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 Vol 9: Polymorphisms in the Insulin-Like Growth Factor Axis Are Associated with Gastrointestinal Cancer.


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This article is from PLoS ONE, volume 9.AbstractIntroduction: Numerous factors influence the development of gastrointestinal GI cancer. The insulin-like growth factor IGF axis plays a role in embryonic and postnatal growth and tissue repair. Elevated levels of IGFs, low levels of IGF binding proteins IGFBPs and over-expression of IGF receptor IGFR-I were associated with several stages of cancer. Here, the prevalence of the single nucleotide polymorphisms SNPs rs6214 in the IGF type I IGF-I gene and rs6898743 in the growth hormone receptor GHR gene in patients with GI cancer and controls was studied. Materials & Methods: In this Dutch case-control study, DNA isolated from blood of 1,457 GI cancer patients; 438 patients with head and neck cancer HNC, 475 with esophageal cancer EC and 544 with colorectal cancer CRC and 1,457 matched controls, was used to determine the rs6214 and rs6898743 genotypes by polymerase chain reaction. The association between these SNPs and GI cancer, HNC, esophageal adenocarcinoma EAC, esophageal squamous-cell carcinoma ESCC and proximal or distal CRC was studied. Odds ratios ORs with 95% confidence interval 95% CI were calculated via unconditional logistic regression. Results: Overall for GI cancer, the ORs for SNPs rs6214 and rs6898743 were approximately 1.0 p-value0.05, using the most common genotypes GG as reference. An OR of 1.54 95% CI, 1.05–2.27 was found for EC for genotype AA of rs6214. The ORs for EAC were 1.45 95% CI, 1.04–2.01 and 1.71 95% CI, 1.10–2.68, for genotypes GA and AA, respectively. Genotype GC of rs6898743 showed an OR of 0.47 95% CI, 0.26–0.86 for ESCC. Conclusion: The A allele of SNP rs6214 in the IGF-I gene was associated with EAC, and with HNC in women. The GC genotype of rs6898743 in the GHR gene was negatively associated with ESCC.



Autor: Ong, Jennie; Salomon, Jody; te Morsche, Rene H. M.; Roelofs, Hennie M. J.; Witteman, Ben J. M.; Dura, Polat; Lacko, Martin; Peters, Wilbert H. M.

Fuente: https://archive.org/







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