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US transplant centers are required to report cancers in transplant recipients to the transplant network. The accuracy and completeness of these data, collected in the Scientific Registry of Transplant Recipients (SRTR), are unknown. We compared diagnoses in the SRTR and 15 linked cancer registries for colorectal, liver, lung, breast, prostate and kidney cancers; melanoma; and non-Hodgkin lymphoma (NHL). Among 187 384 transplants, 9323 cancers were documented in the SRTR or cancer registries. Only 36.8% of cancers were in both, with 47.5% and 15.7% of cases additionally documented solely in cancer registries or the SRTR, respectively. Agreement between the SRTR and cancer registries varied (kappa = 0.28 for liver cancer and kappa = 0.52-0.66 for lung, prostate, kidney, colorectum, and breast cancers). Upon evaluation, some NHLs documented only in cancer registries were identified in the SRTR as another type of posttransplant lymphoproliferative disorder. Some SRTR-only cases were explained by miscoding (colorectal cancer instead of anal cancer, metastases as lung or liver cancers) or missed matches with cancer registries, partly due to recipients' outmigration from catchment areas. Estimated sensitivity for identifying cancer was 52.5% for the SRTR and 84.3% for cancer registries. In conclusion, SRTR cancer data are substantially incomplete, limiting their usefulness for surveillance and research.

One measure of the accuracy of cancer mortality statistics is the concordance between cancer defined as the underlying cause of death from death certificates and cancer diagnoses recorded in central, population-based cancer registries. Previous studies of such concordance are outdated.To characterize the accuracy of cancer mortality statistics from the concordance between cancer cause of death and primary cancer site at diagnosis.Central cancer registry records from California, Colorado, and Idaho in the U.S. were linked with state vital statistics data and evaluated by demographic and tumor information across 79 site categories. A retrospective arm (confirmation rate per 100 deaths) compared death certificate data from 2002 to 2004 with cancer registry diagnoses from 1993 to 2004, while a prospective arm (detection rate per 100 deaths) compared cancer registry diagnoses from 1993 to 1995 with death certificate data from 1993 to 2004 by International Statistical Classification of Diseases and Related Health Problems (ICD) version used to code deaths.With n=265,863 deaths where cancer was recorded as the underlying cause based on the death certificate, the overall confirmation rate for ICD-10 was 82.8% (95% confidence interval [CI], 82.6-83.0%), the overall detection rate for ICD-10 was 81.0% (95% CI, 80.4-81.6%), and the overall detection rate for ICD-9 was 85.0% (95% CI, 84.8-85.2%). These rates varied across primary sites, where some rates were50%, some were 95% or greater, and notable differences between confirmation and detection rates were observed.Important unique information on the quality of cancer mortality data obtained from death certificates is provided. In addition, information is provided for future studies of the concordance of primary cancer site between population-based cancer registry data and data from death certificates, particularly underlying causes of death coded in ICD-10.

Data are limited regarding cancer risk in human immunodeficiency virus (HIV)-infected persons with modest immunosuppression, before the onset of acquired immunodeficiency syndrome (AIDS). For some cancers, risk may be affected by highly active antiretroviral therapy (HAART) widely available since 1996. We linked HIV/AIDS and cancer registries in Colorado, Florida and New Jersey. Standardized incidence ratios (SIRs) compared cancer risk in HIV-infected persons (initially AIDS-free) during the 5-year period after registration with the general population. Poisson regression was used to compare incidence across subgroups, adjusting for demographic factors. Among 57,350 HIV-infected persons registered during 1991-2002 (median CD4 count 491 cells/mm(3)), 871 cancers occurred during follow-up. Risk was elevated for Kaposi sarcoma (KS, SIR 1,300 [n = 173 cases]), non-Hodgkin lymphoma (NHL, 7.3 [n = 203]), cervical cancer (2.9 [n = 28]) and several non-AIDS-defining malignancies, including Hodgkin lymphoma (5.6 [n = 36]) and cancers of the lung (2.6 [n = 109]) and liver (2.7 [n = 14]). KS and NHL incidence declined over time but nonetheless remained elevated in 1996-2002. Incidence increased in 1996-2002 compared to 1991-1995 for Hodgkin lymphoma (relative risk 2.7, 95%CI 1.0-7.1) and liver cancer (relative risk infinite, one-sided 95%CI 1.1-infinity). Non-AIDS-defining cancers comprised 31.4% of cancers in 1991-1995, versus 58.0% in 1996-2002. For KS and NHL, risk was inversely related to CD4 count, but these associations attenuated after 1996. We conclude that KS and NHL incidence declined markedly in recent years, likely reflecting HAART-related improvements in immunity, while incidence of some non-AIDS-defining cancers increased. These trends have led to a shift in the spectrum of cancer among HIV-infected persons.

