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Article

Acquired resistance of EGFR-mutant lung adenocarcinomas to afatinib plus cetuximab is associated with activation of mTORC1.

Cell reports - 22 May 2014

Pirazzoli Valentina, Nebhan Caroline, Song Xiaoling, Wurtz Anna, Walther Zenta, Cai Guoping, Zhao Zhongming, Jia Peilin, de Stanchina Elisa, Shapiro Erik M, Gale Molly, Yin Ruonan, Horn Leora, Carbone David P, Stephens Philip J, Miller Vincent, Gettinger Scott, Pao William, Politi Katerina

Abstract excerpt

Patients with EGFR-mutant lung adenocarcinomas (LUADs) who initially respond to first-generation tyrosine kinase inhibitors (TKIs) develop resistance to these drugs. A combination of the irreversible TKI afatinib and the EGFR antibody cetuximab can be used to overcome resistance to first-generation TKIs; however, resistance to this drug combination eventually emerges. We identified activation of the mTORC1...

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Topics

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Share to Afatinib
Share to Antibodies, Monoclonal, Humanized

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cetuximab

Share to Mechanistic Target of Rapamycin Complex 1

Share to Multiprotein Complexes

Share to Quinazolines

Share to Random Allocation

Share to TOR Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 24813888
DOI: 10.1016/j.celrep.2014.04.014
PMCID: PMC4074596

Genes

EGFR
TSC1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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