Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma

By J. Schwartzentruber, A. Korshunov, Xiao-yang Liu, David T. W. Jones, E. Pfaff, K. Jacob, D. Sturm, A. Fontebasso, Dong Anh Khuong Quang, M. Tönjes and 52 more. Nature, 2012

2,412 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2041cf896a34f537bbb1bb017a602944ea503840

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Citations in the corpus

Epidemiologic and Molecular Prognostic Review of Glioblastoma (2014, background): “Mutations in ATRX have been identified in multiple tumor types and appear to cause alternative lengthening of telomeres (ALT), a presumed precursor to genomic instability (130, 131).”
Epigenetic plasticity and the hallmarks of cancer (2017, background): “3 or its chaperone proteins that promote telomerase-independent telomere lengthening (57, 94), or by nongenetic mechanisms that simulate self-renewing stem cell states (9, 95).”
Cancer epigenetics: from mechanism to therapy. (2012, background): “These tumors with mutations in H3F3A/ATRX/DAXX were associated with increased alternative lengthening of telomeres and genomic instability (Schwartzentruber et al., 2012).”
Neuroblastoma and MYCN (2013, background): “In contrast, elevated expression of MYCN and mutation of ATRX are both associated with mutation of G34 site in Histone 3.3 in pediatric glioblastoma (Schwartzentruber et al. 2012; Wu et al. 2012; Bjerke et al. 2013).”
Histone Lysine Methylation Dynamics: Establishment, Regulation, and Biological Impact (2012, positive): “H3K27 have been observed in some gliomas, suggesting this lysine residue might be important in cancer (Khuong-Quang et al., 2012; Schwartzentruber et al., 2012; Wu et al., 2012).”
Neuronal Activity Promotes Oligodendrogenesis and Adaptive Myelination in the Mammalian Brain (2014, background): “in histone H3 that may prevent effective control of such proliferation (54, 55).”
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).”
Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. (2012, methodology): “The previously reported association of H3F3A mutations, particular the G34 mutation, with loss of ATRX and ALT (Schwartzentruber et al., 2012) is further expanded upon here.”
K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas (2012, methodology): “56)] and almost exclusively in hemispheric GBM [23].”