Volume 22, Issue 92 (9-2012)                   J Mazandaran Univ Med Sci 2012, 22(92): 30-35 | Back to browse issues page

XML Persian Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Karimi K, Arkani M, Safaei A, vahedi M, Mohebi S R, Fatemi S R, et al . Relationship between Insulin Receptor (INSR rs 1799817) and Colorectal Cancer (CRC). J Mazandaran Univ Med Sci. 2012; 22 (92) :30-35
URL: http://jmums.mazums.ac.ir/article-1-1303-en.html
Abstract:   (10063 Views)
Background and purpose: Insulin regulates cell growth and apoptosis by binding to its receptor (INSR). Many studies show that variation in insulin pathway play a plausible role in the development of colorectal cancer (CRC). The goal of this study was to evaluate the incidence of insulin receptor (INSR rs1799817) in people attending Taleghani Hospital and to investigate the role of this polymorphism in increased risk to CRC. Materials and methods: In this case-control study genotyping of the insulin receptor (INSR rs1799817) were determined in a series of 110 colorectal cancer patients and 110 controls using polymerase chain reaction and restriction fragment length polymorphism genotyping assays (PCR-RFLP). To investigate the relationship between genotypes and risk of CRC SPSS (V16) was used. Results: The results showed that polymorphism INSR rs 1799817 was not a predisposing factor for increased risk of CRC (P= 0.49). There was no significant difference in the incidence of mutant allele between the patients and controls (OR= 1.12 95% CI= 0.73-1.69). Conclusion: These findings suggest that polymorphism insulin receptor rs 1799817 is not associated with increased risk of CRC.
Full-Text [PDF 185 kb]   (2133 Downloads)    
Type of Study: Research(Original) |

Add your comments about this article : Your username or Email:
CAPTCHA

Send email to the article author


© 2020 All Rights Reserved | Journal of Mazandaran University of Medical Sciences

Designed & Developed by : Yektaweb