David E. Muench
Cincinnati Children's Hospital Medical Center
23 Papers
13 Citations
David E. Muench is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 12, co-authored 21 publications. Previous affiliations of David E. Muench include University of Cincinnati Academic Health Center & University of Cincinnati.
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Papers
c-Myc and Cancer Metabolism
TL;DR: The interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the “transformed phenotype.”
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Granulocyte-Monocyte Progenitors and Monocyte-Dendritic Cell Progenitors Independently Produce Functionally Distinct Monocytes
Alberto Yáñez,Simon G. Coetzee,Andre Olsson,David E. Muench,Benjamin P. Berman,Dennis J. Hazelett,Nathan Salomonis,H. Leighton Grimes,Helen S. Goodridge +8 more
TL;DR: The balance of GMP and MDP differentiation shapes the myeloid cell repertoire during homeostasis and following infection, and shows that functionally distinct inflammatory monocytes, including those producing monocyte‐derived DCs and a “neutrophil‐like” subset, arise from bone marrow progenitors via two independent pathways
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DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia
Sara E. Meyer,Tingting Qin,David E. Muench,Kohei Masuda,Meenakshi Venkatasubramanian,Emily Orr,Lauren Suarez,Steven D. Gore,Ruud Delwel,Elisabeth Paietta,Martin S. Tallman,Hugo Fernandez,Ari Melnick,Michelle M. Le Beau,Scott C. Kogan,Nathan Salomonis,Maria E. Figueroa,H. Leighton Grimes +17 more
TL;DR: It is demonstrated that mice with Flt3-internal tandem duplication (Flt3(ITD) and inducible deletion of Dnmt3a spontaneously develop a rapidly lethal, completely penetrant, and transplantable AML of normal karyotype.
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Obesity alters the long-term fitness of the hematopoietic stem cell compartment through modulation of Gfi1 expression.
Jung-Mi Lee,Vinothini Govindarajah,Bryan Goddard,Ashwini S. Hinge,David E. Muench,Marie-Dominique Filippi,Bruce J. Aronow,Jose A. Cancelas,Jose A. Cancelas,Nathan Salomonis,H. Leighton Grimes,Damien Reynaud +11 more
TL;DR: It is demonstrated that obesity produces durable changes in HSC function and phenotype and that elevation of Gfi1 expression in response to the oxidative environment is a key driver of the altered HSC properties observed in obesity.
Nanomolar-Potency Small Molecule Inhibitor of STAT5 Protein.
Abbarna A. Cumaraswamy,Andrew M. Lewis,Mulu Geletu,A. Todic,D.B. Diaz,Xin R. Cheng,C.E. Brown,Laister Rc,David E. Muench,Kagan Kerman,H.L. Grimes,Minden,Patrick T. Gunning +12 more
TL;DR: Lead compound 13a, possessing a phosphotyrosyl-mimicking salicylic acid group, potently and selectively binds to STAT5 over STAT3, inhibits STAT5–SH2 domain complexation events in vitro, silences activated STAT5 in leukemic cells, as well as STAT5′s downstream transcriptional targets, including MYC and MCL1, and leads to apoptosis.
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