KRAS Exon 2 Mutations in Patients with Sporadic Colorectal Cancer: Prevalence Variations in Mexican and Latin American Populations

Simple Summary: KRAS is one of the most prominent driver genes implicated in colorectal cancer (CRC), with mutations detected in 33% to 50% of CRC patients. Exon 2 harbors up to 98% of these mutations. Variants in this gene play crucial roles in the progression of the disease, influencing its development, clinical manifestations, and treatment election. This study elucidates a 17% prevalence of mutations in KRAS exon 2 among western Mexican patients with sporadic CRC. Furthermore, a 30% pooled prevalence of mutations in KRAS exon 2 was determined after analyzing an additional 16 studies from Latin America, encompassing 12,604 CRC patients. Due to advances in precision medicine treatments, knowing the pathogenic status of the KRAS gene will become imperative to optimally select targeted therapies. We searched for the prevalence of actionable somatic mutations in exon 2 of the KRAS gene in western Mexican patients with CRC. Tumor tissue DNA samples from 150 patients with sporadic CRC recruited at the Civil Hospital of Guadalajara were analyzed. Mutations in exon 2 of the KRAS gene were identified using Sanger sequencing, and the data were analyzed considering clinical-pathological characteristics. Variants in codon 12 (rs121913529 G>A, G>C, and G>T) and codon 13 (rs112445441 G>A) were detected in 26 patients (with a prevalence of 17%). No significant associations were found between these variants and clinical-pathological characteristics (p > 0.05). Furthermore, a comprehensive search was carried out in PubMed/NCBI and Google for the prevalence of KRAS exon 2 mutations in Latin American populations. The 17 studies included 12,604 CRC patients, with an overall prevalence of 30% (95% CI = 0.26-0.35), although the prevalence ranged from 13 to 43% across the different data sources. Determining the variation and frequency of KRAS alleles in CRC patients will enhance their potential to receive targeted treatments and contribute to the understanding of the genomic profile of CRC.