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ABSTRACT: BACKGROUND: For decades, non-Hodgkin lymphoma (NHL) incidence has been increasing worldwide. NHL risk is strongly increased among HIV-infected people. Our understanding of trends in NHL incidence has been hampered by difficulties in separating HIV-infected NHL cases from general population rates. METHODS: NHL incidence data during 1992-2009 were derived from 10 U.S. SEER cancer registries with information on HIV status at NHL diagnosis. The CDC estimated the number of people living with HIV in the registry areas. The proportion of NHL cases with HIV and NHL rates in the total and the HIV-uninfected populations were estimated. Time trends were assessed with Joinpoint analyses. RESULTS: Of 115,643 NHL cases diagnosed during 1992-2009, 5.9% were HIV-infected. The proportions of NHL cases with HIV were highest for diffuse large B-cell (DLBCL; 7.8%), Burkitt (26.9%), and peripheral T-cell lymphomas (3.2%) with low proportions (≤1.1%) in the other subtypes. NHL rates in the total population increased 0.3% per year during 1992-2009. However, rates of NHL in HIV-uninfected people increased 1.4% per year during 1992-2003, before becoming stable through 2009. Similar trends were observed for DLBCL and follicular lymphoma in HIV-uninfected people; rates increased 2.7% per year until 2003 and 1.7% per year until 2005, respectively, before stabilizing. CONCLUSIONS: NHL incidence rates in the U.S. have plateaued over the last 5-10 years, independent of HIV infection. Impact: Though the causes of the long-term increase in NHL incidence rates in the U.S. remain unknown, general population rates of NHL have stabilized since the early 2000s, independent of HIV.
Cancer Epidemiology Biomarkers & Prevention 04/2013; · 4.12 Impact Factor
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ABSTRACT: BACKGROUND: Solid organ transplantation recipients have elevated cancer incidence. Estimates of absolute cancer risk after transplantation can inform prevention and screening. METHODS: The Transplant Cancer Match Study links the US transplantation registry with 14 state/regional cancer registries. The authors used nonparametric competing risk methods to estimate the cumulative incidence of cancer after transplantation for 2 periods (1987-1999 and 2000-2008). For recipients from 2000 to 2008, the 5-year cumulative incidence, stratified by organ, sex, and age at transplantation, was estimated for 6 preventable or screen-detectable cancers. For comparison, the 5-year cumulative incidence was calculated for the same cancers in the general population at representative ages using Surveillance, Epidemiology, and End Results data. RESULTS: Among 164,156 recipients, 8520 incident cancers were identified. The absolute cancer risk was slightly higher for recipients during the period from 2000 to 2008 than during the period from 1987 to 1999 (5-year cumulative incidence: 4.4% vs 4.2%; P = .006); this difference arose from the decreasing risk of competing events (5-year cumulative incidence of death, graft failure, or retransplantation: 26.6% vs 31.9%; P < .001). From 2000 to 2008, the 5-year cumulative incidence of non-Hodgkin lymphoma was highest at extremes of age, especially in thoracic organ recipients (ages 0-34 years: range, 1.74%-3.28%; aged >50 years; range, 0.36%-2.22%). For recipients aged >50 years, the 5-year cumulative incidence was higher for colorectal cancer (range, 0.33%-1.94%) than for the general population at the recommended screening age (aged 50 years: range, 0.25%-0.33%). For recipients aged >50 years, the 5-year cumulative incidence was high for lung cancer among thoracic organ recipients (range, 1.16%-3.87%) and for kidney cancer among kidney recipients (range, 0.53%-0.84%). The 5-year cumulative incidence for prostate cancer and breast cancer was similar or lower in transplantation recipients than at the recommended ages of screening in the general population. CONCLUSIONS: Subgroups of transplantation recipients have a high absolute risk of some cancers and may benefit from targeted prevention or screening. Cancer 2013. © 2013 American Cancer Society.
Cancer 04/2013; · 4.77 Impact Factor
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Clinical Infectious Diseases 01/2013; · 9.15 Impact Factor
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ABSTRACT: 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.
