Epidermal growth factor receptor (EGFR) and KRAS mutations during chemotherapy plus anti-EGFR monoclonal antibody treatment in metastatic colorectal cancer

Abstract

It is now well established that metastatic colorectal cancer patients without KRAS mutation (codon 12) benefit from treatment with an epidermal growth factor receptor monoclonal antibody (anti-EGFR mAb). Recently, EFGR and KRAS mutations have been shown to exist in patients who developed resistance to anti-EGFR mAb. We analyzed KRAS, BRAF V600E and EGFR S492R mutations in 37 post-anti-EGFR mAb tumor samples from 23 patients treated with chemotherapy plus anti-EGFR mAb. No EGFR S492R mutation was detected. A KRAS mutation was found after anti-EGFR mAb in only one tumor. Our results suggest that acquired EGFR S492R and KRAS mutations do not constitute the main mechanism of resistance to anti-EGFR mAb in combination with chemotherapy.