ArticleScientific reports2016
Variation in KRAS driver substitution distributions between tumor types is determined by both mutation and natural selection.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer.EMBO reports · 2026Article
- Genomic alterations in ovarian endometriosis and subsequently diagnosed ovarian carcinoma.Human reproduction (Oxford, England) · 2024Article
- Signalling dynamics, cell decisions, and homeostatic control in health and disease.Current opinion in cell biology · 2022Review
- Papillary renal neoplasm with reverse polarity with a favorable prognosis: Two cases report and literature review.Frontiers in oncology · 2022Article
- Recurrent KRAS mutations identified in papillary renal neoplasm with reverse polarity-a comparative study with papillary renal cell carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Multiplexed in vivo homology-directed repair and tumor barcoding enables parallel quantification of Kras variant oncogenicity.Nature communications · 2017Article
- KRAS Alleles: The Devil Is in the Detail.Trends in cancer · 2017Review
- Inflammation as a driver and vulnerability of KRAS mediated oncogenesis.Seminars in cell & developmental biology · 2016Review
- Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different tumor types vary greatly in their distribution of driver substitutions. Here, we analyzed how mutation and natural selection contribute to differences in the distribution of KRAS driver substitutions between lung, colon and pancreatic adenocarcinomas. We were able to demonstrate that both differences in mutation and differences in selection drive variation in the distribution of KRAS driver substitutions between tumor types. By accounting for the effects of mutation on the distribution of KRAS driver substitutions, we could identify specific KRAS driver substitutions that are more favored by selection in specific tumor types. Such driver substitutions likely improve fitness most when they occur within the context of the tumor type in which they are preferentially favored. Fitting with this, we found that driver substitutions that are more favored by natural selection in a specific type of tumor tend to associate with worse clinical outcomes specifically in that type of tumor.
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