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Updated: Jan 17, 2026

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
Viral mimicry in cancer therapy
Laura Rosenberg1, Nicolas Vabret1
1Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Immunology and Immunotherapy, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Cancer treatments can trigger viral mimicry by reactivating transposable elements (TEs), leading to immune responses. This review explores TE-mediated immunity in cancer and its therapeutic implications.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Viral mimicry involves transposable element (TE) reactivation, producing nucleic acids that activate innate immunity.
- While initially studied in epigenetic therapies, various cancer treatments now show potential to induce TE reactivation and viral mimicry.
Purpose of the Study:
- To review current knowledge on treatment-induced TE-mediated immune responses in cancer.
- To highlight therapeutic strategies, molecular mechanisms, and implications for tumor-immune interactions and treatment outcomes.
Main Methods:
- Literature review synthesizing current research on TE reactivation and immune responses in cancer.
- Analysis of shared and distinct molecular mechanisms across different cancer treatment modalities.
Main Results:
- Cancer therapies like radiotherapy, chemotherapy, and targeted treatments can induce TE reactivation.
- Induced TE reactivation triggers innate immune pathways, mimicking viral infection responses.
Conclusions:
- Treatment-induced viral mimicry represents a significant factor in cancer-immune interactions.
- Understanding these mechanisms may lead to novel therapeutic strategies and improved treatment outcomes in oncology.
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