Haase, Detlef

[["dc.bibliographiccitation.firstpage","73483"],["dc.bibliographiccitation.issue","43"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","73500"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Valent, Peter"],["dc.contributor.author","Orazi, Attilio"],["dc.contributor.author","Steensma, David P."],["dc.contributor.author","Ebert, Benjamin L."],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Malcovati, Luca"],["dc.contributor.author","van de Loosdrecht, Arjan A."],["dc.contributor.author","Haferlach, Torsten"],["dc.contributor.author","Westers, Theresia M."],["dc.contributor.author","Wells, Denise A."],["dc.contributor.author","Giagounidis, Aristoteles"],["dc.contributor.author","Loken, Michael"],["dc.contributor.author","Orfao, Alberto"],["dc.contributor.author","Lübbert, Michael"],["dc.contributor.author","Ganser, Arnold"],["dc.contributor.author","Hofmann, Wolf-Karsten"],["dc.contributor.author","Ogata, Kiyoyuki"],["dc.contributor.author","Schanz, Julie"],["dc.contributor.author","Béné, Marie C."],["dc.contributor.author","Hoermann, Gregor"],["dc.contributor.author","Sperr, Wolfgang R."],["dc.contributor.author","Sotlar, Karl"],["dc.contributor.author","Bettelheim, Peter"],["dc.contributor.author","Stauder, Reinhard"],["dc.contributor.author","Pfeilstöcker, Michael"],["dc.contributor.author","Horny, Hans-Peter"],["dc.contributor.author","Germing, Ulrich"],["dc.contributor.author","Greenberg, Peter"],["dc.contributor.author","Bennett, John M."],["dc.date.accessioned","2019-12-17T12:21:04Z"],["dc.date.accessioned","2021-10-27T13:21:59Z"],["dc.date.available","2019-12-17T12:21:04Z"],["dc.date.available","2021-10-27T13:21:59Z"],["dc.date.issued","2017"],["dc.description.abstract","Myelodysplastic syndromes (MDS) comprise a heterogeneous group of myeloid neoplasms characterized by peripheral cytopenia, dysplasia, and a variable clinical course with about 30% risk to transform to secondary acute myeloid leukemia (AML). In the past 15 years, diagnostic evaluations, prognostication, and treatment of MDS have improved substantially. However, with the discovery of molecular markers and advent of novel targeted therapies, new challenges have emerged in the complex field of MDS. For example, MDS-related molecular lesions may be detectable in healthy individuals and increase in prevalence with age. Other patients exhibit persistent cytopenia of unknown etiology without dysplasia. Although these conditions are potential pre-phases of MDS they may also transform into other bone marrow neoplasms. Recently identified molecular, cytogenetic, and flow-based parameters may add in the delineation and prognostication of these conditions. However, no generally accepted integrated classification and no related criteria are as yet available. In an attempt to address this challenge, an international consensus group discussed these issues in a working conference in July 2016. The outcomes of this conference are summarized in the present article which includes criteria and a proposal for the classification of pre-MDS conditions as well as updated minimal diagnostic criteria of MDS. Moreover, we propose diagnostic standards to delineate between ´normal´, pre-MDS, and MDS. These standards and criteria should facilitate diagnostic and prognostic evaluations in clinical studies as well as in clinical practice."],["dc.identifier.doi","10.18632/oncotarget.19008"],["dc.identifier.eissn","1949-2553"],["dc.identifier.pmid","29088721"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92060"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Proposed minimal diagnostic criteria for myelodysplastic syndromes (MDS) and potential pre-MDS conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Leukemia"],["dc.contributor.author","Schlenk, R. F."],["dc.contributor.author","Weber, D."],["dc.contributor.author","Herr, W."],["dc.contributor.author","Wulf, G."],["dc.contributor.author","Salih, H. R."],["dc.contributor.author","Derigs, H. G."],["dc.contributor.author","Kuendgen, A."],["dc.contributor.author","Ringhoffer, M."],["dc.contributor.author","Hertenstein, B."],["dc.contributor.author","Martens, U. M."],["dc.contributor.author","Grießhammer, M."],["dc.contributor.author","Bernhard, H."],["dc.contributor.author","Krauter, J."],["dc.contributor.author","Girschikofsky, M."],["dc.contributor.author","Wolf, D."],["dc.contributor.author","Lange, E."],["dc.contributor.author","Westermann, J."],["dc.contributor.author","Koller, E."],["dc.contributor.author","Kremers, S."],["dc.contributor.author","Wattad, M."],["dc.contributor.author","Heuser, M."],["dc.contributor.author","Thol, F."],["dc.contributor.author","Göhring, G."],["dc.contributor.author","Haase, D."],["dc.contributor.author","Teleanu, V."],["dc.contributor.author","Gaidzik, V."],["dc.contributor.author","Benner, A."],["dc.contributor.author","Döhner, K."],["dc.contributor.author","Ganser, A."],["dc.contributor.author","Paschka, P."],["dc.contributor.author","Döhner, H."],["dc.date.accessioned","2019-07-09T11:50:49Z"],["dc.date.available","2019-07-09T11:50:49Z"],["dc.date.issued","2019"],["dc.description.abstract","The aim of this randomized phase-II study was to evaluate the effect of substituting cytarabine by azacitidine in intensive induction therapy of patients with acute myeloid leukemia (AML). Patients were randomized to four induction schedules for two cycles: STANDARD (idarubicin, cytarabine, etoposide); and azacitidine given prior (PRIOR), concurrently (CONCURRENT), or after (AFTER) therapy with idarubicin and etoposide. Consolidation therapy consisted of allogeneic hematopoietic-cell transplantation or three courses of high-dose cytarabine followed by 2-year maintenance therapy with azacitidine in the azacitidine-arms. AML with CBFB-MYH11, RUNX1-RUNX1T1, mutated NPM1, and FLT3-ITD were excluded and accrued to genotype-specific trials. The primary end point was response to induction therapy. The statistical design was based on an optimal two-stage design applied for each arm separately. During the first stage, 104 patients (median age 62.6, range 18–82 years) were randomized; the study arms PRIOR and CONCURRENT were terminated early due to inefficacy. After randomization of 268 patients, all azacitidine-containing arms showed inferior response rates compared to STANDARD. Event-free and overall survival were significantly inferior in the azacitidine-containing arms compared to the standard arm (p < 0.001 and p = 0.03, respectively). The data from this trial do not support the substitution of cytarabine by azacitidine in intensive induction therapy."],["dc.identifier.doi","10.1038/s41375-019-0395-y"],["dc.identifier.pmid","30728457"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59840"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Randomized phase-II trial evaluating induction therapy with idarubicin and etoposide plus sequential or concurrent azacitidine and maintenance therapy with azacitidine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]