MOLECULAR GENETIC MECHANISMS OF THE PATHOGENESIS OF COLORECTAL CANCER

Abstract

A polyp is a benign epithelial tumor, which is a mass on a pedicle or broad base that rises above the mucous membrane. The aim of the work was to study the molecular genetic mechanisms of the pathogenesis of rectal polyps. The study was carried out theoretically, through the analysis of scientific articles related to the pathogenesis of colon polyps, published in the latest issues of well-known scientific journals. As a result of the study, it was established that in the pathogenesis of rectal polyps, 2 main mechanisms can be distinguished: chromosomal instability and microsatellite instability. Chromosomal instability (CIN) is a pathogenetic pathway, the implementation of which consists in a violation of suppressive mechanisms. This pathway of carcinogenesis includes both activation and inactivation of the following genes: APC, KRAS, BRAF, SMAD2 / 4 (DCC), p53. The second mechanism for the development of rectal polyps is associated with the development of microsatellite instability. Microsatellite instability (MSI) is a phenotype characterized by an increased likelihood of mutations occurring as a result of disruption of the unpaired DNA base repair system. The following genes belong to the repair system: MSH2, MSH6, MSH3, MLH1, PMS2. This mechanism is associated with the inactivation of genes of the DNA repair system (MisMatch Repair system - MMR). Thus, the development of rectal polyps is a multistage polyetiological process, in the development of which a number of genes play a primary role, mutations of which lead to the accumulation of these deviations, the differentiation of epithelial cells.