000128928 001__ 128928 000128928 005__ 20240228143357.0 000128928 0247_ $$2doi$$a10.1111/his.12812 000128928 0247_ $$2pmid$$apmid:26291601 000128928 0247_ $$2ISSN$$a0309-0167 000128928 0247_ $$2ISSN$$a1365-2559 000128928 0247_ $$2altmetric$$aaltmetric:4417480 000128928 037__ $$aDKFZ-2017-04940 000128928 041__ $$aeng 000128928 082__ $$a610 000128928 1001_ $$aKoelsche, Christian$$b0 000128928 245__ $$aDifferential nuclear ATRX expression in sarcomas. 000128928 260__ $$aOxford [u.a.]$$bWiley-Blackwell$$c2016 000128928 3367_ $$2DRIVER$$aarticle 000128928 3367_ $$2DataCite$$aOutput Types/Journal article 000128928 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1524482990_2971 000128928 3367_ $$2BibTeX$$aARTICLE 000128928 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000128928 3367_ $$00$$2EndNote$$aJournal Article 000128928 520__ $$aNuclear α-thalassemia/mental retardation X-linked (ATRX) loss and alternative lengthening of telomeres (ALT) are linked in distinct malignancies. We therefore aimed to determine the nuclear ATRX expression correlated with ALT in a comprehensive series of sarcomas.A total of 573 formalin-fixed paraffin-embedded sarcomas comprising 28 entities were investigated for nuclear ATRX expression by immunohistochemistry. Telomere-specific fluorescence in-situ hybridization (FISH) was used to determine the ALT phenotype in 50 sarcomas with complete or heterogeneous ATRX loss. Complete nuclear ATRX loss was detected in 58 of 573 sarcomas, all high-grade, with the highest prevalence in undifferentiated pleomorphic sarcomas (38%) and pleomorphic liposarcomas (38%), followed by dedifferentiated liposarcomas (24%), osteosarcomas (21%), leiomyosarcomas (17%), myxofibrosarcomas (11%) and malignant peripheral nerve sheath tumours (4%). Interestingly, a further 20 sarcomas, all belonging to the aforementioned entities with complete ATRX loss, presented with a heterogeneous ATRX expression pattern. ALT was observed in 41 of 42 sarcomas with complete ATRX loss, but only in two of eight sarcomas with heterogeneous expression.Nuclear ATRX loss, either complete or heterogeneous, is encountered in a considerable number of high-grade sarcomas with non-specific genetic alterations. A causal relationship with ALT might be indicated at least in cases with a complete nuclear ATRX loss. 000128928 536__ $$0G:(DE-HGF)POF3-317$$a317 - Translational cancer research (POF3-317)$$cPOF3-317$$fPOF III$$x0 000128928 588__ $$aDataset connected to CrossRef, PubMed, 000128928 7001_ $$aRenner, Marcus$$b1 000128928 7001_ $$0P:(DE-He78)3fdc3623477264cb5d0e14f256dbfbb8$$aJohann, Pascal$$b2$$udkfz 000128928 7001_ $$0P:(DE-HGF)0$$aLeiss, Irina$$b3 000128928 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b4$$udkfz 000128928 7001_ $$aSchimmack, Simon$$b5 000128928 7001_ $$aWardelmann, Eva$$b6 000128928 7001_ $$aRenker, Eva-Kristin$$b7 000128928 7001_ $$aSchirmacher, Peter$$b8 000128928 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b9$$udkfz 000128928 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, Andreas$$b10$$udkfz 000128928 7001_ $$aMechtersheimer, Gunhild$$b11 000128928 773__ $$0PERI:(DE-600)2006447-0$$a10.1111/his.12812$$gVol. 68, no. 5, p. 738 - 745$$n5$$p738 - 745$$tHistopathology$$v68$$x0309-0167$$y2016 000128928 909CO $$ooai:inrepo02.dkfz.de:128928$$pVDB 000128928 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)3fdc3623477264cb5d0e14f256dbfbb8$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ 000128928 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-HGF)0$$aDeutsches Krebsforschungszentrum$$b3$$kDKFZ 000128928 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aDeutsches Krebsforschungszentrum$$b4$$kDKFZ 000128928 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aDeutsches Krebsforschungszentrum$$b9$$kDKFZ 000128928 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$aDeutsches Krebsforschungszentrum$$b10$$kDKFZ 000128928 9131_ $$0G:(DE-HGF)POF3-317$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vTranslational cancer research$$x0 000128928 9141_ $$y2016 000128928 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz 000128928 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS 000128928 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline 000128928 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database 000128928 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bHISTOPATHOLOGY : 2015 000128928 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search 000128928 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC 000128928 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List 000128928 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index 000128928 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection 000128928 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded 000128928 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine 000128928 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences 000128928 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews 000128928 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5 000128928 9201_ $$0I:(DE-He78)G380-20160331$$kG380$$lKKE Neuropathologie$$x0 000128928 9201_ $$0I:(DE-He78)B062-20160331$$kB062$$lPädiatrische Neuroonkologie$$x1 000128928 9201_ $$0I:(DE-He78)L101-20160331$$kL101$$lDKTK Heidelberg$$x2 000128928 980__ $$ajournal 000128928 980__ $$aVDB 000128928 980__ $$aI:(DE-He78)G380-20160331 000128928 980__ $$aI:(DE-He78)B062-20160331 000128928 980__ $$aI:(DE-He78)L101-20160331 000128928 980__ $$aUNRESTRICTED