Abstract

KRAS mutations are mutually exclusive with other activating mutations on EGFR pathway. Detection of KRAS mutations associated with tumorigenesis, predicates the lack of other mutations on the same pathway and shows that the application of targeted therapy approaches which target other proteins in EGFR-MAPK pathway ineffective. In this study, frequency of KRAS mutations in colorectal cancer and relationship between KRAS mutation status and other clinical features were assessed. KRAS mutations were detected in 47,7% of the cases included in our study. We determined that 76% of the mutations were located in codon 12, 9% of the mutations were located in codon 13, 9% of the mutations were located in codon 61 and 6% of the mutations located in codon 117 or codon 146. Determination of mutation rates and association of mutations with clinical features for different populations are important for planning of the treatment strategies nationwide. In our study, we have demonstrated that KRAS mutation status and clinical features associated with KRAS mutation is in accordance with the literature. We have determined that there is statistically significant correlation between grade and KRAS mutation status.

Highlights

  • Colorectal cancer was the third most common cancer in the World and led second highest cancer related mortality in the year of 2018 (Wong et al, 2021)

  • Our study group is comprised of 44 cases which were diagnosed as “adenocarcinoma colonic type” between the dates of 21.07.2021 and 15.12.2020

  • We have demonstrated that there is statistically significant correlation between grade and KRAS mutation status where well differentiated tumors are associated with lower KRAS mutation rate when Type 1 error value is taken as 0,1

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Summary

Introduction

Colorectal cancer was the third most common cancer in the World and led second highest cancer related mortality in the year of 2018 (Wong et al, 2021). Epidermal Growth Factor Receptor (EGFR) and pathways that EGFR is involved played significant roles in development of Colorectal Carcinoma (London and Gallo, 2020). When EGFR is activated, KRAS and PI3K pathways are activated subsequently directly or indirectly via adaptor proteins harboring SH2 domains (Vitiello et al, 2019). When these pathways are activated, they activate other proteins and transmit extracellular signals to the nucleus where gene expression occurs and these signals were to be effective on cell proliferation and cell survival

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