ArticleCarcinogenesis2014
Integrative post-genome-wide association analysis of CDKN2A and TP53 SNPs and risk of esophageal adenocarcinoma.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Genetic Biomarkers of Barrett's Esophagus Susceptibility and Progression to Dysplasia and Cancer: A Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2016Pooled it
- Pathogenic CDKN2A germline variants are rare in a cohort of unselected pancreatic cancer patients from Pakistan.Familial cancer · 2025Article
- IncreasedMolecular & cellular oncology · 2025Article
- Unraveling the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma: the "omics" era.Frontiers in oncology · 2024Review
- Cancer Risk in Barrett's Esophagus: A Clinical Review.International journal of molecular sciences · 2023Review
- A risk variant for Barrett's esophagus and esophageal adenocarcinoma at chr8p23.1 affects enhancer activity and implicates multiple gene targets.Human molecular genetics · 2022Article
- eQTL Set-Based Association Analysis Identifies Novel Susceptibility Loci for Barrett Esophagus and Esophageal Adenocarcinoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022Article
- Today's Mistakes and Tomorrow's Wisdom in Development and Use of Biomarkers for Barrett's Esophagus.Visceral medicine · 2022Review
- Prioritization and functional analysis of GWAS risk loci for Barrett's esophagus and esophageal adenocarcinoma.Human molecular genetics · 2022Article
- Germline variation in the insulin-like growth factor pathway and risk of Barrett's esophagus and esophageal adenocarcinoma.Carcinogenesis · 2021Observational
- Early TP53 alterations engage environmental exposures to promote gastric premalignancy in an integrative mouse model.Nature genetics · 2020Article
- Identification of genes and pathways in esophageal adenocarcinoma using bioinformatics analysis.Biomedical reports · 2018Article
- Genetic variants of FOXP1 and FOXF1 are associated with the susceptibility of oesophageal adenocarcinoma in Chinese population.Journal of genetics · 2018Article
- Evolution of Premalignant Disease.Cold Spring Harbor perspectives in medicine · 2017Review
- Article
- The Evolving Genomic Landscape of Barrett's Esophagus and Esophageal Adenocarcinoma.Gastroenterology · 2017Review
- Article
- Precancer Atlas to Drive Precision Prevention Trials.Cancer research · 2017Article
- Etiology and Prevention of Esophageal Cancer.Gastrointestinal tumors · 2016Review
- Expression of TP53, BCL-2, and VEGFA Genes in Esophagus Carcinoma and its Biological Significance.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 15 institutions in 5 countries.
Funding
Abstract
Incidence of esophageal adenocarcinoma (EA) in Western countries has increased markedly in recent decades. Although several risk factors have been identified for EA and its precursor, Barrett's esophagus (BE), including reflux, Caucasian race, male gender, obesity, and smoking, less is known about the role of inherited genetic variation. Frequent somatic mutations in the tumor suppressor genes CDKN2A and TP53 were recently reported in EA tumors, while somatic alterations at 9p (CDKN2A) and 17p (TP53) have been implicated as predictors of progression from BE to EA. Motivated by these findings, we used data from a genome-wide association study of 2515 EA cases and 3207 controls to analyze 37 germline single nucleotide polymorphisms at the CDKN2A and TP53 loci. Three CDKN2A polymorphisms were nominally associated (P < 0.05) with reduced risk of EA: rs2518720 C>T [intronic, odds ratio 0.90, P = 0.0121, q = 0.3059], rs3088440 G>A (3'UTR, odds ratio 0.84, P = 0.0186, q = 0.3059), and rs4074785 C>T (intronic, odds ratio 0.85, P = 0.0248, q = 0.3059). None of the TP53 single nucleotide polymorphisms reached nominal significance. Two of the CDKN2A variants identified were also associated with reduced risk of progression from BE to EA, when assessed in a prospective cohort of 408 BE patients: rs2518720 (hazard ratio 0.57, P = 0.0095, q = 0.0285) and rs3088440 (hazard ratio 0.34, P = 0.0368, q = 0.0552). In vitro functional studies of rs3088440, a single nucleotide polymorphism located in the seed sequence of a predicted miR-663b binding site, suggested a mechanism whereby the G>A substitution may attenuate miR-663b-mediated repression of the CDKN2A transcript. This study provides the first evidence that germline variation at the CDKN2A locus may influence EA susceptibility.
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Registered trials
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