ArticleSpringerPlus2015
Genetic variants and risk of gastric cancer: a pathway analysis of a genome-wide association study.
Article in SpringerPlus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Calorie restriction remodels gut microbiota and suppresses tumorigenesis of colorectal cancer in mice.Experimental and therapeutic medicine · 2023Article
- Role of EFNA1 SNP (rs12904) in Tumorigenesis and Metastasis of Colorectal Cancer: A Bioinformatic Analysis and HRM SNP Genotyping Verification.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Review
- Association Between Polymorphisms in Gastric Cancer Related Genes and Risk of Gastric Cancer: A Case-Control Study.Frontiers in molecular biosciences · 2021Article
- ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways.International journal of molecular medicine · 2019Article
- Multi-marker analysis of genomic annotation on gastric cancer GWAS data from Chinese populations.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019Article
- PLCE1 polymorphisms and expression combined with serum AFP level predicts survival of HBV-related hepatocellular carcinoma patients after hepatectomy.Oncotarget · 2017Article
- Genome-wide association studies and epigenome-wide association studies go together in cancer control.Future oncology (London, England) · 2016Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to discover candidate single nucleotide polymorphisms (SNPs) for hypothesizing significant biological pathways of gastric cancer (GC). We performed an Identify Candidate Causal SNPs and Pathways (ICSNPathway) analysis using a GC genome-wide association study (GWAS) dataset, including 472,342 SNPs in 2,240 GC cases and 3,302 controls of Asian ethnicity. By integrating linkage disequilibrium analysis, functional SNP annotation, and pathway-based analysis, seven candidate SNPs, four genes and 12 pathways were selected. The ICSNPathway analysis produced 4 hypothetical mechanisms of GC: (1) rs4745 and rs12904 → EFNA1 → ephrin receptor binding; (2) rs1801019 → UMPS → drug and pyrimidine metabolism; (3) rs364897 → GBA → cyanoamino acid metabolism; and (4) rs11187870, rs2274223, and rs3765524 → PLCE1 → lipid biosynthetic process, regulation of cell growth, and cation homeostasis. This pathway analysis using GWAS dataset suggests that the 4 hypothetical biological mechanisms might contribute to GC susceptibility.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.