Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma.

By Houtan Noushmehr, D. Weisenberger, K. Diefes, H. Phillips, Kanan D. Pujara, Benjamin Paul Berman, F. Pan, C. Pelloski, E. Sulman, K. Bhat and 17 more. Cancer Cell, 2010

2,267 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/609789b3c63b983bcde105f2b69a8e38b4fbc403

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In Cancer Research

1. C. V. Dang
2. Craig B. Thompson
3. Manel Esteller
4. Gad Getz
5. Patrick S. Ward
6. H. Ohgaki
7. Eric S. Lander
8. P. Kleihues

In Genetics

1. Manel Esteller
2. P. Park
3. S. Baylin
4. H. Ohgaki
5. P. Kleihues
6. Peter W. Laird
7. Manolis Kellis
8. Jason Ernst

In Molecular Biology

1. Manolis Kellis
2. Manel Esteller
3. Peter A. Jones
4. S. Baylin
5. David Haussler
6. Eric S. Lander
7. Peter W. Laird
8. Cole Trapnell

Citations in the corpus

• Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “Importantly, these studies have reinforced some early hypotheses about the stem-cell origins in the natural history of cancers (Cairns, 1975) and the clonal evolution of cancers through Darwinian selection (Nowell, 1976).”
• IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype (2012, background): “The fundamental questions regarding these features are (1) how the IDH mutation contributes to oncogenesis, and (2) what the root cause of CIMP is.”
• A User's Guide to the Encyclopedia of DNA Elements (ENCODE) (2011, methodology): “…which enables quantitative analysis of methylcytosines: interrogation of the methylation status of 27,000 CpGs with the Illumina Methyl27 assay [69–72] and Reduced Representation Bisulfite Sequencing (RRBS) [73], which couples Msp I restriction enzyme digestion, size selection, bisulfite…”
• TCGAbiolinks: an R/Bioconductor package for integrative analysis of TCGA data (2015, methodology): “These types of analyses have been performed by our group in our recent TCGA papers (3,6,16,35) but were never implemented in a reproducible and standard package until now.”
• Epigenetic Determinants of Cancer. (2016, background): “These tumors arise in glial cell progenitors (Parsons et al. 2008; Noushmehr et al. 2010).”
• A decade of exploring the cancer epigenome — biological and translational implications (2011, background): “For example, mutations in the TET2 , isocitrate dehydrogenase 1 ( IDH1 ) and IDH2 genes occur in gliomas and leukaemi”
• Tumor evolution of glioma intrinsic gene expression subtype associates with immunological changes in the microenvironment (2017, background): “…a more favorable outcome and MES relating to poor survival (Huse et al., 2011; Phillips et al., 2006; Zheng et al., 2012), but these findings were affected by the relatively favorable outcome of IDH mutant GBMs which are consistently classified as PN (Noushmehr et al., 2010; Verhaak et al., 2010).”
• Absolute quantification of somatic DNA alterations in human cancer (2012, background): “The level of DNA methylation at each probe was summarized with beta values ranging from 0 (unmethylated) to 1 (methylated) 58 .”
• The Cancer Genome Atlas (TCGA): an immeasurable source of knowledge (2015, background): “Therefore, improved molecular understanding of GBM could ultimately result in beneficial personalised therapies [45].”