Interferon signaling restrains renal cell carcinoma heterogeneity
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S., komentáře
Grantová podpora
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-zdroje
- Klíčová slova
- CGAS, CNV, cancer stem cells, cancer/immunity coevolution, immunoevasion,
- MeSH
- interferon typ I * metabolismus MeSH
- karcinom z renálních buněk * genetika MeSH
- lidé MeSH
- nádory ledvin * genetika MeSH
- nukleotidyltransferasy metabolismus MeSH
- signální transdukce MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- komentáře MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Názvy látek
- interferon typ I * MeSH
- nukleotidyltransferasy 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.
Zobrazit více v PubMed
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