Abstract

e14634 Background: Colorectal cancer (CRC) is the third most common malignant tumor in the world. The KRAS gene, associated with CRC, located on chromosome 6, having in the codons 12 and 13 the most frequent mutation site, encodes a protein with an important pathogenic role in CRC. The brazilian northern population, especially in the Amazon region has acquired distinctive eating habits when compared to populations of other brazilian regions and other countries, that can lead to important epigenetic alterations. This reasearch aims to present a molecular panel regarding KRAS mutation in patients with colorectal cancer stage III and IV treated at an advanced oncology center in the Amazon region, comparing molecular findings in this population with other panels held in other centers worldwide. Methods: Retrospective, descriptive and quantitative data obtained in medical records of patients in treatment for CRC submitted to immunohistochemistry evaluation, through samples of colorectal tumor from january 2011 to december 2013. Only patients with pathologic confirmation of colorectal cancer stage III and IV were recruited. Results: The present study assessed a sample of 40 patients, of whom only 4 patients (10 %) showed some codon mutation in the KRAS gene. In the southern of Brazil, COURA et al. found 37/37 patients with mutated KRAS gene, the same percentage that SAMMER et al. found in India, where 53/53 patients had KRAS mutation. In the United States, a study of RASHID et al presented mutations in 60/200 (29.9 %) patients. In Japan, HARAD et al. demonstrated 43/120 (35.8%) patients had mutations in KRAS. An italian study of BAZAN et al. showed 74/160 (43.3 %) patients with a mutation in this gene. In China, a study conducted by LIU et al. showed 65/198 (32.8 %) mutated KRAS tumors. Conclusions: Our study found 90% of patients with wild type KRAS gene profile. This KRAS mutation rate data in CRC was not shown until now neither in brazilian samples nor in any other worldwide studies. It should be determined whether some behavioral or epigenetic pattern contributes to gene mutation or if KRAS patients in the study were subjected to a different carcinogenic pathway. Further studies should be conducted considering NRAS and BRAF mutations.

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