D
Dana E. Cullen
Researcher at Harvard University
Publications - 8
Citations - 2349
Dana E. Cullen is an academic researcher from Harvard University. The author has contributed to research in topics: In vivo & Notch signaling pathway. The author has an hindex of 8, co-authored 8 publications receiving 2205 citations. Previous affiliations of Dana E. Cullen include Brigham and Women's Hospital & Howard Hughes Medical Institute.
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Journal ArticleDOI
FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress.
Zuzana Tothova,Zuzana Tothova,Ramya Kollipara,Brian J. P. Huntly,Benjamin H. Lee,Benjamin H. Lee,Diego H. Castrillon,Dana E. Cullen,Dana E. Cullen,Elizabeth P. McDowell,Elizabeth P. McDowell,Suzan Lazo-Kallanian,Ifor R. Williams,Christopher Sears,Scott A. Armstrong,Emmanuelle Passegué,Ronald A. DePinho,D. Gary Gilliland,D. Gary Gilliland +18 more
TL;DR: FoxO proteins play essential roles in the response to physiologic oxidative stress and thereby mediate quiescence and enhanced survival in the HSC compartment, a function that is required for its long-term regenerative potential.
Journal ArticleDOI
Efficacy of TG101348, a Selective JAK2 Inhibitor, in Treatment of a Murine Model of JAK2V617F-Induced Polycythemia Vera
Gerlinde Wernig,Michael G. Kharas,Rachel Okabe,Sandra A. Moore,Dena S. Leeman,Dana E. Cullen,Maricel Gozo,Elizabeth McDowell,Ross L. Levine,Ross L. Levine,John Doukas,Chi Ching Mak,Glenn Noronha,Michael Martin,Yon D. Ko,Benjamin H. Lee,Richard M. Soll,Ayalew Tefferi,John Hood,D. Gary Gilliland,D. Gary Gilliland,D. Gary Gilliland +21 more
TL;DR: In this article, a small-molecule inhibitor of JAK2 with an in vitro IC50 of approximately 3 nM was used to treat myeloproliferative disease induced by the JAK 2V617F mutation.
Journal ArticleDOI
JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model.
Thomas Mercher,Gerlinde Wernig,Sandra A. Moore,Ross L. Levine,Ting-Lei Gu,Stefan Fröhling,Dana E. Cullen,Roberto D. Polakiewicz,Olivier Bernard,Titus J. Boggon,Benjamin H. Lee,D. Gary Gilliland +11 more
TL;DR: A screening assay for mutations that cause AMKL is developed, based on the hypothesis that constitutive activation of STAT5 would be a biochemical indicator of mutation in an upstream effector tyrosine kinase, and a new JAK2T875N mutation is identified in the AMkL cell line CHRF-288-11.
Journal ArticleDOI
The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRβ and FIP1L1-PDGFRα in vitro and in vivo
Elizabeth H. Stover,Jing Chen,Benjamin H. Lee,Jan Cools,Elizabeth McDowell,Jennifer Adelsperger,Dana E. Cullen,Allison Coburn,Sandra A. Moore,Rachel Okabe,Doriano Fabbro,Paul W. Manley,James D. Griffin,D. Gary Gilliland +13 more
TL;DR: In an in vivo bone marrow transplantation assay, AMN107 effectively treated myeloproliferative disease induced by TEL- PDGFRbeta and FIP1L1-PDGFRalpha, significantly increasing survival and disease latency and reducing disease severity as assessed by histopathology and flow cytometry.
Journal ArticleDOI
The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model
Thomas Mercher,Glen D. Raffel,Sandra A. Moore,Melanie G. Cornejo,Dominique Baudry-Bluteau,Nicolas Cagnard,Jonathan L. Jesneck,Yana Pikman,Dana E. Cullen,Ifor R. Williams,Koichi Akashi,Hirokazu Shigematsu,Jean-Pierre Bourquin,Marco Giovannini,William Vainchenker,Ross L. Levine,Benjamin H. Lee,Olivier Bernard,D. Gary Gilliland,D. Gary Gilliland +19 more
TL;DR: It is established that concomitant activation of RBPJ (Notch signaling) and MPL (cytokine signaling) transforms cells of the megakaryocytic lineage and suggest that specific targeting of these pathways could be of therapeutic value for human AMKL.