期刊
CELL
卷 174, 期 6, 页码 1347-1360出版社
CELL PRESS
DOI: 10.1016/j.cell.2018.08.027
关键词
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资金
- Department of Defense Breast Cancer Research Breakthrough Award [W81XWH-16-1-0315, BC151244]
- Elsa U. Pardee Foundation
- Burroughs Wellcome Fund Career Award for Medical Scientists
- MSKCC core grant [P30-CA008748]
- NIH [R35-CA197588, U54-CA210184]
- Breast Cancer Research Foundation
- Gray Foundation Basser Initiative
- CDMRP [893193, BC151244] Funding Source: Federal RePORTER
Chromosomal instability (CIN) is a hallmark of human cancer, and it is associated with poor prognosis, metastasis, and therapeutic resistance. CIN results from errors in chromosome segregation during mitosis, leading to structural and numerical chromosomal abnormalities. In addition to generating genomic heterogeneity that acts as a substrate for natural selection, CIN promotes inflammatory signaling by introducing double-stranded DNA into the cytosol, engaging the cGAS-STING anti-viral pathway. These multipronged effects distinguish CIN as a central driver of tumor evolution and as a genomic source for the crosstalk between the tumor and its microenvironment, in the course of immune editing and evasion.
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