Objectives/Hypothesis: To document the increasing incidence of oropharyngeal (OP) cancer and to provide evidence that this increase is caused by oncogenic human papilloma virus (HPV). Study Design: Epidemiologic review and retrospective case series analysis. Methods: We collected data from Colorado and the United States comparing the average annual age-adjusted incidence rates of OP and non-OP head and neck cancer between the periods 1980 to 1990 and 1991 to 2001. We obtained data on 72 patients with OP cancer from a single county in Colorado, from 1980 through 2004. HPV status was determined by DNA-polymerase chain reaction. We assessed disease-specific survival. Results: The average annual age-adjusted incidence of OP cancer in males in Colorado increased from 2.54 per 100,000 to 3.47 (P < .05) or 36.6%, whereas the U.S. rate increased from 4.34 to 4.81 (P < .05) or 10.8%. The rates in females and the rates of non-OP head and neck cancer decreased. Of the 72 cases, 50 (69%) were positive for HPV subtype 16. The ratio of HPV-positive to HPV-negative cases prior to 1995 was 0.72 (8:11) but was 3.81 (42:11) afterward. Survival was positively affected by HPV status (hazard ratio of 0.15, confidence intervals 0.07–0.36, P < .001). Disease-specific survival was 83% in the HPV-positive patients and 15% in the HPV-negative group. Conclusions: OP cancer incidence is increasing in Colorado males and to a lesser extent in U.S. males. The HPV-positive OP cancer cases were more frequent in the later years of the study. Disease-specific survival was much better in the HPV-positive patients, confirming that HPV testing defines a unique subset of patients. These findings suggest that HPV oncogenesis accounts for the increase in average annual age-adjusted incidence of OP cancer.

Objective Squamous cell carcinoma (SCC) of the rectum is rare, but as with anal cancer, risk may be increased among immunosuppressed individuals. We assessed risk of rectal SCC in HIV-infected people. Design Population-based registry. Methods We utilized the HIV/AIDS Cancer Match, a linkage of US HIV and cancer registries (1991-2010), to ascertain cases of anal SCC, rectal SCC, rectal non-SCC, and colon non-SCC. We compared risk in HIV-infected persons with the general population using standardized incidence ratios (SIRs) and evaluated risk factors using Poisson regression. We reviewed cancer registry case notes to confirm site and histology for a subset of cases. Results HIV-infected persons had an excess risk of rectal SCC compared with the general population (SIR = 28.9; 95% CI 23.2-35.6), similar to the increase for anal SCC (SIR = 37.3). Excess rectal SCC risk was most pronounced among HIV-infected MSM (SIR = 61.2). Risk was not elevated for rectal non-SCC (SIR = 0.88) or colon non-SCC (SIR = 0.63). Individuals diagnosed with AIDS had higher rectal SCC rates than those with HIV-only (incidence rate ratio = 1.92; 95% CI 1.08-3.42). Based on available information, one-third of rectal SCCs were determined to be misclassified anal cancer. Conclusion HIV-infected individuals, especially with advanced immunosuppression, appear to have substantially elevated risk for rectal SCC. As for anal SCC, rectal SCC risk was highest in MSM, pointing to involvement of a sexually transmitted infection such as human papillomavirus. Site misclassification was present, and detailed information on tumour location is needed to prove that rectal SCC is a distinct entity.

