HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation.

By K. Takezawa, V. Pirazzoli, M. Arcila, C. Nebhan, Xiaoling Song, E. de Stanchina, K. Ohashi, Y. Janjigian, P. Spitzler, M. Melnick and 6 more. Cancer Discovery, 2012

666 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/dbd330514354bec9a90f7a1562280765a2942210

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. Jin-Yuan Shih
2. Carlos L. Arteaga
3. Shang-Gin Wu
4. J. Engelman

In Pulmonary and Respiratory Medicine

1. Carlos L. Arteaga
2. B. Hughes
3. B. Chan
4. Jin-Yuan Shih
5. Marc Ladanyi
6. Shang-Gin Wu
7. J. Engelman

Citations in the corpus

• Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors (2013, neutral): “More recently, ERBB2 amplification has been reported in another subset of AR cases.(318) Several clinical trials aimed at overcoming these distinct mechanisms of AR are underway and it is therefore likely that the further management of these patients will soon require determining T790M status and am”
• Management of acquired resistance to EGFR TKI–targeted therapy in advanced non-small cell lung cancer (2018, positive): “Activation of other alternative pathways, including HER2 amplification [34], PIK3CA mutation [35], BRAF mutation, and increased expression of the receptor tyrosine kinase AXL, have been reported to promote acquired resistance to EGFR TKIs [36].”
• Updated Molecular Testing Guideline for the Selection of Lung Cancer Patients for Treatment With Targeted Tyrosine Kinase Inhibitors: Guideline From the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology (2018, background): “ERBB2 amplification has also been reported rarely as a secondary event in patients with sensitizing EGFR mutations and as a potential mechanism of resistance following treatment with EGFR inhibitors.(90)”
• Targeted therapy for non-small cell lung cancer: current standards and the promise of the future. (2015, background): “Unfortunately a wide variety of mechanisms are being discovered including; ALK amplification, EGFR/HER1, HER2 and HER3 up-regulation, cKIT amplification and various ALK mutations including L1196M (analogous to T790M for EGFR) (107-110).”
• ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “The newer third-generation EGFR TKIs that suppress T790M are showing remarkable progress in this subset of cancers (Ranson et al., 2013; Sequist et al., 2013a; Soria et al., 2013).”