Abstract 156P
Background
The most important direction of modern oncology is the identification of unfavorable prognostic groups of patients, formed on the results of studies of molecular genetic processes occurring in the tumor and tumor microenvironment. The main goal was to assess the information content and determine the prognostic significance of molecular genetic phenotypes of colorectal cancer.
Methods
Analysis of the expression level of 64 genes was carried out using real-time PCR in 226 samples of tumor tissue obtained from the growth zone and 119 samples of morphologically unchanged tissue. The average follow-up period was 28.15±14.7 months. Data Analysis and Predictive Modeling were conducted using the statistical computing environment R 3.6.3 (R Foundation for Statistical Computing, Vienna, Austria) using additional packages rms 5.1-4, survival 3.2-7 and pROC 1.16.2.
Results
In our study, an analysis was carried out that made it possible to identify variables that determine the phenotype characteristic of tumors with a RAS mutation. A discriminant analysis of the classification of patients into RAS+ and RAS – phenotype was also carried out and it was found that the presence of a RAS mutation greatly affects the expression of certain genes and creates a specific phenotype. Impaired expression of genes such as CCND1, BCL2, NDRG1, HER2 and IL2a, characteristic of RAS+ tumors, can affect other signaling pathways. Further studies are needed to understand the relevant role and molecular mechanisms of the RAS+ phenotype in CRC.
Conclusions
Based on the results of an analysis of the gene expression profile in tumor tissue and morphologically unchanged colon tissue, a molecular genetic phenotype of colorectal cancer was identified, including changes in 5 genes, the value of which can accurately separate the “mutant phenotype” (RAS+) from the “non-mutant phenotype” (RAS -). Based on these data, it is possible to create a diagnostic panel that will answer questions regarding the influence of this mutation on other signaling pathways in the pathogenesis of CRC, as well as determine resistance to the use of anti-EGFR targeted therapy.
Legal entity responsible for the study
RNCRR.
Funding
Has not received any funding.
Disclosure
The author has declared no conflicts of interest.