ArticleWorld journal of gastroenterology2009
CDH1 promoter polymorphism (-347G-->GA) is a possible prognostic factor in sporadic colorectal cancer.
Article in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- E-cadherin (CDH1) gene promoter polymorphism and the risk of colorectal cancer : a meta-analysis.International journal of colorectal disease · 2012Pooled it
- Association of CDH1 -160 C → A and -347 G→ GA polymorphisms and expression of E-cadherin and gastric cancer: A case-control study.Turkish journal of surgery · 2021Article
- Correlation of -160C > A and -347GA > G polymorphisms in E-cadherin gene and gastric cancer in north of Iran.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021Article
- A promoter polymorphism in the hMLH1 gene (-93G/A) associated with sporadic colorectal cancer.Oncology letters · 2016Article
- Regulatory Variants and Disease: The E-Cadherin -160C/A SNP as an Example.Molecular biology international · 2014Review
- Association of e-cadherin gene CDH1 polymorphism -160 C/A with susceptibility to develop vitiligo.Anais brasileiros de dermatologiaArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the role of the -347G-->GA polymorphism in the progression of colorectal cancer (CRC).
methodsWe designed a case-control study based on a population of CRC patients in China and normal healthy controls with no history of tumors or inherited diseases. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses were used to genotype the variants, and immunohistochemical staining was performed to measure the expression of E-cadherin in different allele cases among the CRC patients and normal controls.
resultsThe GA-allele (G/GA heterozygous and GA/GA homozygous) did not increase the risk of CRC compared with the G-allele (OR=1.232, 95% CI=0.898-1.691). However, the frequencies of the GA-allele were higher in poorly differentiated (P=0.002) and proximal (P=0.019) CRC patients than in normal controls. We also observed that E-cadherin expression was lower in poorly differentiated CRC patients than in well differentiated CRC patients (P=0.001). Furthermore, E-cadherin expression was lower for the GA-allele than for the G-allele (G/G heterozygous) in CRC patients (P=0.018). In contrast, there was no significant difference in E-cadherin expression for the G-allele and GA-allele in normal controls (P=0.292).
conclusionThe -347G-->GA promoter polymorphism in E-cadherin gene is associated with specific CRC features, and may be a prognostic factor rather than a susceptibility factor during the progression of CRC.
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