Merkel cell carcinoma (MCC) is an uncommon skin cancer of neuroendocrine differentiation. MCC behaves aggressively, and five-year relative survival is only 62% (1). Like other skin cancers, MCC largely affects light-skinned populations (2,3), especially those highly exposed to ultraviolet radiation (UVR) (4). Recently, a previously unknown virus, Merkel cell polyomavirus (MCV), was detected in most but not all MCC tumors tested (5). This discovery has revived interest in MCC epidemiology, especially regarding the role of impaired immunity in promoting viral carcinogenesis. However, details regarding the relevant type of immunosuppression are poorly understood. Immunosuppression is suspected as important to MCC causation, as risk is increased among persons with human immunodeficiency virus (HIV) (6,7), chronic lymphocytic leukemia, (3,8) and other hematologic malignancies (8). MCC risk is also elevated following solid organ transplantation (9–12), after which patients must be pharmacologically immunosuppressed to prevent graft rejection. Also, some immunosuppressant medications used in transplantation may have direct skin carcinogenic effects, including interacting with UVR to enhance DNA damage (13–18). These direct effects may relate to the very high risks of squamous cell skin cancers in transplant recipients (19). Prior studies of transplant-related MCC have included fewer than 50 case patients and have not provided information on how risk differs by age, timing of transplant, or specific immunosuppressive medications (9–12). In the present study, we evaluated the occurrence of MCC among solid organ transplant recipients in the Transplant Cancer Match (TCM) Study, a large, population-based cohort of US transplant recipients for which cancer ascertainment was conducted uniformly via linkage with cancer registries. We quantified MCC risk overall and according to recipient demographic characteristics, transplanted organ, UVR exposure based on place of residence, length of time since transplant, and type of immunosuppressive drugs received.

Background Despite the large number of men diagnosed with localized prostate cancer, there is as yet no consensus concerning appropriate treatment. The purpose of this study was to describe the initial treatment patterns for localized prostate cancer in a population-based sample and to determine the clinical and patient characteristics associated with initial treatment and overall survival. Methods The analysis included 3,300 patients from seven states, diagnosed with clinically localized prostate cancer in 1997. We examined the association of sociodemographic and clinical characteristics with four treatment options: radical prostatectomy, radiation therapy, hormone therapy, and watchful waiting. Diagnostic and treatment information was abstracted from medical records. Socioeconomic measures were derived from the 2000 Census based on the patient's residence at time of diagnosis. Vital status through December 31, 2002, was obtained from medical records and linkages to state vital statistics files and the National Death Index. Multiple logistic regression analysis and Cox proportional hazards models identified factors associated with initial treatment and overall survival, respectively. Results Patients with clinically localized prostate cancer received the following treatments: radical prostatectomy (39.7%), radiation therapy (31.4%), hormone therapy (10.3%), or watchful waiting (18.6%). After multivariable adjustment, the following variables were associated with conservative treatment (hormone therapy or watchful waiting): older age, black race, being unmarried, having public insurance, having non-screen detected cancer, having normal digital rectal exam results, PSA values above 20, low Gleason score (2-4), comorbidity, and state of residence. Among patients receiving definitive treatment (radical prostatectomy or radiation therapy), older age, being unmarried, PSA values above 10, unknown Gleason score, state of residence, as well as black race in patients under 60 years of age, were associated with receipt of radiation therapy. Overall survival was related to younger age, being married, Gleason score under 8, radical prostatectomy, and state of residence. Comorbidity was only associated with risk of death within the first three years of diagnosis. Conclusions In the absence of clear-cut evidence favoring one treatment modality over another, it is important to understand the factors that inform treatment selection. Since state of residence was a significant predictor of both treatment as well as overall survival, true regional differences probably exist in how physicians and patients select treatment options. Factors affecting treatment choice and treatment effectiveness need to be further explored in future population-based studies.