Transfusion 01/2013; · 3.22 Impact Factor
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ABSTRACT: Case reports of Burkitt lymphoma (BL) in transplant recipients suggest that the risk is markedly elevated. Therefore, we investigated the incidence of BL in 203,557 solid organ recipients in the U.S. Transplant Cancer Match Study (1987-2009) and compared it with the general population using standardized incidence ratios. We also assessed associations with demographic and clinical characteristics, and treatments used to induce therapeutic immunosuppression. BL incidence was 10.8 per 100,000 person-years, representing 23-fold (95% confidence interval (CI) 19-28) greater risk than in the general population, and it peaked 3-8 years after the time of transplantation. In adjusted analyses, BL incidence was higher in recipients transplanted when <18 vs. ≥35 years (incidence rate ratio [IRR] 3.49, 95% CI 2.08-5.68) and in those transplanted with a liver (IRR 2.91, 95% CI 1.68-5.09) or heart (IRR 2.39, 95% CI 1.30-4.31) compared with kidney. BL incidence was lower in females than males (IRR 0.45, 95% CI 0.28-0.71), in blacks than whites (IRR 0.33, 95% CI 0.12-0.74), in those with a baseline Epstein-Barr virus (EBV)-seropositive versus EBV-seronegative status (IRR 0.34, 95% CI 0.13-0.93), and in those treated with azathioprine (IRR 0.56, 95% CI 0.34-0.89) or corticosteroids (IRR 0.48, 95% CI 0.29-0.82). Tumors were EBV-positive in 69% of 32 cases with results. EBV positivity was 90% in those aged <18 years and 59% in those aged 18+ years. In conclusion, BL risk is markedly elevated in transplant recipients, and it is associated with certain demographic and clinical features. EBV was positive in most but not all BL cases with results. Am. J. Hematol., 2013. © 2012 Wiley Periodicals, Inc.
American Journal of Hematology 12/2012; · 4.67 Impact Factor
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ABSTRACT: BACKGROUND: Transplant recipients are at risk of posttransplant lymphoproliferative disease (PTLD). METHODS: Thirty-six pediatric transplant recipients were evaluated (18 hematopoietic stem cell and 18 liver recipients; 12 had PTLD). We studied 207 longitudinal plasma samples from these recipients for three markers of B-cell activation or clonality: immunoglobulin free light chains (FLCs), soluble CD30 (sCD30), and monoclonal immunoglobulins (M-proteins). RESULTS: Kappa FLCs, lambda FLCs, and sCD30 were elevated in 20.8%, 28.0%, and 94.2% of plasma specimens, respectively. Free light chain and sCD30 levels increased significantly 1.18 to 1.82 fold per log10 Epstein-Barr virus (EBV) load in peripheral blood. Five PTLD cases manifested elevated FLCs with an abnormal kappa/lambda ratio, suggesting monoclonal FLC production. M-proteins were present in 91% of PTLD cases versus 50% to 67% of other recipients with high or low EBV loads (P=0.13). Concordance of FLCs, M-proteins, and PTLD tumor light chain restriction was imperfect. For example, one PTLD case with an IgG lambda M-protein had a tumor that was kappa restricted, and another case with an M-protein had a T-cell PTLD. In an additional case, an IgM kappa M-protein and excess kappa FLCs were both detected in plasma at PTLD diagnosis; although the tumor was not restricted at diagnosis, kappa restriction was present 5 years later when the PTLD relapsed. CONCLUSIONS: Plasma markers of B-cell dysfunction are frequent after transplantation and associated with poor EBV control. These abnormal markers may be produced by oligoclonal B-cell populations or PTLD tumor cells and could potentially help identify recipients at high risk of PTLD.
