Autophagy facilitates the EGFR-TKI acquired resistance of non-small-cell lung cancer cells

J Formos Med Assoc. 2014 Mar;113(3):141-2. doi: 10.1016/j.jfma.2012.10.017. Epub 2013 Jan 2.

Authors

Donglei Liu¹, Yang Yang¹, Song Zhao²

Affiliations

¹ Department of Thoracic Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
² Department of Thoracic Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: [email protected].

PMID: 24630031
DOI: 10.1016/j.jfma.2012.10.017

No abstract available

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Antineoplastic Agents / therapeutic use
Autophagy*
Benzamides / therapeutic use
Biomarkers, Tumor / antagonists & inhibitors*
Biomarkers, Tumor / metabolism
Carcinoma, Non-Small-Cell Lung / drug therapy
Carcinoma, Non-Small-Cell Lung / physiopathology*
Drug Resistance, Neoplasm / physiology*
ErbB Receptors / antagonists & inhibitors*
ErbB Receptors / metabolism
Erlotinib Hydrochloride
Gefitinib
Humans
Imatinib Mesylate
Lung Neoplasms / drug therapy
Lung Neoplasms / physiopathology*
Piperazines / therapeutic use
Protein Kinase Inhibitors / therapeutic use*
Pyrimidines / therapeutic use
Quinazolines / therapeutic use

Substances

Antineoplastic Agents
Benzamides
Biomarkers, Tumor
Piperazines
Protein Kinase Inhibitors
Pyrimidines
Quinazolines
Imatinib Mesylate
Erlotinib Hydrochloride
EGFR protein, human
ErbB Receptors
Gefitinib