Identification of a novel mutation in codon 31 of kirstein rat sarcoma viral oncogene homologue in colon Cancer: Another evidence of non-canonical mutational pathway

Colorectal cancer (crc) is a disease of the large intestine and regarded as a multistep process resulting from accumulation of different genetic alterations like activation of proto-oncogenes and inactivation of tumour suppressor genes. kirstein rat sarcoma viral oncogene homologue (k ras) is a proto-oncogene and mutations in this gene are considered to be involved in the early transition from normal colonic epithelium to premalignant tissue. mutations at codon 12,13,and 61 are widely studied and considered to be responsible to account for most rasmediated carcinogenesis but some of the recent evidences have suggested that non canonical mutations (outside of codons 12,13,and 61) may also contribute to the genetic aberrations leading to the ras-associated oncogenesis. we have analyzed the whole coding region of the gene and report a non-canonical novel heterozyogous mutation at codon 31 in a colonic tumor. polymerase chain reaction (pcr)-denaturing gradient gel electrophoresis (dgge),subsequent sequencing data revealed,g to a transition at first base of codon substituting glutamic acid (gaa) to lysine (aaa). since this mutation has never been reported before in crc,it is a novel variant in k ras. copyright © 2012 zoological society of pakistan.