000131055 001__ 131055
000131055 005__ 20240228145601.0
000131055 0247_ $$2doi$$a10.1111/ejh.12972
000131055 0247_ $$2pmid$$apmid:28940816
000131055 0247_ $$2ISSN$$a0036-553X
000131055 0247_ $$2ISSN$$a0902-4441
000131055 0247_ $$2ISSN$$a1600-0609
000131055 037__ $$aDKFZ-2017-06122
000131055 041__ $$aeng
000131055 082__ $$a610
000131055 1001_ $$00000-0003-3796-8843$$aKayser, Sabine$$b0
000131055 245__ $$aClinical impact of KMT2C and SPRY4 expression levels in intensively treated younger adult acute myeloid leukemia patients.
000131055 260__ $$aOxford$$bWiley-Blackwell$$c2017
000131055 3367_ $$2DRIVER$$aarticle
000131055 3367_ $$2DataCite$$aOutput Types/Journal article
000131055 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1660805555_8349
000131055 3367_ $$2BibTeX$$aARTICLE
000131055 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000131055 3367_ $$00$$2EndNote$$aJournal Article
000131055 520__ $$aTo evaluate the prognostic impact of gene expression levels (ELs) of two tumor suppressor genes, sprouty 4 (SPRY4, located on 5q) and lysine methyltransferase 2C (KMT2C, located on 7q) in correlation with clinical characteristics and genetic abnormalities assessed at initial diagnosis in acute myeloid leukemia (AML).Gene expression levels were measured on cDNA by RT-qPCR from diagnostic bone marrow samples of 275 intensively treated adult AML patients (median age, 48 years).KMT2C ELs were significantly lower in abn7q/-7 (P = .001), whereas SPRY4 ELs were not associated with abn5q/-5. Higher KMT2C and SPRY4 ELs were significantly associated with lower genetic risk groups as defined by the European LeukemiaNet classification. Additionally, KMT2C ELs were lower in cytogenetically normal patients with DNMT3A (P = .01) or FLT3-ITD mutations (P = .05). KMT2C ELs were not associated with prognosis, whereas higher SPRY4 ELs showed a favorable impact on event-free (EFS, P = .01), relapse-free (RFS, P = .01) and in-trend on overall survival (P = .06) for cytogenetically abnormal patients, which was confirmed in multivariable analysis for EFS (HR, 0.84; 95%-CI, 0.73-0.97; P = .02) and RFS (HR, 0.85; 95%-CI, 0.73-0.98; P = .02).Our data indicate that KMT2C ELs are associated with specific genetic features and that SPRY4 ELs may add prognostic information.
000131055 536__ $$0G:(DE-HGF)POF3-317$$a317 - Translational cancer research (POF3-317)$$cPOF3-317$$fPOF III$$x0
000131055 588__ $$aDataset connected to CrossRef, PubMed,
000131055 7001_ $$0P:(DE-He78)da570a6c45c930fd5ea07868a555101d$$aFeszler, Maximilian$$b1$$udkfz
000131055 7001_ $$0P:(DE-He78)5a7a75d1b29b770f98f1bb2062fc3df9$$aKrzykalla, Julia$$b2
000131055 7001_ $$0P:(DE-He78)c954da35a243d177fdc4a3924f4f8a5c$$aSchick, Matthias$$b3$$udkfz
000131055 7001_ $$aKramer, Michael$$b4
000131055 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b5
000131055 7001_ $$aThol, Felicitas$$b6
000131055 7001_ $$aPlatzbecker, Uwe$$b7
000131055 7001_ $$aMüller-Tidow, Carsten$$b8
000131055 7001_ $$aHo, Anthony D$$b9
000131055 7001_ $$aEhninger, Gerhard$$b10
000131055 7001_ $$aHeuser, Michael$$b11
000131055 7001_ $$0P:(DE-HGF)0$$aSchlenk, Richard F$$b12
000131055 7001_ $$aThiede, Christian$$b13
000131055 7001_ $$aRöllig, Christoph$$b14
000131055 7001_ $$0P:(DE-He78)493c5fbf69f1b20df6f048712f3ad4a0$$aKrämer, Alwin$$b15$$eLast author$$udkfz
000131055 773__ $$0PERI:(DE-600)2027114-1$$a10.1111/ejh.12972$$gVol. 99, no. 6, p. 544 - 552$$n6$$p544 - 552$$tEuropean journal of haematology$$v99$$x0902-4441$$y2017
000131055 909CO $$ooai:inrepo02.dkfz.de:131055$$pVDB
000131055 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)da570a6c45c930fd5ea07868a555101d$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000131055 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)5a7a75d1b29b770f98f1bb2062fc3df9$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000131055 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)c954da35a243d177fdc4a3924f4f8a5c$$aDeutsches Krebsforschungszentrum$$b3$$kDKFZ
000131055 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aDeutsches Krebsforschungszentrum$$b5$$kDKFZ
000131055 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)493c5fbf69f1b20df6f048712f3ad4a0$$aDeutsches Krebsforschungszentrum$$b15$$kDKFZ
000131055 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
000131055 9141_ $$y2017
000131055 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bEUR J HAEMATOL : 2015
000131055 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000131055 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000131055 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000131055 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search
000131055 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC
000131055 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000131055 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000131055 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000131055 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000131055 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000131055 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000131055 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000131055 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000131055 9201_ $$0I:(DE-He78)G330-20160331$$kG330$$lKKE Molekulare Hämatologie/Onkologie$$x0
000131055 9201_ $$0I:(DE-He78)C060-20160331$$kC060$$lC060 Biostatistik$$x1
000131055 9201_ $$0I:(DE-He78)W110-20160331$$kW110$$lBewerunge-Hudler$$x2
000131055 980__ $$ajournal
000131055 980__ $$aVDB
000131055 980__ $$aI:(DE-He78)G330-20160331
000131055 980__ $$aI:(DE-He78)C060-20160331
000131055 980__ $$aI:(DE-He78)W110-20160331
000131055 980__ $$aUNRESTRICTED