Cetuximab Inhibits T790M-Mediated Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in a Lung Adenocarcinoma Patient-Derived Xenograft Mouse Model.

Date publication

septembre 2016

Journal

Clinical lung cancer

Auteurs

Membres identifiés du Cancéropôle Est :
Pr MASCAUX Céline

Tous les auteurs :
Martin P, Stewart E, Pham NA, Mascaux C, Panchal D, Li M, Kim L, Sakashita S, Wang D, Sykes J, Friess T, Shepherd FA, Liu G, Tsao MS

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/26926157

Résumé

The epidermal growth factor receptor (EGFR) kinase domain T790M (amino acid substitution at position 790 in EGFR from threonine [T] to methionine [M]) mutation in non-small-cell lung cancer (NSCLC) results in resistance to EGFR tyrosine kinase inhibitors (TKIs). We used a patient-derived tumor xenograft (PDX) model containing an EGFR exon 19 deletion/T790M mutation to assess response to the EGFR-directed antibody cetuximab. Changes in the EGFR signaling pathway and ligand expression after treatment were investigated.

Mots clés

Cancer, EGFR, Ligand, NSCLC, Signaling

Référence

Clin Lung Cancer. 2016 09;17(5):375-383.e2