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Benjamin H. Lee
Researcher at Harvard University
Publications - 10
Citations - 2161
Benjamin H. Lee is an academic researcher from Harvard University. The author has contributed to research in topics: Receptor tyrosine kinase & Tyrosine kinase. The author has an hindex of 6, co-authored 10 publications receiving 2032 citations. Previous affiliations of Benjamin H. Lee include Howard Hughes Medical Institute & Brigham and Women's Hospital.
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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
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.
Journal ArticleDOI
High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia
Marc M. Loriaux,Ross L. Levine,Ross L. Levine,Jeffrey W. Tyner,Stefan Fröhling,Claudia Scholl,Eric P. Stoffregen,Gerlinde Wernig,Heidi Erickson,Christopher A. Eide,Roland Berger,Olivier Bernard,James D. Griffin,Richard Stone,Benjamin H. Lee,Matthew Meyerson,Matthew Meyerson,Michael Heinrich,Michael W. Deininger,D. Gary Gilliland,D. Gary Gilliland,D. Gary Gilliland,Brian J. Druker,Brian J. Druker +23 more
TL;DR: The findings indicate the majority of these alleles are not potent tyrosine kinase activators in this cellular context and that a significant proportion of nonsynonymous sequence variants identified in HT DNA sequencing screens may not have functional significance.
Journal ArticleDOI
Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells.
Winnie F. Tam,Winnie F. Tam,Winnie F. Tam,Ting-Lei Gu,Ting-Lei Gu,Jing Chen,Jing Chen,Benjamin H. Lee,Benjamin H. Lee,Lars Bullinger,Stefan Fröhling,Andrew Z. Wang,Stefano Monti,Todd R. Golub,Todd R. Golub,D. Gary Gilliland,D. Gary Gilliland,D. Gary Gilliland +17 more
TL;DR: It is indicated that inhibitor of DNA binding 1 (Id1), a gene involved in development, cell cycle, and tumorigenesis, is an important target of constitutively activated tyrosine kinases and may be a therapeutic target for leukemias associated with oncogenic tyrosines.