000124447 001__ 124447
000124447 005__ 20240228145515.0
000124447 0247_ $$2doi$$a10.1111/bpa.12413
000124447 0247_ $$2pmid$$apmid:27380723
000124447 0247_ $$2ISSN$$a1015-6305
000124447 0247_ $$2ISSN$$a1750-3639
000124447 0247_ $$2altmetric$$aaltmetric:9270671
000124447 037__ $$aDKFZ-2017-01324
000124447 041__ $$aeng
000124447 082__ $$a610
000124447 1001_ $$0P:(DE-He78)3fdc3623477264cb5d0e14f256dbfbb8$$aJohann, Pascal$$b0$$eFirst author$$udkfz
000124447 245__ $$aCribriform neuroepithelial tumor: molecular characterization of a SMARCB1-deficient non-rhabdoid tumor with favorable long-term outcome.
000124447 260__ $$aOxford$$bWiley-Blackwell$$c2017
000124447 3367_ $$2DRIVER$$aarticle
000124447 3367_ $$2DataCite$$aOutput Types/Journal article
000124447 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1660747460_30405
000124447 3367_ $$2BibTeX$$aARTICLE
000124447 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000124447 3367_ $$00$$2EndNote$$aJournal Article
000124447 520__ $$aRhabdoid phenotype and loss of SMARCB1 expression in a brain tumor are characteristic features of atypical teratoid/rhabdoid tumors (ATRT). Rare non-rhabdoid brain tumors showing cribriform growth pattern and SMARCB1 loss have been designated cribriform neuroepithelial tumor (CRINET). Small case series suggest that CRINETs may have a relatively favorable prognosis. However, the long-term outcome is unclear and it remains uncertain whether CRINET represents a distinct entity or a variant of ATRT. Therefore, 10 CRINETs were clinically and molecularly characterized and compared with 10 ATRTs of each of three recently described molecular subgroups (i.e. ATRT-TYR, ATRT-SHH and ATRT-MYC) using Illumina Infinium HumanMethylation450 arrays, FISH, MLPA, and sequencing. Furthermore, outcome was compared to a larger cohort of 27 children with ATRT-TYR. Median age of the 6 boys and 4 girls harboring a CRINET was 20 months. On histopathological examination, all CRINETs demonstrated a cribriform growth pattern and distinct tyrosinase staining. On unsupervised cluster analysis of methylation data, all CRINETs examined exclusively clustered within the ATRT-TYR molecular subgroup. As ATRT-TYR, CRINETs mainly showed large heterozygous 22q deletions (9/10) and SMARCB1 mutations of the other allele. In two patients, SMARCB1 mutations were also present in the germline. Estimated mean overall survival in patients with CRINETs was 125 months (95% confidence interval 100-151 months) as compared to only 53 (33-74) months in patients with ATRTs of the ATRT-TYR subgroup (Log-Rank P < 0.05). In conclusion, CRINET represents a SMARCB1-deficient non-rhabdoid tumor, which shares molecular similarities with the ATRT-TYR subgroup but has distinct histopathological features and favorable long-term outcome.
000124447 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
000124447 588__ $$aDataset connected to CrossRef, PubMed,
000124447 7001_ $$0P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc$$aHovestadt, Volker$$b1$$udkfz
000124447 7001_ $$aThomas, Christian$$b2
000124447 7001_ $$aJeibmann, Astrid$$b3
000124447 7001_ $$aHeß, Katharina$$b4
000124447 7001_ $$aBens, Susanne$$b5
000124447 7001_ $$aOyen, Florian$$b6
000124447 7001_ $$aHawkins, Cynthia$$b7
000124447 7001_ $$aPierson, Christopher R$$b8
000124447 7001_ $$aAldape, Kenneth$$b9
000124447 7001_ $$aKim, Sang-Pyo$$b10
000124447 7001_ $$aWiding, Eva$$b11
000124447 7001_ $$aSumerauer, David$$b12
000124447 7001_ $$aHauser, Péter$$b13
000124447 7001_ $$avan Landeghem, Frank$$b14
000124447 7001_ $$aRyzhova, Marina$$b15
000124447 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b16$$udkfz
000124447 7001_ $$0P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aCapper, David$$b17$$udkfz
000124447 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David$$b18$$udkfz
000124447 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b19$$udkfz
000124447 7001_ $$aSchneppenheim, Reinhard$$b20
000124447 7001_ $$aSiebert, Reiner$$b21
000124447 7001_ $$aPaulus, Werner$$b22
000124447 7001_ $$aFrühwald, Michael C$$b23
000124447 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b24$$udkfz
000124447 7001_ $$aHasselblatt, Martin$$b25
000124447 773__ $$0PERI:(DE-600)2029927-8$$a10.1111/bpa.12413$$gVol. 27, no. 4, p. 411 - 418$$n4$$p411 - 418$$tBrain pathology$$v27$$x1015-6305$$y2017
000124447 909CO $$ooai:inrepo02.dkfz.de:124447$$pVDB
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)3fdc3623477264cb5d0e14f256dbfbb8$$aDeutsches Krebsforschungszentrum$$b0$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aDeutsches Krebsforschungszentrum$$b16$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aDeutsches Krebsforschungszentrum$$b17$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)551bb92841f634070997aa168d818492$$aDeutsches Krebsforschungszentrum$$b18$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aDeutsches Krebsforschungszentrum$$b19$$kDKFZ
000124447 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aDeutsches Krebsforschungszentrum$$b24$$kDKFZ
000124447 9131_ $$0G:(DE-HGF)POF3-312$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunctional and structural genomics$$x0
000124447 9141_ $$y2017
000124447 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000124447 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000124447 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bBRAIN PATHOL : 2015
000124447 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000124447 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000124447 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000124447 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000124447 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000124447 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000124447 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000124447 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bBRAIN PATHOL : 2015
000124447 9201_ $$0I:(DE-He78)B062-20160331$$kB062$$lB062 Pädiatrische Neuroonkologie$$x0
000124447 9201_ $$0I:(DE-He78)L101-20160331$$kL101$$lDKTK Heidelberg$$x1
000124447 9201_ $$0I:(DE-He78)B060-20160331$$kB060$$lB060 Molekulare Genetik$$x2
000124447 9201_ $$0I:(DE-He78)G380-20160331$$kG380$$lKKE Neuropathologie$$x3
000124447 980__ $$ajournal
000124447 980__ $$aVDB
000124447 980__ $$aI:(DE-He78)B062-20160331
000124447 980__ $$aI:(DE-He78)L101-20160331
000124447 980__ $$aI:(DE-He78)B060-20160331
000124447 980__ $$aI:(DE-He78)G380-20160331
000124447 980__ $$aUNRESTRICTED