Mathematical Approach in Colitis-Related Colon Cancer Genomics

Abstract

Ulcerative colitis or Crohn's illness patients are in danger of colon cancer due to chronic inflammation, resulting from the reaction of the immune system to bacterial disease caused by genetic alterations in the colonic mucosa. Somatic cells gain genomic changes, such as TP53 that regulates MUC2 production and APC alterations linked with 𝛽-catenin and MUC1 contribution in the slight proliferation of cells. Mathematical modeling describes developmental modifications and uses the phrases to link parameter to curves of age-dependent incidence of epidemiological cancer. By using the long-lasting investigation of IBD patients to gather the genomic estimations for increasingly exact computations of IBD-explicit developmental parameters as initiation, birth, and death. Colon cancer genetic trajectory follows the structure of the composition of functions that leads to malignancies. Models of population level can be utilized to consolidate epidemiological information and in this manner describe malignant growth advancement in a population with IBD.