ArticlePloS one2012
Genetic susceptibility on CagA-interacting molecules and gene-environment interaction with phytoestrogens: a putative risk factor for gastric cancer.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Risk Factors for Gastric Cancer: A Systematic ReviewAsian Pacific journal of cancer prevention : APJCP · 2018Pooled it
- Validation of the ABC Method for Gastric Cancer Risk Stratification Across Helicobacter pylori Infections With Diverse CagA Status and Subtypes in Brazil.Cancer medicine · 2025Article
- Personalizing Dietary Polyphenols for Health Maintenance and Disease Management: A Nutrigenetic Approach.Current nutrition reports · 2025Review
- The Impact ofJournal of Cancer · 2025Article
- Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology.Frontiers in medicine · 2024Article
- The Association between Plasma Concentration of Phytoestrogens and Hypertension within the Korean Multicenter Cancer Cohort.Nutrients · 2021Article
- Variant of SNPs at lncRNA NEAT1 contributes to gastric cancer susceptibility in Chinese Han population.International journal of clinical oncology · 2021Article
- Factors Explaining Interpersonal Variation in Plasma Enterolactone Concentrations in Humans.Molecular nutrition & food research · 2019Review
- Anticancer and antimetastatic potential of enterolactone: Clinical, preclinical and mechanistic perspectives.European journal of pharmacology · 2019Review
- Overexpression of CrkL as a novel biomarker for poor prognosis in gastric cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- Equol inhibits proliferation of human gastric carcinoma cells via modulating Akt pathway.World journal of gastroenterology · 2015Article
- Association Analysis of MET Gene Polymorphism with Papillary Thyroid Carcinoma in a Chinese Population.International journal of endocrinology · 2015Article
- Cyanidin 3-O-glucoside reduces Helicobacter pylori VacA-induced cell death of gastric KATO III cells through inhibition of the SecA pathway.International journal of medical sciences · 2014Article
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo evaluate whether genes that encode CagA-interacting molecules (SRC, PTPN11, CRK, CRKL, CSK, c-MET and GRB2) are associated with gastric cancer risk and whether an interaction between these genes and phytoestrogens modify gastric cancer risk.
methodsIn the discovery phase, 137 candidate SNPs in seven genes were analyzed in 76 incident gastric cancer cases and 322 matched controls from the Korean Multi-Center Cancer Cohort. Five significant SNPs in three genes (SRC, c-MET and CRK) were re-evaluated in 386 cases and 348 controls in the extension phase. Odds ratios (ORs) for gastric cancer risk were estimated adjusted for age, smoking, H. pylori seropositivity and CagA strain positivity. Summarized ORs in the total study population (462 cases and 670 controls) were presented using pooled- and meta-analysis. Plasma concentrations of phytoestrogens (genistein, daidzein, equol and enterolactone) were measured using the time-resolved fluoroimmunoassay.
resultsSRC rs6122566, rs6124914, c-MET rs41739, and CRK rs7208768 showed significant genetic effects for gastric cancer in both the pooled and meta-analysis without heterogeneity (pooled OR = 3.96 [95% CI 2.05-7.65], 1.24 [95% CI = 1.01-1.53], 1.19 [95% CI = 1.01-1.41], and 1.37 [95% CI = 1.15-1.62], respectively; meta OR = 4.59 [95% CI 2.74-7.70], 1.36 [95% CI = 1.09-1.70], 1.20 [95% CI = 1.00-1.44], and 1.32 [95% CI = 1.10-1.57], respectively). Risk allele of CRK rs7208768 had a significantly increased risk for gastric cancer at low phytoestrogen levels (p interaction<0.05).
conclusionsOur findings suggest that SRC, c-MET and CRK play a key role in gastric carcinogenesis by modulating CagA signal transductions and interaction between CRK gene and phytoestrogens modify gastric cancer risk.
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