946-1952) had lower overall cancer risk (age-adjusted relative risk [RR] = 0.86, 95% confidence interval [CI] = 0.81 to 0.91 and RR = 0.79, 95% CI = 0.75 to 0.84, respectively; P<.001 for both) than unexposed individuals (i.e., born 1964-1970, after the vaccine was cleared of SV40 contamination). Specifically, SV40 exposure was not associated with increased incidence of mesothelioma, ependymoma, choroid plexus tumor, or non-Hodgkin's lymphoma. After 19.5 million person-years of follow-up, incidence of all cancers combined, of intracranial tumors, and of leukemia among children aged 0-4 years was also not associated with SV40 exposure. Ependymoma incidence was higher during the exposed period than during the unexposed period (RR = 2.59, 95%CI = 1.36 to 4.92; P =.004 versus the period before contamination); however, incidence peaked in 1969, after the vaccine was cleared of SV40.Conclusion: Exposure to SV40-contaminated poliovirus vaccine in Denmark was not associated with increased cancer incidence. [ABSTRACT FROM AUTHOR]

Tests for human herpesvirus-8 (HHV-8) often disagree on which individuals are infected. To evaluate HHV8 antibody changes over many years, 245 homosexual men enrolled in a prospective study between 1982 and 1999 were studied. Samples collected annually were evaluated by immunofluorescence to HHV-8 latent nuclear antigen and by an ELISA for antibody against the HHV-8 lytic antigen K8.1. When positive, samples from most subjects were persistently reactive in both assays. Titers to both lytic and latent antibodies increased for many years, usually in parallel, and were higher in human immunodeficiency virus-infected men. The increasing titers and expanding epitope recognition suggest ongoing, low-grade replication of HHV-8. Use of multiple assays is important in determining prevalence in asymptomatic populations. Because persons with more advanced infections have higher antibody titers, they are easier to detect, which may skew our understanding of the epidemiology of HHV-8. [ABSTRACT FROM AUTHOR]

Studies the risk for hepatocellular carcinoma (HCC) and non-Hodgkin lymphoma (NHL) in adults with AIDS in the U.S. Correlation between HCC risk and high prevalence of hepatitis C virus (HCV) infection; Overview on the NHL grades developed by patients; Level of NHL risk in groups with prevalent HCV.

Presents a study which investigated the virus load trends in male children with hemophilia who acquired HIV-1 postnatally. Background information on HIV-1; Characteristics of the patients; Methods used; Results and discussion.

Presents information on a study which examined the risk of T-cell lymphomas in persons with AIDS. Methods; T- and B-cell immunohistochemistry markers; HIV-exposure categories of persons developing non-Hodgkin's lymphoma; Conclusion.

Presents information on a study which evaluated the performance characteristics of serologic assays for the identification of human herpesvirus 8 infection. Methodology of the study; Results and discussion on the study.

Background: Incidence of hepatocellular carcinoma (HCC) had been increasing steadily among older Americans but plateaued in 2015–2017. Chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) are important causes of HCC. The impact of improved treatments for these infections on recent trends in HCC incidence is unclear. Aims: To examine the relationship between use of antiviral therapy for chronic viral hepatis and HCC incidence in older Americans. Methods: We used 2007–2017 data from the Surveillance, Epidemiology, and End Results—Medicare database to estimate age-standardized incidence rates and average annual percent changes (AAPCs) for viral hepatitis-attributable HCC among individuals ≥66 years. We analyzed data from Medicare Part D to determine the frequency of HBV and HCV treatment utilization in this population. Results: Overall HCC incidence increased 10.5%, from 22.2/100,000 in 2007 to 24.5/100,000 in 2017 (AAPC, 1.3%). During that time, HBV-attributable HCC rates decreased from 2.5 to 2.0/100,000 (AAPC, -1.6%), while HCV-attributable HCC rose from 6.6 to 8.0/100,000 (AAPC, 2.0%). HBV treatment among patients with HBV infection increased by 66% (2007, 7.4%; 2015, 12.3%). Treatment for HCV was stable at <2% during 2006–2013 but rose to 6.9% in 2014 and 12.7% in 2015, coinciding with the introduction of direct acting antiviral agents for HCV. Conclusions: A decreased incidence of HBV-attributable HCC corresponded with an increased uptake in treatment for that infection. Despite a marked increase in the effectiveness and frequency of HCV treatment in 2014 and 2015, HCV-attributable HCC had not begun to fall as of 2017. [ABSTRACT FROM AUTHOR]

