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Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade.

Shengqing Stan Gu1,2, Wubing Zhang1,3, Xiaoqing Wang4

  • 1Department of Data Science, Dana-Farber Cancer Institute, Boston, Massachusetts.

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|February 16, 2021
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This study identifies SMAC mimetics, like birinapant, as drugs that can increase MHC-I expression. This approach may help overcome resistance to immune checkpoint blockade (ICB) therapy in cancer patients with low MHC-I levels.

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Area of Science:

  • Oncology
  • Immunology
  • Genetics

Background:

  • Immune checkpoint blockade (ICB) therapy is effective for cancer, but resistance occurs, often due to impaired MHC-I expression.
  • Identifying therapeutic strategies to restore MHC-I expression is crucial for improving ICB efficacy.

Purpose of the Study:

  • To identify drugs that upregulate MHC-I expression without increasing PD-L1.
  • To explore novel therapeutic approaches for enhancing ICB response in tumors with low MHC-I.

Main Methods:

  • Utilized FACS-based genome-wide CRISPR screens to identify regulators of MHC-I.
  • Employed a data-mining approach to screen for drugs with specific transcriptional signatures.
  • Experimentally validated the efficacy of identified drug candidates in preclinical models.

Main Results:

  • TRAF3 was identified as a negative regulator of MHC-I expression.
  • A gene expression signature associated with TRAF3 loss correlated with improved survival and ICB response.
  • Second Mitochondria-derived Activator of Caspase (SMAC) mimetics, specifically birinapant, were found to upregulate MHC-I and enhance T cell-mediated killing.
  • Birinapant demonstrated additive efficacy with ICB in preclinical settings.

Conclusions:

  • SMAC mimetics, such as birinapant, represent a promising strategy to enhance ICB efficacy in tumors with low MHC-I expression.
  • This approach offers potential new immunotherapy opportunities for refractory cancer patients.
  • The methodology can be generalized to discover other drugs that potentiate immunotherapy.