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Validation of a Blood Biomarker for Identification of Individuals at High Risk for Gastric Cancer
Epplein, Meira,Butt, Julia,Zhang, Yang,Hendrix, Laura H.,Abnet, Christian C.,Murphy, Gwen,Zheng, Wei,Shu, Xiao-Ou,Tsugane, Shoichiro,Qiao, You-lin,Taylor, Philip R.,Shimazu, Taichi,Yoo, Keun-Young,Par American Association for Cancer Research 2018 Cancer Epidemiology, Biomarkers & Prevention Vol.27 No.12
<P><B>Background:</B></P><P><I>Helicobacter pylori</I> is the leading cause of gastric cancer, yet the majority of infected individuals will not develop neoplasia. Previously, we developed and replicated serologic <I>H. pylori</I> biomarkers for gastric cancer risk among prospective cohorts in East Asia and now seek to validate the performance of these biomarkers in identifying individuals with premalignant lesions.</P><P><B>Methods:</B></P><P>This cross-sectional study included 1,402 individuals from Linqu County screened by upper endoscopy. <I>H. pylori</I> protein-specific antibody levels were assessed using multiplex serology. Multivariable-adjusted logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for prevalent intestinal metaplasia, indefinite dysplasia, or dysplasia, compared with superficial or mild atrophic gastritis.</P><P><B>Results:</B></P><P>Compared with individuals seronegative to Omp and HP0305, individuals seropositive to both were seven times more likely to have precancerous lesions (OR, 7.43; 95% CI, 5.59–9.88). A classification model for precancerous lesions that includes age, smoking, and seropositivity to <I>H. pylori</I>, Omp, and HP0305 resulted in an area under the curve (AUC) of 0.751 (95% CI, 0.725–0.777), which is significantly better than the same model, including the established gastric cancer risk factor CagA (AUC, 0.718; 95% CI, 0.691–0.746, <I>P</I><SUB>difference</SUB> = 0.0002).</P><P><B>Conclusions:</B></P><P>The present study of prevalent precancerous gastric lesions provides support for two new serum biomarkers of gastric cancer risk, Omp and HP 0305.</P><P><B>Impact:</B></P><P>Our results support further research into the serological biomarkers Omp and HP0305 as possible improvements over the established virulence marker CagA for identifying individuals with precancerous lesions in East Asia.</P>
Sampson, Joshua N.,Wheeler, William A.,Yeager, Meredith,Panagiotou, Orestis,Wang, Zhaoming,Berndt, Sonja I.,Lan, Qing,Abnet, Christian C.,Amundadottir, Laufey T.,Figueroa, Jonine D.,Landi, Maria Teres U.S. Dept. of Health, Education, and Welfare, Publ 2015 Journal of the National Cancer Institute Vol.107 No.12
<P>Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.</P>
Butt, Julia,Varga, Matthew G.,Wang, Tianyi,Tsugane, Shoichiro,Shimazu, Taichi,Zheng, Wei,Abnet, Christian C.,Yoo, Keun-Young,Park, Sue K.,Kim, Jeongseon,Jee, Sun Ha,Qiao, You-lin,Shu, Xiao-Ou,Waterboe AMERICAN ASSOCIATION FOR CANCER RESEARCH INC 2019 CANCER PREVENTION RESEARCH Vol.12 No.10
<P>Smoking is an established risk factor for gastric cancer development. In this study, we aimed to assess prospectively the association of smoking with gastric cancer risk in 1,446 non-cardia gastric cancer cases and 1,796 controls from China, Japan, and Korea with consideration of <I>Helicobacter pylori</I> infection as a potential effect modifier. Applying logistic regression models stratified by study and adjusted for age and sex we found that current, but not former, smoking was significantly associated with gastric cancer risk [OR = 1.33; 95% confidence interval (CI), 1.07–1.65]. However, the association was significant only in <I>H. pylori</I> sero-positive individuals determined by 3 different sero-markers: overall sero-positivity, sero-positivity to the onco-protein CagA, and sero-positivity to the gastric cancer associated sero-marker HP0305 and HP1564. Specifically, a significant interaction was found when stratifying by HP0305/HP1564 (<I>P</I><SUB>interaction</SUB> = 0.01) with a 46% increased risk of gastric cancer among HP0305/HP1564 sero-positive current smokers (95% CI, 1.10–1.93) as opposed to no increased gastric cancer risk among HP0305/HP1564 sero-negative current smokers (OR = 0.93; 95% CI, 0.65–1.33). We confirmed that current smoking is associated with an increased gastric cancer risk, however, only among individuals that are simultaneously sero-positive for the leading causal factor for gastric cancer, <I>H. pylori</I>.</P>
Epstein-Barr Virus Antibody Titers Are Not Associated with Gastric Cancer Risk in East Asia
Varga, Matthew G.,Cai, Hui,Waterboer, Tim,Murphy, Gwen,Shimazu, Taichi,Taylor, Phil R.,Qiao, You-Lin,Park, Sue K.,Yoo, Keun-Young,Jee, Sun Ha,Cho, Eo Rin,Kim, Jeongseon,Abnet, Christian C.,Tsugane, Sh Springer-Verlag 2018 Digestive diseases and sciences Vol.63 No.10