F
Florian H. Heidel
Researcher at National Institutes of Health
Publications - 144
Citations - 3549
Florian H. Heidel is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Medicine & Haematopoiesis. The author has an hindex of 27, co-authored 107 publications receiving 2734 citations. Previous affiliations of Florian H. Heidel include Harvard University & Schiller International University.
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Journal ArticleDOI
Randomized comparison of low dose cytarabine with or without glasdegib in patients with newly diagnosed acute myeloid leukemia or high-risk myelodysplastic syndrome
Jorge E. Cortes,Florian H. Heidel,Andrzej Hellmann,Walter Fiedler,B. Douglas Smith,Tadeusz Robak,Pau Montesinos,Daniel A. Pollyea,Pierre Desjardins,Oliver G. Ottmann,Weidong Wendy Ma,Naveed Shaik,A. Douglas Laird,Mirjana Zeremski,Ashleigh O'Connell,Geoffrey Chan,Michael Heuser +16 more
TL;DR: Glasdegib plus LDAC has a favorable benefit–risk profile and may be a promising option for AML patients unsuitable for intensive chemotherapy and clinical efficacy was evident across patients with diverse mutational profiles.
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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain
Florian H. Heidel,Fian K. Solem,Frank Breitenbuecher,Daniel B. Lipka,Stefan Kasper,M. H. Thiede,Christian Brandts,Hubert Serve,Johannes Roesel,Francis J. Giles,Eric J. Feldman,Gerhard Ehninger,Gary J. Schiller,Stephen D. Nimer,Richard Stone,Yanfeng Wang,Thomas Kindler,Pamela S. Cohen,Christoph Huber,Thomas Fischer +19 more
TL;DR: In vivo and in vitro investigation of primary blasts at relapse revealed persistent TK phosphorylation of FLT3 despite sufficient PKC412 serum levels, pointing out that a genetically complex malignancy such as AML may retain dependence on a single oncogenic signal.
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Genetic and pharmacologic inhibition of β-catenin targets imatinib-resistant leukemia stem cells in CML.
Florian H. Heidel,Lars Bullinger,Lars Bullinger,Zhaohui Feng,Zhaohui Feng,Zhu Wang,Zhu Wang,Tobias Neff,Tobias Neff,Lauren Stein,Lauren Stein,Demetrios Kalaitzidis,Demetrios Kalaitzidis,Steven W. Lane,Steven W. Lane,Scott A. Armstrong,Scott A. Armstrong +16 more
TL;DR: In this paper, the authors used a conditional mouse model to show that deletion of β-catenin after CML initiation does not lead to a significant increase in survival, but deletion synergizes with IM to delay disease recurrence after imatinib discontinuation and to abrogate CML stem cells.
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Oncogenic JAK2 V617F causes PD-L1 expression, mediating immune escape in myeloproliferative neoplasms
Alessandro Prestipino,Alica J. Emhardt,Konrad Aumann,David O’Sullivan,Sivahari P. Gorantla,Sandra Duquesne,Wolfgang Melchinger,Lukas Braun,Slavica Vuckovic,Slavica Vuckovic,Melanie Boerries,Melanie Boerries,Hauke Busch,Hauke Busch,Sebastian Halbach,Sandra Pennisi,Teresa Poggio,Petya Apostolova,Pia Veratti,Pia Veratti,Michael Hettich,Gabriele Niedermann,Mark Bartholomä,Khalid Shoumariyeh,Jonas S. Jutzi,Julius Wehrle,Christine Dierks,Heiko Becker,Annette Schmitt-Graeff,Marie Follo,Dietmar Pfeifer,Jan Rohr,Sebastian Fuchs,Stephan Ehl,Frederike A. Hartl,Susana Minguet,Cornelius Miething,Cornelius Miething,Florian H. Heidel,Nicolaus Kröger,Ioanna Triviai,Tilman Brummer,Jürgen Finke,Anna Lena Illert,Eliana Ruggiero,Chiara Bonini,Justus Duyster,Justus Duyster,Heike L. Pahl,Steven W. Lane,Steven W. Lane,Steven W. Lane,Geoffrey R. Hill,Geoffrey R. Hill,Geoffrey R. Hill,Bruce R. Blazar,Nikolas von Bubnoff,Nikolas von Bubnoff,Erika L. Pearce,Robert Zeiser +59 more
TL;DR: In MPN, constitutive JAK2/STAT3/STAT5 activation, mainly in monocytes, megakaryocytes, and platelets, caused PD-L1–mediated immune escape by reducing T cell activation, metabolic activity, and cell cycle progression, which paving the way for immunomodulatory approaches relying on PD-1 inhibition.
Journal ArticleDOI
Requirement for CDK6 in MLL-rearranged acute myeloid leukemia
Theresa Placke,Katrin Faber,Atsushi Nonami,Sarah L. Putwain,Helmut R. Salih,Florian H. Heidel,Alwin Krämer,David E. Root,David A. Barbie,David A. Barbie,Andrei V. Krivtsov,Scott A. Armstrong,William C. Hahn,William C. Hahn,Brian J. P. Huntly,Stephen M. Sykes,Michael D. Milsom,Claudia Scholl,Stefan Fröhling +18 more
TL;DR: CDK6 is identified as critical effector of MLL fusions in leukemogenesis that might be targeted to overcome the differentiation block associated with MLL-rearranged AML, and underscores that cell-cycle regulators may have distinct, noncanonical, and nonredundant functions in different contexts.