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Reimagining HER2 therapy: Bridging oncogene addiction and immune modulation
Luke Tillman1, Lajos Pusztai2, Seth A Wander3
1School of Clinical Medicine, University of Cambridge, Cambridge CB2 0SP, UK.
Cancer Cell
|May 21, 2026
Summary
Human epidermal growth factor receptor 2 (HER2) drives cancer by altering the tumor microenvironment, creating immune resistance. Strategies targeting HER2 must address its immunomodulatory effects for improved cancer treatment efficacy.
Area of Science:
- Oncology
- Immunology
- Cancer Biology
Background:
- Human epidermal growth factor receptor 2 (HER2) is a key oncogenic driver in various cancers.
- HER2 signaling extends beyond direct tumor cell proliferation to profoundly influence the tumor microenvironment.
- This influence includes suppression of antigen presentation and promotion of immune checkpoints, fostering an immune-resistant tumor state.
Purpose of the Study:
- To elucidate the immunomodulatory roles of HER2 in the tumor microenvironment.
- To discuss strategies for enhancing HER2-targeted therapies by addressing immune evasion mechanisms.
- To highlight the importance of overcoming HER2-driven immunosuppression for effective cancer control.
Main Methods:
- Review of existing literature on HER2 signaling and tumor immunology.
- Analysis of HER2's impact on immune cell function and cytokine profiles within the tumor microenvironment.
- Synthesis of data to propose therapeutic strategies.
Main Results:
- HER2 actively remodels the tumor microenvironment to suppress anti-tumor immunity.
- Key mechanisms include reduced antigen presentation and increased immune checkpoint expression.
- Cytokine-mediated suppression is also a significant factor in HER2-driven immune resistance.
Conclusions:
- HER2-targeted therapies require integration with immunomodulatory strategies for optimal efficacy.
- Addressing HER2-driven immunosuppression is critical for achieving durable tumor control.
- Future therapeutic approaches should focus on overcoming the immune-resistant phenotype induced by HER2.
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