Transplantation 12/2012; · 4.00 Impact Factor
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ABSTRACT: Depletion of gut-associated lymphocytes by HIV infection facilitates microbial translocation, which may contribute to non-Hodgkin lymphoma (NHL) risk via chronic immune activation and B-cell hyperstimulation. We therefore examined associations of four microbial translocation markers with subsequent NHL risk in a case-control study nested within 4 prospective cohort studies of HIV-infected individuals. Pre-diagnostic blood specimens for 56 NHL cases and 190 controls matched on age, sex, race, specimen type, cohort, and CD4+ T-cell count were tested for the endotoxin lipopolysaccharide (LPS), anti-endotoxin core antibody (EndoCab), LPS binding protein (LBP), and soluble CD14 (sCD14). Elevated levels of sCD14 were associated with significantly increased NHL risk (OR: 2.72 [95% CI:1.29, 5.76]). In sub-group analyses, elevated LPS levels were also associated with significantly increased NHL risk (OR: 3.24 [95% CI:1.10, 9.53]). EndoCab and LBP levels were not associated with NHL risk. The association of sCD14 and LPS with NHL risk supports an etiologic role for gut microbial translocation in lymphomagenesis among HIV-infected individuals. Additional studies with larger sample sizes are needed to confirm these observations.
AIDS (London, England) 11/2012; · 4.91 Impact Factor
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Benjamin M Cherry,
Rene Costello,
Adriana Zingone,
Jason Burris,
Neha Korde,
Elisabet Manasanch,
Mary Kwok,
Christina Annunziata,
Mark J Roschewski, Eric A Engels,
Ola Landgren
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ABSTRACT: Immunoparesis and a skewed serum free light chain (FLC) ratio are indicators of immune dysfunction predictive of progression from monoclonal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM). Previous studies have reported increased prevalence of MGUS by age, but no study has examined the relationship between immunoparesis and abnormal FLC ratios in the elderly. We screened 453 older adults (median age, 80 years; range, 65-96) to characterize the patterns of immunoparesis and abnormal FLC ratio in relation to MGUS. We defined MGUS in 4.4% of the subjects; the prevalence was 12.5% among individuals of >90 years. In MGUS (vs. non-MGUS) cases, immunoparesis and abnormal FLC ratios were detected in 70.0% (vs. 49.0%; P = 0.07) and 50.0% (vs. 12.9%; P = 0.0001), respectively. Based on small numbers, MGUS patients with abnormal FLC ratio were borderline (P = 0.07) more likely to have immunoparesis. Overall, the prevalence of immunoparesis varied in a nonlinear fashion, with lowest frequencies in the youngest and oldest groups. Our observed disassociation between MGUS prevalence and impaired immunoglobulin production suggests that separate mechanisms are involved in the development of MGUS and immunoparesis in advanced age. These findings emphasize the need for molecularly defined methods to characterize myeloma precursor states and better predict progression to MM. Am. J. Hematol. 2012. Published 2012 Wiley Periodicals, Inc.
American Journal of Hematology 10/2012; · 4.67 Impact Factor
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ABSTRACT: OBJECTIVES:: HIV-infected people have elevated risk for lung cancer and higher mortality following cancer diagnosis than HIV-uninfected individuals. It is unclear whether HIV-infected people with lung cancer receive similar cancer treatment as HIV-uninfected people. DESIGN/METHODS:: We studied adults 18+ years old with lung cancer reported to the Texas Cancer Registry (N = 156,930) from 1995-2009. HIV status was determined by linkage with the Texas enhanced HIV/AIDS Reporting System. For non-small cell lung cancer (NSCLC) cases, we identified predictors of cancer treatment using logistic regression. We used Cox regression to evaluate effects of HIV and cancer treatment on mortality. RESULTS:: Compared with HIV-uninfected lung cancer cases (N = 156,593), HIV-infected lung cancer cases (N = 337) were more frequently young, non-Hispanic black, male, and with distant stage disease. HIV-infected NSCLC cases less frequently received cancer treatment than HIV-uninfected cases (60.3% vs. 77.5%; odds ratio 0.39, 95% confidence interval [CI] 0.30-0.52, after adjustment for diagnosis year, age, sex, race, stage, and histologic subtype). HIV infection was associated with higher lung cancer-specific mortality (hazard ratio [HR] 1.34, 95%CI 1.15-1.56, adjusted for demographics and tumor characteristics). Inclusion of cancer treatment in adjusted models slightly attenuated the effect of HIV on lung cancer-specific mortality (HR 1.25; 95%CI 1.06-1.47). Also, there was a suggestion that HIV was more strongly associated with mortality among untreated than among treated cases (adjusted HR 1.32 vs. 1.16, p-interaction = 0.34). CONCLUSION:: HIV-infected NSCLC cases were less frequently treated for lung cancer than HIV-uninfected cases, which may have affected survival.
