Medulloblastoma comprises four distinct molecular variants.
By P. Northcott, A. Korshunov, H. Witt, T. Hielscher, C. Eberhart, S. Mack, E. Bouffet, S. Clifford, C. Hawkins, P. French and 3 more. Journal of Clinical Oncology, 2011
1,170 citations recorded by the source corpus.
Subfields: Epidemiology, Genetics, Neurology
View Paper: https://www.semanticscholar.org/paper/8d9a1c1243f6814fc8fc160c323e4eb040eb9e02
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Citations in the corpus
- Genome Sequencing of Pediatric Medulloblastoma Links Catastrophic DNA Rearrangements with TP53 Mutations (2012, neutral): “SHHMBs form the clinically and histopathologically most heterogeneousmedulloblastomasubtype,making it challenging topredict response to therapy and patient outcome solely based on subtype affiliation (Northcott et al., 2011a; Remke et al., 2011).”
- Molecular subgroups of medulloblastoma: the current consensus (2011, methodology): “Others approaches to identify Shh medulloblastomas have included immunohistochemical staining for SFRP1 [2, 28, 48], or GAB1 [11].”
- The whole-genome landscape of medulloblastoma subtypes (2017, neutral): “Notable similarities between Group 3 and Group 4 have been discussed, including ambiguous cases that exhibit features characteristic of either subgroup 33–35 .”
- TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal (2013, background): “OTX2 expression was >100-fold higher in medulloblastoma patients without TERT promoter mutations than in those patients with TERT promoter mutations (note the log scale in Fig.”
- Genome Sequencing of SHH Medulloblastoma Predicts Genotype-Related Response to Smoothened Inhibition (2014, methodology): “All patients in this discovery cohort (n = 67) were confirmed to have a MB of the SHH subtype by either gene expression profiling, DNA methylation, or immunohistochemistry (SFRP1 Northcott et al., 2011b and GAB1 Ellison et al., 2011).”
- Molecular subgroups of medulloblastoma: an international meta-analysis of transcriptome, genetic aberrations, and clinical data of WNT, SHH, Group 3, and Group 4 medulloblastomas (2012, methodology): “They are transcriptionally, genetically, demographically, clinically, and prognostically distinct, confirming earlier reports in smaller series [1, 3, 9, 15, 19, 25].”