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

被引：15

作者：

Tougeron D. ^{[1
,2
,3
]}

Cortes U. ^{[4
,5
]}

Ferru A. ^{[2
]}

Villalva C. ^{[4
,5
]}

Silvain C. ^{[1
]}

Tourani J.M. ^{[2
]}

Levillain P. ^{[6
]}

Karayan-Tapon L. ^{[4
,5
]}

机构：

[1] Department of Gastroenterology, Poitiers University Hospital, 86000 Poitiers Cedex

[2] Department of Oncology, Poitiers University Hospital

[3] Laboratoire Inflammation Tissus Epithéliaux et Cytokines, EA 4331, University of Poitiers

[4] INSERM U935, University of Poitiers

[5] Department of Molecular Oncology, Poitiers University Hospital

[6] Department of Pathology, Poitiers University Hospital

来源：

Cancer Chemotherapy and Pharmacology | 2013年 / 72卷 / 2期

关键词：

Anti-EGFR monoclonal antibodies; Colorectal cancer; EGFR mutation; KRAS mutation;

D O I：

10.1007/s00280-013-2211-0

中图分类号：

学科分类号：

摘要：

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. © 2013 Springer-Verlag Berlin Heidelberg.

引用

页码：397 / 403

页数：6

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