AIDS (London, England) 10/2012; · 4.91 Impact Factor
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ABSTRACT: 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 (P(trend) ) were calculated. For statistically significant SNPs (P(trend) < .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 (P(trend) < .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 P(trend) = .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.
Cancer 10/2012; · 4.77 Impact Factor
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ABSTRACT: Background The risk of anal cancer is substantially increased in HIV-infected individuals. Thus, the HIV epidemic may have influenced the increasing anal cancer trends in the United States. We estimated the impact of the HIV epidemic on trends in anal cancer incidence in the United States during 1980-2005. Methods Data on anal cancer cases with and without AIDS were obtained from the HIV/AIDS Cancer Match Study. The number of HIV-infected anal cancer cases without AIDS was estimated from the number of anal cancers occurring before diagnosis of AIDS. The proportion of anal cancer cases with HIV infection in the general population was calculated. We estimated temporal trends in the incidence rates of anal cancer in the general population overall and after exclusion of HIV-infected cancer cases by calculating annual percent changes and 95% confidence intervals (CIs) using a Joinpoint log-linear model. All incidence rates were standardized to the 2000 US population by age, sex, and race. Results During 1980-2005, of the 20 533 estimated anal cancer cases, 1665 (8.1%) were HIV-infected. During 2001-2005, the proportion of anal cancer cases with HIV infection was the highest-1.2% (95% CI = 0.93 to 1.4%) among females and 28.4% (95% CI = 26.6 to 29.4%) among males. During 1980-2005, HIV infection did not have an impact on the trends in anal cancer among females (incidence rates increased by 3.3% [95% CI = 3.0 to 3.7%] annually overall, and by 3.3% [95% CI = 2.9 to 3.6%] annually without HIV-infected anal cancer cases) but had a strong impact on the trends in anal cancer among males (incidence rates increased by 3.4% [95% CI = 2.9 to 3.9%] annually overall, and by 1.7% [95% CI = 1.2 to 2.3%] annually without HIV infection). Conclusion During 1980-2005, the increasing anal cancer incidence rates in the United States were strongly influenced by the HIV epidemic in males but were independent of HIV infection in females.
CancerSpectrum Knowledge Environment 10/2012; 104(20):1591-8. · 14.07 Impact Factor
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ABSTRACT: Background. The relevance of B-cell dysfunction for progression to AIDS among human immunodeficiency virus (HIV)-infected individuals has not been clearly defined. We evaluated the association between circulating κ and λ free light chains (FLCs), which are markers of B-cell dysfunction, and risk of developing an AIDS-defining opportunistic infection in HIV-infected men. Methods. The study included 252 case patients with clinical AIDS and 252 HIV-infected controls from the Multicenter Hemophilia Cohort Study I. Case patients were matched to controls on birth date, specimen type, blood sample collection date, and CD4 cell count. Levels of κ and λ FLCs were measured in serum or plasma collected 0-2.5 years before selection. Elevated FLC levels (κ or λ, above the upper limit of normal) were classified as polyclonal (normal κ-λ ratio) or monoclonal (abnormally skewed κ-λ ratio). We used conditional logistic regression to estimate odds ratios (ORs) for AIDS. Results. FLC levels were higher in case patients than in controls, for κ (median, 4.03 vs 2.98 mg/dL) and λ (3.77 vs 2.42 mg/dL) FLCs. Compared with normal levels, above-normal FLC levels were associated with AIDS (OR, 3.13 [95% confidence interval (CI), 1.78-5.49] for κ and 3.47 [2.31-5.20] for λ FLCs), and the association with AIDS was strengthened with increasing κ and λ FLC levels (P trends < .0001). Polyclonal FLC elevation was associated with a 4-fold increase in the risk of AIDS (OR, 3.85; 95% CI, 1.97-7.54), but monoclonal FLC elevation was not associated with AIDS. Conclusions. Circulating FLCs are associated with elevated risk of AIDS in HIV-infected individuals. Polyclonal B-cell dysfunction may contribute to HIV-related immune suppression and predispose to clinical AIDS events.
