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Cancer Chemother Pharmacol. 2013 Aug;72(2):397-403. doi: 10.1007/s00280-013-2211-0. Epub 2013 Jun 14.

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

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  • 1Department of Gastroenterology, Poitiers University Hospital, 2 rue de la Mil├ętrie, Poitiers Cedex, France. davidtougeron@hotmail.fr

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.

PMID:
23765179
[PubMed - indexed for MEDLINE]
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