| Abstract: |
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. Chromosomal instability is well recognized as a hallmark of many cancers and a driver of tumor evolution. In this Perspective, Bakhoum and Cantley discuss how this instability directly impacts the tumor micro-environment via cGAS and STING-dependent signaling. © 2018 Elsevier Inc. |