Clinical Infectious Diseases 08/2012; 55(10):e103-8. · 9.15 Impact Factor
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ABSTRACT: Patients with end-stage renal disease (ESRD) have elevated cancer risk. Cancer risk increases with age, but associations of ESRD with specific malignancies are incompletely studied for older individuals.
We conducted a population-based case-control study (1,029,695 cancer and 99,610 controls) among the U.S. elderly using SEER-Medicare linked data. We defined ESRD as presence of dialysis claims in the 3 months prior to selection.
Although ESRD was not associated with excess cancer risk overall (odds ratio 1.02; 95%CI 0.91-1.14), risk was specifically increased for cancers of the stomach (1.45; 1.16-1.81), small intestine (1.92; 1.27-2.92), colon (1.17; 1.00-1.36), liver (1.53; 1.16-2.01), biliary tract (1.78; 1.20-2.65), lung (1.17; 1.02-1.34), cervix (2.12; 1.39-3.23), kidney (2.42; 2.01-2.92), and for multiple myeloma (1.77; 1.40-2.24) and chronic myeloid leukemia (1.74; 1.08-2.80). The association between liver cancer and ESRD was attenuated upon adjustment for hepatitis B and C infection or diabetes mellitus. Multiple myeloma risk was highest with short ESRD duration (p < 0.0001), possibly reflecting reverse causality, while kidney cancer risk showed a borderline rise over time (p = 0.08).
Among elderly individuals with ESRD, the excess risks for some cancers may reflect immune dysfunction or a high prevalence of other risk factors, such as viral infections or diabetes mellitus. Our results underscore the need for studying biological pathways of carcinogenesis in ESRD.
BMC Nephrology 07/2012; 13:65. · 2.18 Impact Factor
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ABSTRACT: People infected with human immunodeficiency virus (HIV) have an increased risk of some malignancies, but little is known about the effects of infection on risk of cancers of the upper gastrointestinal tract. We evaluated the risks of different histologic and anatomic subtypes of carcinomas and non-Hodgkin lymphomas (NHLs) of the stomach and esophagus in people with acquired immunodeficiency syndrome (AIDS).
We analyzed data from the HIV/AIDS Cancer Match Study, which links data collected from 1980 to 2007 for 16 US population-based HIV and AIDS and cancer registries. We compared risks of stomach and esophageal malignancies in people with AIDS (N = 596,955) with those of the general population using standardized incidence ratios (SIRs). We assessed calendar trends using Poisson regression.
People with AIDS had increased risks of carcinomas of the esophagus (SIR, 1.69; 95% confidence interval [CI], 1.37-2.07; n = 95) and stomach (SIR, 1.44; 95% CI, 1.17-1.76; n = 96). Risk was increased for esophageal adenocarcinoma (SIR, 1.91; 95% CI, 1.31-2.70) and squamous cell carcinoma (SIR, 1.47; 95% CI, 1.10-1.92). People with AIDS had greater risks of carcinomas of the gastric cardia (SIR, 1.36; 95% CI, 0.83-2.11) and noncardia (SIR, 1.53; 95% CI, 1.12-2.05) than the general population. Although most stomach and esophageal NHLs that developed in people with AIDS were diffuse large B-cell lymphomas, these individuals also had an increased risk of stomach mucosa-associated lymphoid tissue lymphoma (SIR, 5.99; 95% CI, 3.19-10.2; n = 13). The incidence of carcinomas remained fairly constant over time, but rates of NHL decreased from 1980 to 2007 (P(trend) < .0001).
