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- W4214577736 abstract "A person develops cancer when changes in a cell's DNA (called mutations) allow the cell to grow rapidly and spread around the body. The mutated genes are often involved in controlling the growth of cells, such as two genes called EGFR and KRAS, which are associated with forms of lung cancer. In a type of lung cancer called adenocarcinoma, the KRAS gene is mutated in about one-third of tumors and the EGFR gene is mutated in about 15%. However, the two mutations rarely or never occur in the same tumor. This could be because the effects of the mutations overlap, so that cells with both mutations have no advantages over cells with just one. Alternatively, it is possible that having both mutations may be harmful to tumor cells. Here, Unni, Lockwood et al. analyzed genetic data from over 600 lung tumors and confirmed that none of them have cancer-causing mutations in both KRAS and EGFR. Then, Unni, Lockwood et al. carried out experiments using genetically engineered mice with mutated forms of both KRAS and EGFR that are activated by a drug called doxycycline. As expected, the mice developed lung tumors when exposed to the drug, but these tumors didn't grow any faster than mouse tumors that had mutations in only one of the genes. In the mice with both mutant genes, only one of the two genes was actually active in most of the tumor cells. Unni, Lockwood et al. manipulated human lung tumor cells in the laboratory so that the cells had mutated versions of both genes. These cells developed serious abnormalities and died, which may be due to the over-activation of a communication pathway within the cells called MAPK signaling. The next challenges are to understand why the combination of these two mutant genes kills these cancer cells and to look for other combinations of mutations that can be toxic to cancer cells. In the future, it might be possible to develop drugs that can mimic the effects of these gene mutations to treat cancers." @default.
- W4214577736 created "2022-03-02" @default.
- W4214577736 date "2015-04-11" @default.
- W4214577736 modified "2023-09-26" @default.
- W4214577736 title "Decision letter: Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma" @default.
- W4214577736 doi "https://doi.org/10.7554/elife.06907.014" @default.
- W4214577736 hasPublicationYear "2015" @default.
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