Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma.

By D. Sturm, H. Witt, V. Hovestadt, Dong-Anh Khuong-Quang, David T. W. Jones, Carolin Konermann, E. Pfaff, M. Tönjes, M. Sill, S. Bender and 68 more. Cancer Cell, 2012

1,735 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics

View Paper: https://www.semanticscholar.org/paper/d545dc096e786e2828043275f35d8640ddcd99b8

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Citations in the corpus

DNA methylation-based classification of central nervous system tumours (2018, positive): “Subsets of the reference cohort have been previously published 4,9–16 , 26– 33 .”
Similarity network fusion for aggregating data types on a genomic scale (2014, background): “05×10−4) to be associated with Subtype 3 [14, 8].”
Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion (2015, neutral): “…thalamic HGGs typically occurring inmid-childhood, cortical gliomas of childhood occurring in older children and young adults, and HGG of later adulthood occurring chiefly in the frontotemporal lobes (Khuong-Quang et al., 2012; Schwartzentruber et al., 2012; Sturm et al., 2012; Wu et al., 2012).”
Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma (2017, background): “520), as reported previously (Sturm et al., 2012); however it was also found to be significantly elevated in PXA-like tumors (median beta value 0.”
Glioma Subclassifications and Their Clinical Significance (2017, background): “3 appear mostly in pericallosal GBMs in adolescent and young adults aged 9–42 years [35].”
Machine Learning Identifies Stemness Features Associated with Oncogenic Dedifferentiation (2018, methodology): “Additionally, we downloaded independent, non-TCGA datasets of gliomas [(Sturm et al., 2012) (GSE36245, GSE36278) and (Turcan et al.”
Recurrent somatic alterations of FGFR1 and NTRK2 in pilocytic astrocytoma (2013, neutral): “Three experienced neuropathologists agreed on pilocytic astrocytoma histology for this case, although a diagnosis of GBM cannot be conclusively excluded, owing to limited material.”
The Somatic Genomic Landscape of Glioblastoma (2013, background): “reported that adult and pediatric GBM with alterations of IDH1, H3F3A, and receptor tyrosine kinases (RTK)were associatedwith epigenetic subtypes (Sturm et al., 2012).”
High-grade glioma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. (2014, background): “Prognosis of mixed anaplastic oligoastrocytoma and anaplastic astrocytoma is intermediate between GBM and pure anaplastic oligodendroglioma.”
Mesenchymal glioma stem cells are maintained by activated glycolytic metabolism involving aldehyde dehydrogenase 1A3 (2013, background): “(24) reported that a small subset of PN GBM (after removing IDH1 mutant samples) has a worse prognosis.”