People with AIDS are at increased risk for developing esophageal and stomach carcinomas and NHLs. Although the incidence of NHL decreased from 1980 to 2007 as treatments for HIV infection improved, HIV-infected individuals face continued risks of esophageal and stomach carcinomas.
Gastroenterology 07/2012; 143(4):943-950.e2. · 11.68 Impact Factor
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ABSTRACT: BACKGROUND: Hepatocellular carcinoma (HCC) is a concern among individuals with human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS). METHODS: The authors analyzed population-based registry linkage data from the US HIV/AIDS Cancer Match Study (1980-2009) to examine the risk and trends of HCC among individuals with AIDS. Standardized incidence ratios (SIRs) were used to measure HCC risk relative to the general population, and Poisson regression was used to calculate incidence rate ratios (RR) comparing incidence among individuals with AIDS. People with AIDS were categorized according to their HIV risk group into high and low hepatitis C virus (HCV) prevalence groups based on their HIV transmission risk category. RESULTS: Among 615,150 individuals with AIDS, HCC risk was elevated almost 4 times compared with the risk in the general population (N = 366; SIR, 3.8; 95% confidence interval, 3.5-4.3). Although HCC incidence increased steadily across calendar periods (P(trend) < .0001; adjusted for sex and age), the excess risk in individuals with AIDS compared with the general population remained somewhat constant (SIRs range, 3.5-3.9) between the monotherapy/dual therapy era (1990-1995) and the recent highly active antiretroviral therapy era (2001-2009). In a multivariate model adjusting for sex, race/ethnicity, and attained calendar period, HCC incidence increased with advancing age (P(trend) < .0001) and was associated with HIV risk groups with a known higher prevalence of HCV (adjusted RR, 2.2; 95% confidence interval, 1.8-2.8). CONCLUSIONS: HCC incidence in individuals with AIDS has increased over time despite improved HIV treatment regimens, likely reflecting prolonged survival with chronic liver disease. The high incidence in older adults suggests that this cancer will increase in importance with aging of the HIV-infected population. Cancer 2012. Published 2012 by the American Cancer Society.
Cancer 06/2012; · 4.77 Impact Factor
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ABSTRACT: In immunodeficiency, an increased sarcoma risk is confirmed for Kaposi's sarcoma. Whether rates of other sarcoma subtypes are elevated in the setting of immunodeficiency is not known. We therefore reviewed published case reports on HIV and AIDS patients and organ transplant recipients with sarcomas. For comparison, we assessed sarcomas in the U.S. general population using Surveillance Epidemiology End Results (SEER) data.
A total of 176 non-Kaposi sarcoma were identified, 75 in people with HIV and AIDS and 101 in transplant recipients. Leiomyosarcomas (n = 101) were the most frequently reported sarcomas, followed by angiosarcomas (n = 23) and fibrohistiocytic tumors (n = 17). Leiomyosarcomas were reported with two age peaks, in children and young adults. Epstein-Barr virus (EBV) was detected in the tumor cells in 85 and 88% of leiomyosarcomas in HIV-infected people and transplant recipients, respectively. Angiosarcomas and fibrohistiocytic tumors were most frequently reported in men. Among kidney transplant recipients, 20% of sarcomas arose at the site of an arteriovenous fistula. In comparison, leiomyoscarcomas, angiosarcomas, and fibrohistiocytic tumors comprised 16.9, 3.8, and 18.7% of sarcomas in the U.S. general population.
Leiomyosarcoma and angiosarcoma may occur disproportionately in immunodeficiency. Leiomyosarcomas appear causatively linked to EBV, whereas angiosarcomas might be correlated with an arteriovenous fistula. Additional studies are necessary to understand the contribution of immunodeficiency to the cause of these sarcomas.