Infections remain common life-threatening complications of bone marrow transplantation. To examine clinical factors that affect infection risk, we retrospectively studied patients who received bone marrow transplants (53 autologous and 51 allogeneic). Over a median of 27 hospital days, 44 patients developed documented infections. Both autologous transplantation and hematopoietic growth factor use were associated with less prolonged neutropenia and decreased occurrence of infection (P ≤ .05). In a survival regression model, variables independently associated with infection risk were the log10 of the neutrophil count (hazard ratio [HR], 0.49; 95% confidence interval [CI], 0.32-0.75), ciprofloxacin prophylaxis (HR, 0.42; 95% CI, 0.19-0.95), empirical intravenous antibiotic use (HR, 0.09; 95% CI, 0.03-0.32), and an interaction between neutrophil count and intravenous antibiotic use (HR, 1.86; 95% CI, 1.06-3.29). In this model, infection risk increases steeply at low neutrophil counts for patients receiving no antibiotic therapy. Ciprofloxacin prophylaxis and particularly intravenous antibiotic therapy provide substantial protection at low neutrophil counts. These results can be used to model management strategies for transplant recipients. [ABSTRACT FROM AUTHOR]

Background: For patients infected with HIV, plasma HIV viral load in early disease predicts long-term prognosis. However, the implications of viral load measurements late in HIV disease are uncertain.Objective: To evaluate the relation between plasma HIV viral load and subsequent risk for disease progression in patients with late-stage HIV disease.Design: Retrospective cohort study.Setting: 16 treatment centers for patients with hemophilia.Patients: 389 patients with hemophilia and late-stage HIV disease (CD4 count < 200 cells/mm3).Measurements: Plasma HIV viral load was measured at baseline. Patients were followed for AIDS-related illnesses (primary outcome) and, specifically, Pneumocystis carinii pneumonia (secondary outcome).Results: HIV viral load strongly predicted AIDS-related illness. For patients with viral loads less than 4.00 log10 copies/mL, the 1-year actuarial risk was 0% and the 5-year risk was 25%. For patients with viral loads of at least 6.00 log10 copies/mL, the 1-year actuarial risk was 42% and the 5-year risk was 78%. A linear relation existed between viral load and risk for AIDS-related illness (hazard ratio, 2.37 per 1og10 copies/mL; P < 0.001). In addition, viral load most strongly predicted risk for illness immediately after viral load testing; this predictive relation attenuated over time (P = 0.002). These findings changed little after adjustment for CD4 cell counts that were updated during follow-up. In the first year after viral load was measured, it predicted occurrence of P. carinii pneumonia (hazard ratio, 4.69 per 1og10 copies/mL; P < 0.001).Conclusions: In patients with hemophilia and late-stage HIV disease, viral load predicts disease progression independently of CD4 cell counts. Because viral load most strongly predicts progression immediately after load is measured, it seems to reflect the current level of immunosuppression. [ABSTRACT FROM AUTHOR]

Zoster is an important clinical problem for human immunodeficiency virus type 1 (HIV)-infected patients. Risk factors for zoster and trends in incidence in HIV-infected hemophiliacs and homosexual men (n = 1218) were examined. From 1984 to 1997, 174 zoster cases were identified (average yearly incidence, 2.5%). Prior zoster episodes were associated with increased risk for a subsequent episode (relative risk [RR], 4.30; 95% confidence interval [CI], 3.11-5.95). Among hemophiliacs, children and adolescents had the highest zoster risk, and zoster risk declined with age (RR, 0.80 per decade; 95% CI, 0.68-0.93). These findings suggest that HIV-infected persons do not produce or maintain adequate booster responses after varicella zoster virus exposure. Zoster risk was relatively constant when CD4 cell counts >200 cells/mm[sup3] but increased steeply below this level. During the 14 years of follow-up, zoster incidence declined 9% per year. This trend occurred despite decreasing CD4 cell counts and was unexplained by zidovudine or acyclovir use. [ABSTRACT FROM AUTHOR]

Presents a meta-analysis of randomized efficacy trials to estimate the efficacy and toxicity of typhoid fever vaccines. Subjects of the study; Background information about the study; Discussion on the method used for the study; Results of the study; Discussion. INSET: Key messages.

Anal cancer is common among people infected with human immunodeficiency virus (HIV). This cancer is caused by human papillomavirus, and immunosuppression likely contributes to its development. In this issue of the Journal, Bertisch et al. (Am J Epidemiol. 2013;178(6):877-884) present the results of a case-control study of anal cancer among HIV-infected people in Switzerland. They demonstrate that anal cancer risk is increased in association with a low CD4+ cell count (a clinical measurement of immune status). In particular, HIV-induced immunosuppression was most severe among cases approximately 6-7 years prior to the diagnosis of anal cancer. A plausible biological interpretation is that immunosuppression is important at an early stage of the development of anal cancer, but that the neoplastic process becomes irreversible over time with persistent human papillomavirus infection and genetic damage. With current efforts to provide earlier combination antiretroviral therapy to HIV-infected people, anal cancer incidence may start to decline. Bertisch et al. also demonstrate a strong association between serum antibodies against the human papillomavirus type 16 protein E6 and anal cancer risk, highlighting the role of this viral oncoprotein in carcinogenesis. Additional biomarkers could help refine clinical approaches to anal cancer screening and prevention for the HIV-infected population. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which highlights the results of a study that examines the epidemiology of urinary tract cancers among people with AIDS in the United States.

Discusses issues related to human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) and cancer. Long-term cancer risks of HIV infections and AIDS; Role of Epstein Barr virus in the etiology of lymphoma.