Oncogenic MET as an Effective Therapeutic Target in Non–Small Cell Lung Cancer Resistant to EGFR Inhibitors: The Rise of the Phoenix

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Abstract

Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non–small cell lung cancer carrying EGFR mutations and MET amplifi cation, but large phase III trials in genetically unselected individuals have failed to confi rm the benefi t of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifi es a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode.
Original languageEnglish
JournalCancer Discovery
Publication statusPublished - 2016

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Non-Small Cell Lung Carcinoma
Mutation
Cations
Lung Neoplasms
Phosphotransferases
Therapeutics

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@article{ab7379c5bcc1457e9c1deb7cc18dd9e4,
title = "Oncogenic MET as an Effective Therapeutic Target in Non–Small Cell Lung Cancer Resistant to EGFR Inhibitors: The Rise of the Phoenix",
abstract = "Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non–small cell lung cancer carrying EGFR mutations and MET amplifi cation, but large phase III trials in genetically unselected individuals have failed to confi rm the benefi t of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifi es a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode.",
author = "Livio Trusolino",
year = "2016",
language = "English",
journal = "Cancer Discovery",
issn = "2159-8274",
publisher = "American Association for Cancer Research Inc.",

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T1 - Oncogenic MET as an Effective Therapeutic Target in Non–Small Cell Lung Cancer Resistant to EGFR Inhibitors: The Rise of the Phoenix

AU - Trusolino, Livio

PY - 2016

Y1 - 2016

N2 - Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non–small cell lung cancer carrying EGFR mutations and MET amplifi cation, but large phase III trials in genetically unselected individuals have failed to confi rm the benefi t of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifi es a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode.

AB - Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non–small cell lung cancer carrying EGFR mutations and MET amplifi cation, but large phase III trials in genetically unselected individuals have failed to confi rm the benefi t of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifi es a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode.

M3 - Article

JO - Cancer Discovery

JF - Cancer Discovery

SN - 2159-8274

ER -