Background Mutations of the KRAS gene are common in cancers; they are detected at a very high rate in colon cancer (CC) and are considered a negative disease factor. CC is among the deadliest cancers in Vietnam, and KRAS status for non-polyp colon cancer (NPCC) was rarely reported from the country. In this study, we aim to determine KRAS mutations and the associations of mutation status with clinicopathological features in Vietnamese NPCC patients. Methods Patients with NPCC (stages II or III) and without historical or current polyp appearance were included. Genomic DNA samples were prepared from dissected tumors, and specific sequences of the KRAS gene were amplified by PCR. The mutations at codons 12, 13, 59, 60, 61, 117, and 146 of the gene were determined by using a commercial kit. Possible associations of the KRAS mutation with clinicopathological properties were analyzed using SPSS and GraphPad Prism. Results The KRAS mutation rate was 47.9% in NPCC patients; mutations in exon 2 accounted for 91.4% of all detected mutations. Moreover, the KRAS mutation rate was higher in females (57.1%) than in males (39.8%). The association of KRAS mutation with female NPCC patients was further confirmed by multivariate regression data with OR=2.144 and p = 0.012. Conclusion The KRAS mutation rate was also higher in patients with right colon cancers. The mutated-KRAS-carrying patients potentially experienced anemia. The data provide important scientific background for the treatment and management of the disease.

Background: Mutations of KRAS gene are common in cancers; they are detected at a very high rate in colon cancer (CC) and considered the negative factor of the disease. CC is among deadliest cancers in Vietnam, and KRAS status for non-polyp colon cancer (NPCC) was rarely reported from the country. We, in this study, aim to determine KRAS mutations and associations of mutation status with clinicopathological features in Vietnamese NPCC patients. Methods: Patients with NPCC (stages II or III) and without historical or current polyp appearance were included. Genomic DNA samples were prepared from dissected tumors and specific sequences of KRAS gene were amplified by PCR. The mutations at codons 12, 13, 59, 60, 61, 117 and 146 of the gene were determined by using a commercial kit. Possible associations of the KRAS mutation with clinicopathological properties were analyzed by using SPSS and GraphPad Prism. Key findings: KRAS mutation rate was 47.9% in NPCC patients; mutations in exon 2 accounted for 91.4% of all detected mutations. Moreover, the KRAS mutation rate was higher in females (57.1%) than in males (39.8%).