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000128541 1001_ $$0P:(DE-He78)2d0c564eca775a62ff86225f7717af12$$aWiestler, Benedikt Paul Otmar$$b0$$eFirst author$$udkfz
000128541 245__ $$aIntegrated DNA methylation and copy-number profiling identify three clinically and biologically relevant groups of anaplastic glioma.
000128541 260__ $$aBerlin$$bSpringer$$c2014
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000128541 520__ $$aThe outcome of patients with anaplastic gliomas varies considerably. Whether a molecular classification of anaplastic gliomas based on large-scale genomic or epigenomic analyses is superior to histopathology for reflecting distinct biological groups, predicting outcomes and guiding therapy decisions has yet to be determined. Epigenome-wide DNA methylation analysis, using a platform which also allows the detection of copy-number aberrations, was performed in a cohort of 228 patients with anaplastic gliomas (astrocytomas, oligoastrocytomas, and oligodendrogliomas), including 115 patients of the NOA-04 trial. We further compared these tumors with a group of 55 glioblastomas. Unsupervised clustering of DNA methylation patterns revealed two main groups correlated with IDH status: CpG island methylator phenotype (CIMP) positive (77.5 %) or negative (22.5 %). CIMP(pos) (IDH mutant) tumors showed a further separation based on copy-number status of chromosome arms 1p and 19q. CIMP(neg) (IDH wild type) tumors showed hallmark copy-number alterations of glioblastomas, and clustered together with CIMP(neg) glioblastomas without forming separate groups based on WHO grade. Notably, there was no molecular evidence for a distinct biological entity representing anaplastic oligoastrocytoma. Tumor classification based on CIMP and 1p/19q status was significantly associated with survival, allowing a better prediction of outcome than the current histopathological classification: patients with CIMP(pos) tumors with 1p/19q codeletion (CIMP-codel) had the best prognosis, followed by patients with CIMP(pos) tumors but intact 1p/19q status (CIMP-non-codel). Patients with CIMP(neg) anaplastic gliomas (GBM-like) had the worst prognosis. Collectively, our data suggest that anaplastic gliomas can be grouped by IDH and 1p/19q status into three molecular groups that show clear links to underlying biology and a significant association with clinical outcome in a prospective trial cohort.
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000128541 650_7 $$2NLM Chemicals$$aNuclear Proteins
000128541 650_7 $$2NLM Chemicals$$aTumor Suppressor Proteins
000128541 650_7 $$0EC 2.1.1.-$$2NLM Chemicals$$aDNA Modification Methylases
000128541 650_7 $$0EC 2.1.1.63$$2NLM Chemicals$$aMGMT protein, human
000128541 650_7 $$0EC 2.7.7.49$$2NLM Chemicals$$aTelomerase
000128541 650_7 $$0EC 3.6.4.-$$2NLM Chemicals$$aDNA Helicases
000128541 650_7 $$0EC 3.6.4.12$$2NLM Chemicals$$aATRX protein, human
000128541 650_7 $$0EC 6.5.1.-$$2NLM Chemicals$$aDNA Repair Enzymes
000128541 7001_ $$0P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aCapper, David$$b1$$eFirst author$$udkfz
000128541 7001_ $$0P:(DE-He78)45440b44791309bd4b7dbb4f73333f9b$$aSill, Martin$$b2$$udkfz
000128541 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David$$b3$$udkfz
000128541 7001_ $$0P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc$$aHovestadt, Volker$$b4$$udkfz
000128541 7001_ $$0P:(DE-He78)a46a5b2a871859c8e2d63d2f8c666807$$aSturm, Dominik$$b5$$udkfz
000128541 7001_ $$0P:(DE-HGF)0$$aKoelsche, Christian$$b6
000128541 7001_ $$0P:(DE-HGF)0$$aBertoni, Anna$$b7
000128541 7001_ $$0P:(DE-HGF)0$$aSchweizer, Leonille$$b8
000128541 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b9$$udkfz
000128541 7001_ $$0P:(DE-HGF)0$$aWeiß, Elisa K$$b10
000128541 7001_ $$0P:(DE-He78)2970cb1f38e9cb41d755455acd14893e$$aSchliesser, Maximilian$$b11$$udkfz
000128541 7001_ $$0P:(DE-He78)77588f5b9413339755a66e739d316c7d$$aRadbruch, Alexander$$b12$$udkfz
000128541 7001_ $$0P:(DE-He78)c146c0b611b8fb654444ec078766f5ea$$aHerold-Mende, Christel$$b13$$udkfz
000128541 7001_ $$aRoth, Patrick$$b14
000128541 7001_ $$aUnterberg, Andreas$$b15
000128541 7001_ $$0P:(DE-HGF)0$$aHartmann, Christian$$b16
000128541 7001_ $$aPietsch, Torsten$$b17
000128541 7001_ $$0P:(DE-HGF)0$$aReifenberger, Guido$$b18
000128541 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b19$$udkfz
000128541 7001_ $$0P:(DE-He78)d1939d434dd885fad08106329e3db719$$aRadlwimmer, Bernhard$$b20$$udkfz
000128541 7001_ $$0P:(DE-He78)5ef8651b0f857b9c640aa5b1498c43b5$$aPlatten, Michael$$b21$$udkfz
000128541 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b22$$udkfz
000128541 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, Andreas$$b23$$udkfz
000128541 7001_ $$aWeller, Michael$$b24
000128541 7001_ $$0P:(DE-He78)92e9783ca7025f36ce14e12cd348d2ee$$aWick, Wolfgang$$b25$$eLast author$$udkfz
000128541 773__ $$0PERI:(DE-600)1458410-4$$a10.1007/s00401-014-1315-x$$gVol. 128, no. 4, p. 561 - 571$$n4$$p561 - 571$$tActa neuropathologica$$v128$$x1432-0533$$y2014
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