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• W2803325987 abstract "Abstract The majority of glioblastomas can be classified into molecular subgroups based on mutations in the TERT promoter ( TERTp ) and isocitrate dehydrogenase 1 or 2 ( IDH ). These molecular subgroups utilize distinct genetic mechanisms of telomere maintenance, either TERTp mutation leading to telomerase activation or ATRX- mutation leading to an alternative lengthening of telomeres phenotype (ALT). However, about 20% of glioblastomas lack alterations in TERTp and IDH . These tumors, designated TERTp WT - IDH WT glioblastomas, do not have well-established genetic biomarkers or defined mechanisms of telomere maintenance. Here we report the genetic landscape of TERTp WT - IDH WT glioblastoma and identify SMARCAL1 inactivating mutations as a novel genetic mechanism of ALT. Furthermore, we identify a novel mechanism of telomerase activation in glioblastomas that occurs via chromosomal rearrangements upstream of TERT . Collectively, our findings define novel molecular subgroups of glioblastoma, including a telomerase-positive subgroup driven by TERT -structural rearrangements ( IDH WT - TERT SV ), and an ALT-positive subgroup ( IDH WT -ALT) with mutations in ATRX or SMARCAL1 ." @default.
• W2803325987 created "2018-06-01" @default.
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• W2803325987 date "2018-05-25" @default.
• W2803325987 modified "2023-10-11" @default.
• W2803325987 title "The genomic landscape of TERT promoter wildtype-IDH wildtype glioblastoma" @default.
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• W2803325987 doi "https://doi.org/10.1038/s41467-018-04448-6" @default.
• W2803325987 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5970234" @default.
• W2803325987 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29802247" @default.
• W2803325987 hasPublicationYear "2018" @default.
• W2803325987 type Work @default.

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