Interferon signaling restrains renal cell carcinoma heterogeneity
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Comment
Grant support
R01 CA271915
NCI NIH HHS - United States
U54 CA274291
NCI NIH HHS - United States
PubMed
37658022
PubMed Central
PMC11075004
DOI
10.1016/j.trecan.2023.08.008
PII: S2405-8033(23)00168-1
Knihovny.cz E-resources
- Keywords
- CGAS, CNV, cancer stem cells, cancer/immunity coevolution, immunoevasion,
- MeSH
- Interferon Type I * metabolism MeSH
- Carcinoma, Renal Cell * genetics MeSH
- Humans MeSH
- Kidney Neoplasms * genetics MeSH
- Nucleotidyltransferases metabolism MeSH
- Signal Transduction MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Comment MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Names of Substances
- Interferon Type I * MeSH
- Nucleotidyltransferases MeSH
Type I interferon (IFN) is central to cancer surveillance as it mediates both direct and immune-mediated oncosuppressive effects. A recent study by Perelli et al. suggests that the ability of renal cancer cells to tolerate complex karyotypic alterations elicited by chromosomal instability (CIN), and ultimately acquire full metastatic potential, is also negatively regulated by IFN signaling.
See more in PubMed
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