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- W2755660258 abstract "Significance Identifying the drivers of tumorigenesis provides insight into mechanisms of transformation and can suggest novel therapeutic targets. IDH1 mutations in gliomas are one such promising target. Drivers of tumor initiation may be distinct from those at tumor recurrence, however. Here, we demonstrate that in a subset of initially IDH1 mutant gliomas IDH1 is deleted or amplified at recurrence, yielding a higher grade tumor with a reprogrammed epigenome. We also report systematic selection for cells with IDH1 CNA in vitro and in vivo. Thus, while IDH1 mutation likely initiates gliomagenesis, neither mutant IDH1 nor the oncometabolite 2HG that it produces are required at recurrence. These findings have important implications for emerging therapeutic strategies targeting mutant IDH1." @default.
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- W2755660258 date "2017-09-15" @default.
- W2755660258 modified "2023-10-16" @default.
- W2755660258 title "Clonal expansion and epigenetic reprogramming following deletion or amplification of mutant <i>IDH1</i>" @default.
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- W2755660258 doi "https://doi.org/10.1073/pnas.1708914114" @default.
- W2755660258 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5635900" @default.
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