Cumulative haploinsufficiency and triplosensitivity drive aneuploidy patterns and shape the cancer genome
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Aneuploidy has been recognized as a hallmark of cancer for more than 100 years, yet no general theory to explain the recurring patterns of aneuploidy in cancer has emerged. Here, we develop Tumor Suppressor and Oncogene (TUSON) Explorer, a computational method that analyzes the patterns of mutational signatures in tumors and predicts the likelihood that any individual gene functions as a tumor suppressor (TSG) or oncogene (OG). By analyzing >8,200 tumor-normal pairs, we provide statistical evidence suggesting that many more genes possess cancer driver properties than anticipated, forming a continuum of oncogenic potential. Integrating our driver predictions with information on somatic copy number alterations, we find that the distribution and potency of TSGs (STOP genes), OGs, and essential genes (GO genes) on chromosomes can predict the complex patterns of aneuploidy and copy number variation characteristic of cancer genomes. We propose that the cancer genome is shaped through a process of cumulative haploinsufficiency and triplosensitivity.
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Abraxas fits the criteria for a tumor suppressor gene according to TUSON Explorer.
“Abraxas also fits the criteria as a tumor suppressor gene using the Tumor Suppressor and Oncogene (TUSON) Explorer, a recently proposed computational method for predicting oncogene/tumor suppressor genes (Davoli et al., 2013).”
From The BRCA1-Interacting Protein Abraxas Is Required for Genomic Stability and Tumor Suppression (2014) · cites this paper as Davoli et al., 2013
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Genome Sequencing during a Patient’s Journey through Cancer
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A genetic interaction analysis identifies cancer drivers that modify EGFR dependency
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The BRCA1-Interacting Protein Abraxas Is Required for Genomic Stability and Tumor Suppression
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- Authors
- Davoli, T., Xu, A. W., Mengwasser, K. E., Sack, L. M., Yoon, J. C., Park, P. J., & Elledge, S. J.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Elledge, Stephen J.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 155
- Issue
- 4
- Pages
- 948-962
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3891052
- OpenAlex
- W1987908519
- Cited by
- 815
- References
- 64
- Citations by year
- 2026: 36 · 2025: 57 · 2024: 63 · 2023: 69 · 2022: 68 · 2021: 68 · 2020: 76 · 2019: 68 · 2018: 76 · 2017: 62 · 2016: 60 · 2015: 69 · 2014: 40 · 2013: 2
- FWCI
- 20.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- Howard Hughes Medical Institute
- Wellcome Trust
- National Institutes of Health
- National Institute of General Medical Sciences (T32GM007753, R01GM044664)
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK081612)
- U.S. National Library of Medicine (U54LM008748)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- aneuploidy, haploinsufficiency, cancer genome, tumor suppressor, oncogenes, mutational signatures, cancer driver genes, essential genes, somatic copy number alterations, copy number variation
- MeSH terms
- Algorithms, Aneuploidy, Humans, Neoplasms, Oncogenes, Genes, Tumor Suppressor, Gene Dosage
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