Relationship of special molecular mechanisms in colorectal cancer. Literature review
Pokitko O.V.1, Sulayeva O.M.2, Mashukov A.O.3, Merlich S.V.1, Zgura O.M.1, Ratsiborskyi D.V.1, Shilin I.V.1, Shkurat O.V.1, Syrbu V.M.1, Petrosyan M.A.1, Yukhymchuk B.S.1, Brailovska V.V.3, Letinsky I.H.1, Brailovskyi B.Y.3
- 1Municipal Non-Commercial Enterprise «Odesa Regional Clinical Antitumor Center» of the Odesa Regional Council», Odesa, Ukraine
- 2CSD LAB Medical laboratory, Kyiv, Ukraine
- 3International Humanitarian University, Odesa, Ukraine
Summary. Modern oncology raises a rapidly developing specialty that uses increasingly complex and multi-level models in order to describe multiple processes occurring inside tumor surface. From the understanding of some «simple» colony of malignant cells, we first of all have been moved to understanding the heterogeneity of those processes occurring in its various parts to realizing the significant role of «corrupted» tumor genetics. One of the most vivid and well-studied is the genetics of colorectal cancer, the formation of which is preceded by series of scenarios. Theoretical models describing the appearance of a specific oncological phenotype are considered to be quite well developed. But, as it turned out, the events taking place in the process of accumulating signs of malignant growth do not have a linear-like character. They accumulate simultaneously, and its accumulation occurs at different speeds. «Changes accumulate gradually, and are implemented in leaps and bounds». The most vivid example of this, from the point of view of the authors of the publication, is a comparison of 2 lines of mutations: driver mutations, included in the so-called «Full House» (Vogelgram) and, accordingly, a set of mutations had been not included in it yet. The first point includes APC, DCC, TP 53, KRAS and DNA hypomethylation, the second — PIK3CA, BRAF, NRAS, HER2, PTEN STAT3, RAF1. Instead of one, which was previously considered the «leading» phenotype — microsatellite instability (MSI), there raises a second, competing phenotype of CpG-island methylator (CIMP). In this review, we have tried to clarify the direction of those trends, to comprehend their role in the biology and mechanisms of the colorectal cancer progression.
Leave a comment