Summary Temporal trends in the incidence of esophageal and gastric cancers during 1972 to 1989 were addressed in urban Shanghai, the location of China's longest standing cancer registry. Over the 18 year study period, esophageal cancer rates decreased more than 50% from 28.8/100,000 person-years in 1972-74 to 13.3/100,000 in 1987-89 among men and from 11.3/100,000 to 5.4/100,000 among women. Reductions Materials and methodsDetails on the materials and methods used in this analysis have been described elsewhere (Jin et al., 1993 (Table I). In the 18 year period, the incidence rates for esophageal cancer decreased more than 50% from 28.8/100,000 person-years in 1972-74 to 13.3/100,000 in 1987-89 among men and from 11.3/100,000 to 5.4/100,000 among women. Gastric cancer also declined steadily over time, although not as rapidly. The incidence among men was 50.1/100,000 in 1987-89, about four-fifths that in 1972-74. Among women, however, the rates showed only a 2.9% decline over the entire period. Both esophageal and gastric cancers were more common among men than women; male/ female rate ratios ranged from 2.2 to 2.6, with little change over time. The gastric/esophageal cancer rate ratios almost doubled from two to about four from 1972-74 to 1987-89 among both men and women, reflecting a sharper decline in esophageal cancer incidence over the study period. Table II presents the age-specific trends in esophageal and gastric cancer incidence rates. Esophageal cancer decreased across all age groups, with greater rates of decline in the younger age groups among both men and women (Figure 1) When the age-specific trends for gastric cancer are plotted according to cohort year of birth, some interesting patterns emerge (Figure 3). Among men and women, risk increased among the earliest cohorts, levelled off, declined among those born during the 1910s-1930s, and rose subsequently. The downward trend for esophageal cancer incidence, however, was observed for all birth cohorts (Figure 4). DiscussionAs seen in many developing regions in the world (Muir et al., 1987), cancers of the esophagus and stomach are among the most common forms of malignancy in Shanghai. From 1972-74 to 1987-89, however, age-adjusted incidence rates
A recent comparison of 493 dead and 697 living controls from a case-control study of cancer in the Minneapolis-St. Paul area showed that the dead controls of both sexes were reported to have been significantly heavier consumers of cigarettes, hard liquor, beer, and certain drugs, and to have had more adulthood diseases than living controls. The present analysis examines the effect of excluding causes of death associated with those exposures found in excess in the dead controls. Exclusion of individuals with smoking-related causes of death reduced but did not eliminate the excess of cigarette smokers among the dead controls. Deletion of individuals with alcohol-related causes of death only slightly reduced the excess among dead controls. Adjustment for cigarette smoking, however, nearly eliminated the association with alcohol consumption, particularly among males. For certain adulthood diseases and medications, the exclusion of individuals with exposure-associated causes of death also virtually eliminated the excesses found in the dead controls when compared with the living controls. Thus, it appears that even after extensive exclusion of smoking-related causes of death, the association between dead controls and cigarette smoking still remains, and the use of dead controls in case-control studies where cigarette smoking is the risk factor being evaluated may lead to a biased underestimated of risk. For the other exposures found in significant excess among the dead controls, the exclusion of exposure-related causes of death and proper adjustment for confounders may eliminate much or all of the excess.
Background: Multiple common susceptibility loci for breast cancer (BC) have been identified/confirmed in Caucasian women. Combination of these SNPs into a polygenic risk score (PRS) could improve risk stratification and provide guidance for preventive and screening strategies. However, due to differences in allele frequencies of genetic variants, tumor characteristics between women of African and European ancestries, we sought to evaluate the association of PRS with BC in a large consortium of African women. Methods: The GWAS in BC in the African Diaspora (ROOT consortium) included 3686 participants of African ancestry from Nigeria, USA, and Barbados (1657 cases, 2029 controls). PRS was constructed from the published odds ratios (ORs) from 90 susceptibility loci for BC. Logistic regression was used to examine its association with overall BC risk as well as associations by hormone receptor status, family history and other clinical features. Results: One unit change in the PRS was associated with an OR of 1.13 (95% CI: 