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https://github.com/jhrcook/comutation-manuscript
Manuscript for the KRAS comutation research project.
https://github.com/jhrcook/comutation-manuscript
cancer cancer-genetics comutation haigis haigis-lab kras krasalleles latex manuscript overleaf
Last synced: 25 days ago
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Manuscript for the KRAS comutation research project.
- Host: GitHub
- URL: https://github.com/jhrcook/comutation-manuscript
- Owner: jhrcook
- Created: 2019-12-18T21:29:19.000Z (almost 5 years ago)
- Default Branch: master
- Last Pushed: 2020-06-22T13:46:15.000Z (over 4 years ago)
- Last Synced: 2024-01-27T08:03:38.016Z (9 months ago)
- Topics: cancer, cancer-genetics, comutation, haigis, haigis-lab, kras, krasalleles, latex, manuscript, overleaf
- Language: TeX
- Homepage: https://github.com/jhrcook/comutation
- Size: 37.7 MB
- Stars: 0
- Watchers: 1
- Forks: 0
- Open Issues: 0
-
Metadata Files:
- Readme: README.md
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README
# KRAS comutation manuscript
Joshua Cook, Giorgio Melloni, Peter J. Park ([lab](https://compbio.hms.harvard.edu/index)), Kevin M. Haigis ([lab](https://www.haigislab.org))
## Abstract
Mutational activation of the *KRAS* oncogene promotes initiation and/or progression of cancer in a variety of tissues.
Though the mutant variants seemingly exert similar biological outputs, the biochemical properties and downstream signaling of each is distinct and highly context-dependent.
As such, the genetic interactions associated with *KRAS* mutants are likely to vary according to the specific allele and the tissue-of-origin of the cancer.
To explore this concept, 13,492 samples were collated from four tumor types with the highest frequency of mutation in *KRAS*: colorectal adenocarcinoma, lung adenocarcinoma, multiple myeloma, and pancreatic adenocarcinoma.
Each cancer had a distinct spectrum of *KRAS* activating mutations that could not be predicted by the prevalence of known mutagenic mechanisms.
Moreover, each allele was associated with a distinct comutation network that was also tissue-specific.
Analyzing genetic dependencies highlighted cellular functions and individual genes that were or were not required for tumors with specific *KRAS* alleles.
Overall, this analysis demonstrates that the *KRAS* alleles have distinct genetic interactions likely linked to their biological differences that can be further investigated as therapeutic targets.
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