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Updated: Feb 6, 2026

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
Published on: November 22, 2021
ERBBal Remedies: Combination Therapy for EGFR-mutant Lung Cancers
Pang-Dian Fan1, Helena A Yu2,3
1Department of Pathology and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
Abstract:
Multiple members of the ERBB/HER family of the receptor tyrosine kinases have been implicated in mediating acquired resistance to EGFR inhibitors that are used to treat EGFR-mutant lung cancers. New single agents and combination therapies targeting the ERBB/HER family members are being investigated to either prevent or overcome the emergence of acquired resistance. Clin Cancer Res; 24(22); 5499-501. ©2018 AACR See related article by Romaniello et al., p. 5610.
Insights
Acquired resistance to EGFR inhibitors in lung cancer is linked to ERBB/HER family kinases. New therapies targeting these kinases are being developed to overcome or prevent this resistance.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Epidermal Growth Factor Receptor (EGFR) inhibitors are crucial for treating EGFR-mutant lung cancers.
- Acquired resistance to these inhibitors is a significant clinical challenge.
- Members of the ERBB/HER family of receptor tyrosine kinases are implicated in resistance mechanisms.
Purpose of the Study:
- To review the role of ERBB/HER family members in acquired resistance to EGFR inhibitors.
- To discuss emerging single-agent and combination therapies targeting ERBB/HER family members.
- To explore strategies for preventing or overcoming acquired resistance in EGFR-mutant lung cancer.
Main Methods:
- Literature review of studies investigating ERBB/HER family kinases in EGFR inhibitor resistance.
- Analysis of preclinical and clinical data on novel therapeutic strategies.
- Synthesis of information on targeted therapies and resistance mechanisms.
Main Results:
- Multiple ERBB/HER family members contribute to acquired resistance to EGFR inhibitors.
- Targeting these ERBB/HER family members shows promise in preclinical and early clinical studies.
- Combination therapies may offer enhanced efficacy in overcoming resistance.
Conclusions:
- Understanding the role of ERBB/HER family kinases is critical for developing effective lung cancer treatments.
- New therapeutic approaches targeting ERBB/HER family members are essential for managing acquired resistance.
- Further investigation into these targeted therapies is warranted to improve patient outcomes.
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