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000137576 1001_ $$0P:(DE-He78)d20d08adc992abdb6ccffa1686f1ba17$$aStichel, Damian$$b0$$eFirst author
000137576 245__ $$aDistribution of EGFR amplification, combined chromosome 7 gain and chromosome 10 loss, and TERT promoter mutation in brain tumors and their potential for the reclassification of IDHwt astrocytoma to glioblastoma.
000137576 260__ $$aBerlin$$bSpringer$$c2018
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000137576 520__ $$aEGFR amplification (EGFRamp), the combination of gain of chromosome 7 and loss of chromosome 10 (7+/10-), and TERT promoter mutation (pTERTmut) are alterations frequently observed in adult IDH-wild-type (IDHwt) glioblastoma (GBM). In the absence of endothelial proliferation and/or necrosis, these alterations currently are considered to serve as a surrogate for upgrading IDHwt diffuse or anaplastic astrocytoma to GBM. Here, we set out to determine the distribution of EGFRamp, 7+/10-, and pTERTmut by analyzing high-resolution copy-number profiles and next-generation sequencing data of primary brain tumors. In addition, we addressed the question whether combinations of partial gains on chromosome 7 and partial losses on chromosome 10 exhibited a diagnostic and prognostic value similar to that of complete 7+/10-. Several such combinations proved relevant and were combined as the 7/10 signature. Our results demonstrate that EGFRamp and the 7/10 signature are closely associated with IDHwt GBM. In contrast, pTERTmut is less specific for IDHwt GBM. We conclude that, in the absence of endothelial proliferation and/or necrosis, the detection of EGFRamp is a very strong surrogate marker for the diagnosis of GBM in IDHwt diffuse astrocytic tumors. The 7/10 signature is also a strong surrogate marker. However, care should be taken to exclude pleomorphic xanthoastrocytoma. pTERTmut is less restricted to this entity and needs companion analysis by other molecular markers to serve as a surrogate for diagnosing IDHwt GBM. A combination of any two of EGFRamp, the 7/10 signature and pTERTmut, is highly specific for IDHwt GBM and the combination of all three alterations is frequent and exclusively seen in IDHwt GBM.
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000137576 7001_ $$0P:(DE-HGF)0$$aEbrahimi, Azadeh$$b1$$eFirst author
000137576 7001_ $$0P:(DE-HGF)0$$aReuss, David$$b2
000137576 7001_ $$0P:(DE-He78)e54a1e0999c1d8c95869ef9188b794cc$$aSchrimpf, Daniel$$b3
000137576 7001_ $$aOno, Takahiro$$b4
000137576 7001_ $$aShirahata, Mitsuaki$$b5
000137576 7001_ $$0P:(DE-HGF)0$$aReifenberger, Guido$$b6
000137576 7001_ $$aWeller, Michael$$b7
000137576 7001_ $$aHänggi, Daniel$$b8
000137576 7001_ $$0P:(DE-He78)92e9783ca7025f36ce14e12cd348d2ee$$aWick, Wolfgang$$b9
000137576 7001_ $$aHerold-Mende, Christel$$b10
000137576 7001_ $$aWestphal, Manfred$$b11
000137576 7001_ $$aBrandner, Sebastian$$b12
000137576 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b13
000137576 7001_ $$0P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aCapper, David$$b14
000137576 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b15
000137576 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, Andreas$$b16$$eLast author
000137576 773__ $$0PERI:(DE-600)1458410-4$$a10.1007/s00401-018-1905-0$$n5$$p793-803$$tActa neuropathologica$$v136$$x1432-0533$$y2018
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