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Objective. To estimate the prevalence, incidence, survival, and disease characteristics of systemic sclerosis (SSc) in the Detroit tricounty area.Methods. A census of SSc cases for the period 1989-1991 was conducted in the Detroit area, using multiple sources for case identification. Diagnoses were verified by medical record review. Capture-recapture analysis was used to estimate the total SSc population. Cases of localized scleroderma (morphea and linear disease) were excluded.Results. Based on 706 verified cases of SSc, prevalence was initially estimated to be 242.0 cases per million adults (95% confidence interval [95% CI] 213-274), with an annual incidence of 19.3 new cases per million adults per year (95% CI 12.4-30.2). Capturerecapture analysis, based on the degree of overlap of verified cases among multiple sources, resulted in a revised prevalence estimate of 276 cases per million adults (95% CI 245-310). Sex-and race-specific prevalence estimates were significantly higher for women than for men, and for blacks than for whites. The average age at diagnosis was significantly younger for blacks than for whites. Compared with white patients, black patients were almost twice as likely to have diffuse disease (prevalence proportion ratio 1.86, 95% CI 1.48-2.35). Median survival was ϳ11 years. Factors negatively affecting survival included male sex (hazard ratio 1.81, 95% CI 1.29-2.55) and older age at diagnosis (hazard ratio 1.04, 95% CI 1.03-1.05).Conclusion. This study establishes baseline estimates of SSc occurrence and characteristics in a large US cohort consisting primarily of black adults and white adults. These data should facilitate research regarding the role of geographic, ethnic, racial, and environmental factors for this disease in comparison populations.

A causal link between chronic inflammation and carcinogenesis is explored by reviewing illustrative examples of specific cancers and causal agents and mechanisms. The causal agents or pathologic conditions include microbial agents, gastroesophageal reflux, chronic cholecystitis and cholelithiasis, inflammatory bowel disease, and specific agents that cause chronic obstructive or diffuse interstitial lung disease. The proportion of total cancer deaths attributable to infectious agents is estimated to be about 20% to 25% in developing countries and 7% to 10% in more industrialized countries. Recurrent or persistent inflammation may induce, promote, or influence susceptibility to carcinogenesis by causing DNA damage, inciting tissue reparative proliferation, and/or creating a stromal "soil" that is enriched with cytokines and growth factors. Future research on the complex cascade of cellular and humoral factors participating in the chronic inflammatory process will further understanding of the pathogenesis of various cancers and potentially provide a rationale for targeted chemopreventive interventions.

PURPOSE: The mucosa of the small intestine encompasses about 90% of the luminal surface area of the digestive system, but only 2% of the total annual gastrointestinal cancer incidence in the United States. METHODS: The remarkable contrast in age-standardized cancer incidence between the small and large intestine has been reviewed with respect to the cell type patterns, demographic features, and molecular characteristics of neoplasms. RESULTS: Particularly noteworthy is the predominance of adenocarcinoma in the colon, which exceeds 98% of the total incidence by cell type, in contrast to that of 30% to 40% in the small intestine, resulting in an age-standardized ratio of rates exceeding 50-fold. The prevalence of adenomas and carcinomas is most prominent in the duodenum and proximal jejunum. The positive correlation in global incidence rates of small and large intestinal neoplasms and the reciprocal increases in risk of second primary adenocarcinomas suggest that there are common environmental risk factors. The pathophysiology of Crohn inflammatory bowel disease and the elevated risk of adenocarcinoma demonstrate the significance of the impaired integrity of the mucosal barrier and of aberrant immune responses to luminal indigenous and potentially pathogenic microorganisms. CONCLUSION: In advancing a putative mechanism for the contrasting mucosal susceptibilities of the small and large intestine, substantial differences are underscored in the diverse taxonomy, concentration and metabolic activity of anaerobic organisms, rate of intestinal transit, changing pH, and the enterohepatic recycling and metabolism of bile acids. Experimental and epidemiologic studies are cited that suggest that the changing microecology, particularly in the colon, is associated with enhanced metabolic activation of ingested and endogenously formed procarcinogenic substrates.

Background Biliary tract cancers (BTCs) are rare but deadly cancers (gallbladder cancer [GBC], intrahepatic cholangiocarcinoma [ICC], extrahepatic cholangiocarcinoma [ECC], and ampulla of Vater cancer [AVC]). A recent US study reported increasing GBC incidence among people younger than 45 years and blacks; however, it did not examine trends for other biliary tract sites. Methods This study characterized demographic differences in BTC incidence rates and time trends by anatomic site. Population‐based North American Association of Central Cancer Registries data were used to calculate age‐adjusted incidence rates, incidence rate ratios (IRRs), and estimated annual percent changes (eAPCs) for 1999‐2013 by site and demographic group. For sites with significant differences in eAPC by age group, IRRs were compared by age group. Results GBC incidence rates declined among women (eAPC, –0.5%/y; P = .01) and all racial/ethnic groups except for non‐Hispanic blacks, among whom rates increased (1.8%/y; P < .0001). Although GBC rates increased among 18‐ to 44‐year‐olds (eAPC, 1.8%/y; P = .01), they decreased among people 45 years old or older (–0.4%/y; P = .009). Sex (P < .0001) and racial/ethnic differences (P = .003 to .02) in GBC incidence were larger for younger people than older people. During this period, ICC (eAPC, 3.2%/y; P < .0001) and ECC rates (1.8%/y; P = .001) steadily increased across sex and racial/ethnic groups. Although AVC incidence rates increased among younger adults (eAPC, 1.8%/y; P = .03) but not older adults (–0.20%/y; P = .30), sex and racial/ethnic IRRs did not differ by age. Conclusions Differential patterns of BTC rates and temporal trends have been identified by anatomic site and demographic groups. These findings highlight the need for large pooling projects to evaluate BTC risk factors by anatomic site.