Current opinion in oncology 06/2012; 24(5):537-46. · 4.09 Impact Factor
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ABSTRACT: BACKGROUND: The cause of chronic fatigue syndrome (CFS) is unknown but is thought to be associated with immune abnormalities or infection. Because cancer can arise from similar conditions, associations between CFS and cancer were examined in a population-based case-control study among the US elderly. METHODS: Using linked Surveillance, Epidemiology, and End Results (SEER)-Medicare registry data, approximately 1.2 million cancer cases and 100,000 controls (age range, 66-99 years; 1992-2005) were evaluated. CFS was identified in the period more than 1 year prior to selection, using linked Medicare claims. Unconditional logistic regression was used to estimate the odds ratios (ORs) comparing the CFS prevalence in cases and controls, adjusting for age, sex, and selection year. All statistical tests were 2-sided. RESULTS: CFS was present in 0.5% of cancer cases overall and 0.5% of controls. CFS was associated with an increased risk of non-Hodgkin lymphoma (NHL) (OR = 1.29, 95% confidence interval [CI] = 1.16-1.43, P = 1.7 × 10(-6) ). Among NHL subtypes, CFS was associated with diffuse large B cell lymphoma (OR = 1.34, 95% CI = 1.12-1.61), marginal zone lymphoma (OR = 1.88, 95% CI = 1.38-2.57), and B cell NHL not otherwise specified (OR = 1.51, 95% CI = 1.03-2.23). CFS associations with NHL overall and NHL subtypes remained elevated after excluding patients with medical conditions related to CFS or NHL, such as autoimmune conditions. CFS was also associated, although not after multiple comparison adjustment, with cancers of the pancreas (OR = 1.25, 95% CI = 1.07-1.47), kidney (OR = 1.27, 95% CI = 1.07-1.49), breast (OR = 0.85, 95% CI = 0.74-0.98), and oral cavity and pharynx (OR = 0.70, 95% CI = 0.49-1.00). CONCLUSIONS: Chronic immune activation or an infection associated with CFS may play a role in explaining the increased risk of NHL. Cancer 2012. © 2012 American Cancer Society.
Cancer 05/2012; · 4.77 Impact Factor
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Infectious Agents and Cancer 05/2012; 5:1-2.
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ABSTRACT: Deaths related to HIV/AIDS have declined due to improved HIV therapies. However, people with AIDS remain at elevated risk for cancer and cancer deaths. Prior studies evaluated cancer deaths using death certificates, which may be inaccurate. We utilized population attributable risk methods (which do not rely on death certificates) to assess cancer mortality.
Data from a US population-based record linkage study were used to identify incident cancers and deaths in 372 364 people with AIDS (1980-2006) followed for up to 5 years after AIDS onset. We utilized Cox regression to compare mortality in individuals with and without cancer and to calculate cancer-attributable mortality across calendar periods (AIDS onset in 1980-1989, 1990-1995, and 1996-2006).
Mortality declined across calendar periods for all people with AIDS but remained higher among those with cancer relative to those without. During 1996-2006, among individuals with an AIDS-defining cancer (ADC) who died, 88.3% of deaths were attributable to their ADC; likewise, among individuals with a non-AIDS-defining cancer (NADC), 87.1% of deaths were attributable to their NADC. The fraction of all deaths in people with AIDS attributable to ADC (i.e. population-attributable risk) decreased significantly from 6.3% (1980-1990) to 3.9% (1996-2006), but NADC population attributable mortality increased significantly over time from 0.5% (1980-1989) to 2.3% (1996-2006).
Among individuals with AIDS and cancer who subsequently die, most deaths are attributable to cancer. With a decline in overall mortality, the proportion of all deaths attributable to NADCs has increased. These results highlight the need for improved cancer prevention and treatment.
AIDS (London, England) 03/2012; 26(10):1311-8. · 4.91 Impact Factor
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ABSTRACT: 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).
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).
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).
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.
Cancer 02/2012; 118(19):4869-76. · 4.77 Impact Factor
