TP53 codon 72 polymorphism and type 2 diabetes: a case–control study in South Indian population
Molecular Biology Reports, ISSN: 1573-4978, Vol: 48, Issue: 6, Page: 5093-5097
2021
- 4Citations
- 10Captures
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Metrics Details
- Citations4
- Citation Indexes4
- Captures10
- Readers10
- 10
Article Description
TP53 functions primarily as a tumor suppressor, controlling a myriad of signalling pathways that prevent a cell from undergoing malignant transformation. This tumor suppressive function requires an activation and stabilization of TP53 in response to cell stressors. However, besides its cancer-preventive functions, TP53 is also known to be involved in diverse cellular processes including metabolism, reproduction, stem cell renewal and development. Indeed, several lines of evidence strongly suggest that TP53 plays crucial role in diabetes. A number of studies have evaluated the association of genetic alterations (single nucleotide variations) in TP53 gene with the development of diabetes. However, the results have not been consistent. The aim of this study was to evaluate whether the C/G polymorphism at codon 72 (Pro72/Arg72), located in exon 4 of TP53, is associated with type 2 diabetes in South Indian population. A total of 74 type 2 diabetic patients and 54 non-diabetic subjects were screened. None of the three genotypes, namely C/C (Pro/Pro), C/G (Pro/Arg), and G/G (Arg/Arg) was found to be significantly associated with type 2 diabetes in our study group. The findings of this study indicate that TP53 codon 72 polymorphism is not associated with increased risk of type 2 diabetes in South Indian population. Further studies with a large cohort size would be necessary to corroborate the observations of this study. Nevertheless, this study represents the first genetic analysis of TP53 variants in South Indian type 2 diabetic patients.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85111360940&origin=inward; http://dx.doi.org/10.1007/s11033-021-06505-8; http://www.ncbi.nlm.nih.gov/pubmed/34181170; https://link.springer.com/10.1007/s11033-021-06505-8; https://dx.doi.org/10.1007/s11033-021-06505-8; https://link.springer.com/article/10.1007/s11033-021-06505-8
Springer Science and Business Media LLC
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