Met receptor amplification drives resistance to anti-egfr therapies

Patricia Martin Romano; Eduardo Castanon; Antoine Hollebecque; Ludovic Lacroix; Nathalie Auger; Eric Angevin; Lambros Tselikas; Sami Ammari; Jean Charles Soria; Christophe Massard

doi:10.4103/JIPO.JIPO_7_19

Met receptor amplification drives resistance to anti-egfr therapies

Patricia Martin Romano, Eduardo Castanon, Antoine Hollebecque, Ludovic Lacroix, Nathalie Auger, Eric Angevin, Lambros Tselikas, Sami Ammari, Jean Charles Soria, Christophe Massard

Résultats de recherche: Contribution à un journal › Article › Revue par des pairs

Résumé

Mesenchymal–epithelial transition factor (MET) amplification has been suggested either as a de novo or acquired mechanism of resistance to anti-epidermal growth factor receptor (anti-EGFR) therapy. However, even if MET amplification has been widely described in the preclinical setting, only a few clinical data have confirmed the role of MET in the resistance to anti-EGFR treatment. A 60-year-old man presenting cholangiocarcinoma with EGFR amplification had a tumor response to anti-EGFR therapy. A new on-purpose tumor biopsy performed during tumor progression confirmed the known EGFR amplification as well as a new MET amplification. This clinical observation highlights the role of MET amplification as a mechanism of resistance to EGFR inhibitors.

langue originale	Anglais
Pages (de - à)	152-155
Nombre de pages	4
journal	Journal of Immunotherapy and Precision Oncology
Volume	2
Numéro de publication	4
Les DOIs	https://doi.org/10.4103/JIPO.JIPO_7_19
état	Publié - 1 janv. 2019

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10.4103/JIPO.JIPO_7_19

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title = "Met receptor amplification drives resistance to anti-egfr therapies",

abstract = "Mesenchymal–epithelial transition factor (MET) amplification has been suggested either as a de novo or acquired mechanism of resistance to anti-epidermal growth factor receptor (anti-EGFR) therapy. However, even if MET amplification has been widely described in the preclinical setting, only a few clinical data have confirmed the role of MET in the resistance to anti-EGFR treatment. A 60-year-old man presenting cholangiocarcinoma with EGFR amplification had a tumor response to anti-EGFR therapy. A new on-purpose tumor biopsy performed during tumor progression confirmed the known EGFR amplification as well as a new MET amplification. This clinical observation highlights the role of MET amplification as a mechanism of resistance to EGFR inhibitors.",

keywords = "Anti-epidermal growth factor receptor, Cholangiocarcinoma, Gene amplificationmesenchymal–epithelial transition factor, Resistance",

author = "Romano, {Patricia Martin} and Eduardo Castanon and Antoine Hollebecque and Ludovic Lacroix and Nathalie Auger and Eric Angevin and Lambros Tselikas and Sami Ammari and Soria, {Jean Charles} and Christophe Massard",

note = "Publisher Copyright: {\textcopyright} 2019 Journal of Immunotherapy and Precision Oncology.",

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T1 - Met receptor amplification drives resistance to anti-egfr therapies

AU - Romano, Patricia Martin

AU - Castanon, Eduardo

AU - Hollebecque, Antoine

AU - Lacroix, Ludovic

AU - Auger, Nathalie

AU - Angevin, Eric

AU - Tselikas, Lambros

AU - Ammari, Sami

AU - Soria, Jean Charles

AU - Massard, Christophe

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Mesenchymal–epithelial transition factor (MET) amplification has been suggested either as a de novo or acquired mechanism of resistance to anti-epidermal growth factor receptor (anti-EGFR) therapy. However, even if MET amplification has been widely described in the preclinical setting, only a few clinical data have confirmed the role of MET in the resistance to anti-EGFR treatment. A 60-year-old man presenting cholangiocarcinoma with EGFR amplification had a tumor response to anti-EGFR therapy. A new on-purpose tumor biopsy performed during tumor progression confirmed the known EGFR amplification as well as a new MET amplification. This clinical observation highlights the role of MET amplification as a mechanism of resistance to EGFR inhibitors.

AB - Mesenchymal–epithelial transition factor (MET) amplification has been suggested either as a de novo or acquired mechanism of resistance to anti-epidermal growth factor receptor (anti-EGFR) therapy. However, even if MET amplification has been widely described in the preclinical setting, only a few clinical data have confirmed the role of MET in the resistance to anti-EGFR treatment. A 60-year-old man presenting cholangiocarcinoma with EGFR amplification had a tumor response to anti-EGFR therapy. A new on-purpose tumor biopsy performed during tumor progression confirmed the known EGFR amplification as well as a new MET amplification. This clinical observation highlights the role of MET amplification as a mechanism of resistance to EGFR inhibitors.

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KW - Cholangiocarcinoma

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KW - Resistance

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