Journal
CELL SYSTEMS
Volume 6, Issue 3, Pages 282-+Publisher
CELL PRESS
DOI: 10.1016/j.cels.2018.03.003
Keywords
-
Categories
Funding
- NIH [4U01CA176303-04, U24CA143867, RO1CA57138, 5R01CA149707]
- SEngine Precision Medicine
- Cure First
- Shriners Hospitals for Children
- Leukemia and Lymphoma Society
- [U54 HG003273]
- [U54 HG003067]
- [U54 HG003079]
- [U24 CA143799]
- [U24 CA143835]
- [U24 CA143840]
- [U24 CA143843]
- [U24 CA143845]
- [U24 CA143848]
- [U24 CA143858]
- [U24 CA143866]
- [U24 CA143882]
- [U24 CA143867]
- [U24 CA143883]
- [U24 CA144025]
- [P30 CA016672]
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Although the MYC oncogene has been implicated in cancer, a systematic assessment of alterations of MYC, related transcription factors, and co-regulatory proteins, forming the proximal MYC network (PMN), across human cancers is lacking. Using computational approaches, we define genomic and proteomic features associated with MYC and the PMN across the 33 cancers of The Cancer Genome Atlas. Pan-cancer, 28% of all samples had at least one of the MYC paralogs amplified. In contrast, the MYC antagonists MGA and MNT were the most frequently mutated or deleted members, proposing a role as tumor suppressors. MYC alterations were mutually exclusive with PIK3CA, PTEN, APC, or BRAF alterations, suggesting that MYC is a distinct oncogenic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such as immune response and growth factor signaling; chromatin, translation, and DNA replication/repair were conserved pan-cancer. This analysis reveals insights into MYC biology and is a reference for biomarkers and therapeutics for cancers with alterations of MYC or the PMN.
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