1.01-1.28, P=0.042) for overall BC risk, 1.15 (95%CI: 0.95-1.41, P=0.160) for ER+ BC risk, and 1.17 (95%CI: 0.95-1.44, P=0.133) for ER- BC risk. The ORs for developing BC by percentiles of the PRS, relative to women in the middle quintile, showed weak linear trend. The discriminative accuracy of the PRS, as measured by the C-statistic, was 0.524 (95% CI: 0.505-0.542) for overall BC, 0.511(95% CI: 0.479-0.543) for ER+ BC, and 0.513 (95% CI: 0.481-0.545) for ER- BC. There was a statistically significant interaction between PRS and age, the association between PRS and overall BC risk were stronger in two age groups (aged <40 years and ≥60 years). The PRS was also more strongly associated with PR+ (OR=1.26, 95%CI: 1.01-1.58) compared to PR- (OR=1.08, 95%CI: 0.95-1.44) BC. Association between PRS and BC were similarly non-significant across different strata of family history of BC, BMI, alcohol consumption, oral contraceptive use, menopausal, ER and HER2 status. Table 1. Performance of the 90-SNP polygenic risk score (PRS) in the GWAS in Breast Cancer in the African DiasporaPercentile of PRS (%) OR (95%CI) Overall BC (n=1657) vs Ctrl (n=2029)ER+ BC (n=403) vs Ctrl (n=2029)ER- BC (n=374) vs Ctrl (n=2029)<51.01 (0.73-1.41)1.32 (0.28-2.13)0.89 (0.51-1.55)5-100.83 (0.59-1.15)0.71 (0.40-1.26)0.63 (0.34-1.17)10-200.74 (0.57-0.95)0.69 (0.44-1.07)0.72 (0.46-1.12)20-400.97 (0.79-1.19)0.80 (0.56-1.14)0.98 (0.69-1.39)40-601.00 (ref)1.00(ref)1.00(ref)60-800.89 (0.73-1.10)0.94 (0.66-1.33)0.90 (0.63-1.28)80-901.14 (0.89-1.47)0.87 (0.56-1.34)0.90 (0.63-1.28)90-951.14 (0.82-1.58)1.54 (0.92-2.58)0.88 (0.48-1.61)>951.10 (0.79-1.52)1.15 (0.67-1.99)1.34 (0.79-2.25)Note: Odds ratios are for different percentiles of the PRS relative to the middle quintile (40% to 60%). Odds ratios were adjusted for study site and the first ten eigenvectors from principal components analysis. Conclusion: BC PRS obtained from prior GWASs conducted in Caucasian women didn't provide a comparable degree of risk stratification for African Americans. Additional studies are needed to identify SNPs specific to women of African ancestry that could provide improved risk prediction. Further studies can also combine the PRS with lifestyle/environmental factors. Citation Format: Wang S, Qian F, Zheng Y, Ogundiran T, Ojengbede O, Zheng W, Blot W, Nathanson KL, Hennis A, Nemesure B, Ambs S, Olopade OI, Huo D. Breast cancer risk prediction using a polygenic risk score in women of African ancestry: Findings from GWAS in breast cancer in the African diaspora [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P5-09-02.
Auto-antibodies to tumor suppressor p53 are found in a subset of colorectal cancer (CRC) patients. A prospective cohort study in the US (Cancer Prevention Study II) has recently reported a statistically significant 1.8-fold increased odds for the development of CRC based on pre-diagnostic sero-positivity for p53; the magnitude of this association decreased with longer time-span between blood sampling and diagnosis. In the present study, we sought to examine this association in a large US CRC cohort consortium to evaluate the potential utility of p53 auto-antibodies as an early CRC detection biomarker. Methods: Antibody responses to p53 were measured in pre-diagnostic blood samples of 3,702 incident CRC cases (median [range] follow-up: 7.3 years [0–40 years]) and an equal number of controls, matched by age, race, and sex, from 9 US prospective cohorts. The association of sero-positivity to p53 with CRC risk, overall and by time between blood draw and diagnosis, was determined by conditional logistic regression. Results: Overall, 5% of controls and 7% of cases were sero-positive to p53, resulting in a statistically significant 33% increased CRC risk (OR: 1.33; 95% CI: 1.09, 1.61). The association was strongest for CRC diagnoses within 2 years after blood draw (OR: 2.73; 95% CI: 1.67, 4.45), with 15% sero-positive cases compared to 6% sero-positive controls. The number of sero-positive cases decreased with longer follow-up time (2–<5 years: 9%; 5–<10 years: 6%; ≥10 years: 3%) down to a proportion similar to that in controls resulting in the absence of an association of p53 sero-positivity with CRC risk after more than 5 years between blood draw and CRC diagnosis. Conclusion: In this large consortium of prospective cohorts, we found that pre-diagnostic sero-positivity to the tumor suppressor p53 was statistically significantly associated with a 2.7-fold increased risk of a subsequent CRC diagnosis within 2 years after blood draw, replicating the findings of the one previous cohort study examining this association. The findings suggest that while p53 sero-positivity may not be a useful predictor of long-term CRC risk, p53 auto-antibodies might be considered as part of a marker panel for early detection of this cancer.
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