BACKGROUND The survival of men diagnosed with prostate cancer has improved over time, and the current 10-year relative survival rate is 99.7%. The long survival of patients with this common cancer raises questions about the risk of a second primary cancer and the need for continued surveillance. METHODS A population-based cohort of 441,504 men who were diagnosed with prostate cancer between 1992 and 2010 was identified from Surveillance, Epidemiology and End Results Program (SEER) data (SEER13). The standardized incidence ratio (SIR) was calculated as an estimate of the risk of a second primary malignancy based on the incidence in the general population. RESULTS Prostate cancer survivors had a lower risk of being diagnosed with another cancer overall compared with the US population (SIR = 0.60; 95% confidence interval, 0.60–0.61). The risks of leukemia and cancers of the oral cavity and pharynx, esophagus, stomach, colon and rectum, liver, gallbladder, pancreas, lung and bronchus, and larynx were significantly lower. Conversely, these patients had a greater risk of bladder, kidney, and endocrine and soft tissue cancers. Men who received treatment with radiation therapy (external-beam radiation therapy) had long-term increases in their risk of bladder cancer (SIR = 1.42) and rectal cancer (SIR = 1.70) risk compared with who did not receive radiation (SIRbladder = 0.76; SIRrectal = 0.74). There were significant racial differences in the risk of being diagnosed with a second primary cancer, and the magnitude and direction of these risks depended on tumor type. CONCLUSIONS Prostate cancer survivors remain at risk of subsequent malignancies, and race and treatment choice important determinants of long-term risk.

Evidence of the existence of major prostate cancer (PC)-susceptibility genes has been provided by multiple segregation analyses. Although genomewide screens have been performed in over a dozen independent studies, few chromosomal regions have been consistently identified as regions of interest. One of the major difficulties is genetic heterogeneity, possibly due to multiple, incompletely penetrant PC-susceptibility genes. In this study, we explored two approaches to overcome this difficulty, in an analysis of a large number of families with PC in the International Consortium for Prostate Cancer Genetics (ICPCG). One approach was to combine linkage data from a total of 1,233 families to increase the statistical power for detecting linkage. Using parametric (dominant and recessive) and nonparametric analyses, we identified five regions with "suggestive" linkage (LOD score >1.86): 5q12, 8p21, 15q11, 17q21, and 22q12. The second approach was to focus on subsets of families that are more likely to segregate highly penetrant mutations, including families with large numbers of affected individuals or early age at diagnosis. Stronger evidence of linkage in several regions was identified, including a "significant" linkage at 22q12, with a LOD score of 3.57, and five suggestive linkages (1q25, 8q13, 13q14, 16p13, and 17q21) in 269 families with at least five affected members. In addition, four additional suggestive linkages (3p24, 5q35, 11q22, and Xq12) were found in 606 families with mean age at diagnosis of < or = 65 years. Although it is difficult to determine the true statistical significance of these findings, a conservative interpretation of these results would be that if major PC-susceptibility genes do exist, they are most likely located in the regions generating suggestive or significant linkage signals in this large study.

BACKGROUND.Metabolic syndrome refers to a cluster of conditions that includes hypertension, dyslipidemia, central adiposity, and high blood glucose levels. Over the past decade, a growing body of literature suggests that metabolic syndrome may be associated with several different forms of cancer. Because prostate cancer risk is highest among African Americans, and these men, similarly, are more prone to developing specific features of the metabolic syndrome, including hypertension and type‐2 diabetes, any relationships would have a significant impact on developing strategies for the primary prevention of prostate cancer.METHODS.The Flint Men's Health Study is a community‐based, case‐control study of prostate cancer conducted exclusively among African Americans. Prostate cancer cases and controls completed an interviewer‐administered questionnaire that asked about the respondent's history of high blood pressure and diabetes. All men also participated in a physical examination in which several measures of body composition, including waist circumference, were collected.RESULTS.Hypertension was reported more commonly among men with prostate cancer (cases) compared with men in the control group (odds ratio [OR]. 2.4; 95% confidence interval [95% CI], 1.5–3.7), and cases were more likely to have a waist circumference >102 cm (OR, 1.8; 95% CI, 1.2–2.9). However, self‐reported diabetes was not associated with prostate cancer risk. The men with prostate cancer also were more likely than controls to exhibit multiple syndrome characteristics (OR, 1.9; 95% CI, 1.2–3.0).CONCLUSIONS.The current results indicated that features of the metabolic syndrome, specifically abdominal obesity and hypertension, are associated with prostate cancer in African‐American men. This relationship, if it is proved causal, suggests that prevention or control of these conditions eventually may lead to a reduction in the incidence of prostate cancer in this high‐risk minority group. Cancer 2007 © 2007 American Cancer Society.