Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis

Wendy De Roock, Bart Claes, David Bernasconi, Jef De Schutter, Bart Biesmans, George Fountzilas, Konstantine T Kalogeras, Vassiliki Kotoula, Demetris Papamichael, Pierre Laurent-Puig, Frédérique Penault-Llorca, Philippe Rougier, Bruno Vincenzi, Daniele Santini, Giuseppe Tonini, Federico Cappuzzo, Milo Frattini, Francesca Molinari, Piercarlo Saletti, Sara De DossoMiriam Martini, Alberto Bardelli, Salvatore Siena, Andrea Sartore-Bianchi, Josep Tabernero, Teresa Macarulla, Frédéric Di Fiore, Alice Oden Gangloff, Fortunato Ciardiello, Per Pfeiffer, Camilla Qvortrup, Tine Plato Hansen, Eric Van Cutsem, Hubert Piessevaux, Diether Lambrechts, Mauro Delorenzi, Sabine Tejpar

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Abstract

Following the discovery that mutant KRAS is associated with resistance to anti-epidermal growth factor receptor (EGFR) antibodies, the tumours of patients with metastatic colorectal cancer are now profiled for seven KRAS mutations before receiving cetuximab or panitumumab. However, most patients with KRAS wild-type tumours still do not respond. We studied the effect of other downstream mutations on the efficacy of cetuximab in, to our knowledge, the largest cohort to date of patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab plus chemotherapy in the pre-KRAS selection era.
OriginalsprogEngelsk
TidsskriftLancet Oncology
Vol/bind11
Udgave nummer8
Sider (fra-til)753-62
Antal sider10
ISSN1470-2045
DOI
StatusUdgivet - 1. aug. 2010

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