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Related Experiment Video

Updated: May 3, 2026

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Molecular pathways: HER3 targeted therapy.

Kinisha Gala¹, Sarat Chandarlapaty

¹Authors' Affiliations: Gerstner Sloan Kettering Graduate School of Biomedical Sciences; and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research

|February 13, 2014

Summary

HER3 signaling is crucial in cancer, driving resistance to therapies and acting as a therapeutic target. Combination therapies show promise for HER3-targeting drugs, despite challenges with single-agent efficacy.

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Area of Science:

Oncology
Molecular Biology
Pharmacology

Background:

The HER family of receptor tyrosine kinases (EGFR, HER2, HER3, HER4) regulates cell growth and is frequently deregulated in cancer.
HER3, despite lacking intrinsic kinase activity, is a key signaling hub implicated in therapy resistance and cancer progression.
Activating mutations in HER3 have been identified in various cancers, positioning it as a direct therapeutic target.

Purpose of the Study:

To review the role of HER3 activation in cancer.
To discuss current pharmacologic strategies targeting HER3.
To explore opportunities for future HER3-directed therapeutic development.

Main Methods:

Review of preclinical and clinical data on HER3 signaling and targeted therapies.
Analysis of strategies to inhibit HER3 activation, including targeting dimerization partners and the HER3 extracellular domain (ECD).
Evaluation of single-agent versus combination therapy approaches for HER3-targeted drugs.

Main Results:

HER3 plays a significant role in mediating resistance to HER2 and PI3K pathway inhibitors.
Directly targeting HER3 with antibodies shows limited single-agent activity, potentially due to biomarker limitations and antibody potency.
Combination therapies involving HER3-targeted agents demonstrate improved efficacy in preclinical and clinical settings.

Conclusions:

HER3 is an important target in oncology, particularly for overcoming therapeutic resistance.
Developing effective HER3-targeted therapies requires addressing challenges in biomarker identification and drug potency.
Combination strategies represent a promising avenue for enhancing the clinical benefit of HER3-directed treatments.