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Cited by 585

The DOI matches its Crossref record; 92 of the 92 references it cites were found in a registry or an index.

Mechanisms of resistance to EGFR tyrosine kinase inhibitors

Open access
Huang, Lihua, Fu, Liwu·2015·Acta Pharmaceutica Sinica B

Abstract

Since the discovery that non-small cell lung cancer (NSCLC) is driven by epidermal growth factor receptor (EGFR) mutations, the EGFR tyrosine kinase inhibitors (EGFR-TKIs, e.g., gefitinib and elrotinib) have been effectively used for clinical treatment. However, patients eventually develop drug resistance. Resistance to EGFR-TKIs is inevitable due to various mechanisms, such as the secondary mutation (T790M), activation of alternative pathways (c-Met, HGF, AXL), aberrance of the downstream pathways (K-RAS mutations, loss of PTEN), impairment of the EGFR-TKIs-mediated apoptosis pathway (BCL2-like 11/BIM deletion polymorphism), histologic transformation, ATP binding cassette (ABC) transporter effusion, etc. Here we review and summarize the known resistant mechanisms to EGFR-TKIs and provide potential targets for development of new therapeutic strategies.

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Metadata

Authors
Huang, L., & Fu, L.
Venue
Acta Pharmaceutica Sinica B
Publisher
Elsevier BV
Published
2015-09
Volume
5
Issue
5
Pages
390-401
ISSN
2211-3835 (ISSN-L)
OpenAlex
W950232622
Cited by
585
References
92
FWCI
32.35
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Mechanisms of resistance to EGFR tyrosine kinase inhibitors. https://app.cochat.ai/papers/10.1016/j.apsb.2015.07.001
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Huang, L., & Fu, L. (2015). Mechanisms of resistance to EGFR tyrosine kinase inhibitors. Acta Pharmaceutica Sinica B. https://doi.org/10.1016/j.apsb.2015.07.001

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.