BACKGROUND. Understanding the ways in which socioeconomic status (SES) affects mortality is important for defining strategies to eliminate the unequal burden of cancer by race and ethnicity in the United States. METHODS. Disease stage, treatment, and 5-year mortality rates were ascertained by reviewing medical records, and SES was determined by analyzing income and education at the census tract level for 4844 women with breast cancer, 4332 men with prostate cancer, and 4422 men and women with colorectal cancer who were diagnosed in 7 U.S. states in 1997. RESULTS. Low SES was associated with more advanced disease stage and with less aggressive treatment for all 3 cancers. The hazard ratio (HR) for 5-year all-cause mortality associated with low SES was elevated after a diagnosis of breast cancer when the analysis was adjusted for age (HR, 1.59; 95% confidence interval [CI], 1.35-1.87). Adjustment for mediating factors of race/ethnicity, comorbid conditions, cancer stage, and treatment reduced the association. The age-adjusted mortality risk associated with low SES was elevated after a diagnosis of prostate cancer (HR, 1.33; 95% CI, 1.13-1.57), and multivariate adjustments for mediating factors also reduced that association. There was less association between SES and mortality after a diagnosis of colorectal cancer. For all 3 cancer sites, low SES was a much stronger predictor of mortality among individuals aged

Context Solid organ transplant recipients have elevated cancer risk due to immunosuppression and oncogenic viral infections. Because most prior research has concerned kidney recipients, large studies that include recipients of differing organs can inform cancer etiology. Objective To describe the overall pattern of cancer following solid organ transplantion. Design, Setting, and Participants Cohort study using linked data on solid organ transplant recipients from the US Scientific Registry of Transplant Recipients (1987-2008) and 13 state and regional cancer registries. Main Outcome Measures Standardized incidence ratios (SIRs) and excess absolute risks (EARs) assessing relative and absolute cancer risk in transplant recipients compared with the general population. Results The registry linkages yielded data on 175 732 solid organ transplants (58.4% for kidney, 21.6% for liver, 10.0% for heart, and 4.0% for lung). The overall cancer risk was elevated with 10 656 cases and an incidence of 1375 per 100 000 person-years (SIR, 2.10 [95% CI, 2.06-2.14]; EAR, 719.3 [95% CI, 693.3-745.6] per 100 000 person-years). Risk was increased for 32 different malignancies, some related to known infections (eg, anal cancer, Kaposi sarcoma) and others unrelated (eg, melanoma, thyroid and lip cancers). The most common malignancies with elevated risk were non-Hodgkin lymphoma (n = 1504; incidence: 194.0 per 100 000 person-years; SIR, 7.54 [95% CI, 7.17-7.93]; EAR, 168.3 [95% CI, 158.6-178.4] per 100 000 person-years) and cancers of the lung (n = 1344; incidence: 173.4 per 100 000 person-years; SIR, 1.97 [95% CI, 1.86-2.08]; EAR, 85.3 [95% CI, 76.2-94.8] per 100 000 person-years), liver (n = 930; incidence: 120.0 per 100 000 person-years; SIR, 11.56 [95% CI, 10.83-12.33]; EAR, 109.6 [95% CI, 102.0-117.6] per 100 000 person-years), and kidney (n = 752; incidence: 97.0 per 100 000 person-years; SIR, 4.65 [95% CI, 4.32-4.99]; EAR, 76.1 [95% CI, 69.3-83.3] per 100 000 person-years). Lung cancer risk was most elevated in lung recipients (SIR, 6.13 [95% CI, 5.18-7.21]) but also increased among other recipients (kidney: SIR, 1.46 [95% CI, 1.34-1.59]; liver: SIR, 1.95 [95% CI, 1.74-2.19]; and heart: SIR, 2.67 [95% CI, 2.40-2.95]). Liver cancer risk was elevated only among liver recipients (SIR, 43.83 [95% CI, 40.90-46.91]), who manifested exceptional risk in the first 6 months (SIR, 508.97 [95% CI, 474.16-545.66]) and a 2-fold excess risk for 10 to 15 years thereafter (SIR, 2.22 [95% CI, 1.57-3.04]). Among kidney recipients, kidney cancer risk was elevated (SIR, 6.66 [95% CI, 6.12-7.23]) and bimodal in onset time. Kidney cancer risk also was increased in liver recipients (SIR, 1.80 [95% CI, 1.40-2.29]) and heart recipients (SIR, 2.90 [95% CI, 2.32-3.59]). Conclusion Compared with the general population, recipients of a kidney, liver, heart, or lung transplant have an increased risk for diverse infection-related and unrelated cancers.