Journal
CELL
Volume 177, Issue 6, Pages 1375-1383Publisher
CELL PRESS
DOI: 10.1016/j.cell.2019.05.005
Keywords
-
Categories
Funding
- US National Institutes of Health [U54CA209891, R01HG009979]
- Netherlands Organization for Scientific Research Gravitation Program
- Dutch Cancer Society [NKI 2016-1/10014]
Ask authors/readers for more resources
Recent studies of the tumor genome seek to identify cancer pathways as groups of genes in which mutations are epistatic with one another or, specifically, mutually exclusive. Here, we show that most mutations are mutually exclusive not due to pathway structure but to interactions with disease subtype and tumor mutation load. In particular, many cancer driver genes are mutated preferentially in tumors with few mutations overall, causing mutations in these cancer genes to appear mutually exclusive with numerous others. Researchers should view current epistasis maps with caution until we better understand the multiple cause-and-effect relationships among factors such as tumor subtype, positive selection for mutations, and gross tumor characteristics including mutational signatures and load.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available