Abstract
Signal pathway inhibition is a well-validated approach for treating cancers driven by activated kinases such as KIT. However, kinase inhibitors may make tumor cells less responsive to tumor immune surveillance and less sensitive to immunotherapies. In this issue, Liu and colleagues report that, in a mouse model, inhibition of oncogenic KIT in gastrointestinal stromal tumors reduces type I interferon (IFN) production and signaling, and the effectiveness of the immune system in controlling tumor growth. They were able to partially overcome the immunosuppressive effects of KIT inhibition using agonists of the type I IFN response, pointing the way toward intelligently combining kinase inhibitors and immune modulators for therapy. See article by Liu et al., p. 542.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 489 |
| Number of pages | 1 |
| Journal | Cancer Immunology Research |
| Volume | 9 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 1 2021 |
Bibliographical note
Funding Information:D.A. Largaespada reports other support from NeoClone Biotechnology, Inc., Luminary Therapeutics, Inc., Recombinetics, Inc., Luminary Therapeutics, Inc., Styx Biotechnologies, Inc., and Immusoft, Inc. and grants from Genentech, Inc. outside the submitted work.
Publisher Copyright:
2021 American Association for Cancer Research.
Keywords
- Animals
- Gastrointestinal Stromal Tumors
- Imatinib Mesylate/pharmacology
- Mice
- Proto-Oncogene Proteins c-kit/metabolism
- Signal Transduction
PubMed: MeSH publication types
- Journal Article
- Comment
