De novo ERBB2 amplification causing intrinsic resistance to erlotinib in EGFR-L858R mutated TKI-naïve lung adenocarcinoma

Lung Cancer. 2017 Dec:114:108-110. doi: 10.1016/j.lungcan.2017.08.018. Epub 2017 Aug 24.

Authors

Brian J Carney¹, Deepa Rangachari², Paul A VanderLaan³, Kyle Gowen⁴, Alexa B Schrock⁴, Siraj M Ali⁴, Daniel B Costa¹

Affiliations

¹ Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
² Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: drangach@bidmc.harvard.edu.
³ Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
⁴ Foundation Medicine Inc, Cambridge, MA, United States.

PMID: 28870636
DOI: 10.1016/j.lungcan.2017.08.018

No abstract available

Publication types

Case Reports
Letter

MeSH terms

Adenocarcinoma / drug therapy*
Adenocarcinoma / genetics
Adenocarcinoma / pathology
Adenocarcinoma of Lung
Aged
Antineoplastic Agents / therapeutic use
Drug Resistance, Neoplasm / drug effects
Drug Resistance, Neoplasm / genetics*
ErbB Receptors / genetics
Erlotinib Hydrochloride / therapeutic use*
Female
Gene Amplification
Humans
Lung Neoplasms / drug therapy*
Lung Neoplasms / genetics
Lung Neoplasms / pathology
Mutation
Protein Kinase Inhibitors / therapeutic use*
Receptor, ErbB-2 / genetics*

Substances

Antineoplastic Agents
Protein Kinase Inhibitors
Erlotinib Hydrochloride
EGFR protein, human
ERBB2 protein, human
ErbB Receptors
Receptor, ErbB-2