Molecular Biology of Colon Cancer

Abstract

SummaryColorectal cancer affects approx 140,000 people in the United States each year, resulting in more than 55,000 deaths. Colorectal cancer develops as the result of the progressive accumulation of genetic and epigenetic alterations that lead to the transformation of normal colonic epithelium to colon adenocarcinoma. The loss of genomic stability is a key molecular and pathophysiological step in this process and serves to create a permissive environment for the occurrence of alterations in tumor suppressor genes and oncogenes. Alterations in these genes, which include APC, CTNNB1, KRAS2, BRAF, MADH4/SMAD4, TP53, PI3KCA, and TGFBR2, appear to promote colon tumorigenesis by perturbing the function of signaling pathways, such as the transforming growth factor-␤ and PI3K signaling pathways, or by affecting genes that regulate genomic stability, such as the mutation mismatch repair genes.

MMP7 as a potential biomarker of colon cancer and its prognostic value by bioinformatics analysis

“…In particular, mutations of APC , KRAS , SMAD4 , DCC , TP53 and DNA mismatch repair genes are the most common and characteristic molecular events. [ 21 – 23 ] Due to the popularity of single cell sequencing and the study of gene and genomics, more and more new tumor markers have been applied, especially in colorectal cancer. Yang et al found seven differentially expressed mRNAs which were associated with prognosis in colon cancer patients by transcriptomic analysis, involving (SGCG, CLDN23, SLC4A4, CCDC78, SLC17A7, OTOP3, and SMPDL3A).…”