D
D. Gary Gilliland
Researcher at Merck & Co.
Publications - 82
Citations - 22071
D. Gary Gilliland is an academic researcher from Merck & Co.. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 53, co-authored 80 publications receiving 20768 citations. Previous affiliations of D. Gary Gilliland include Massachusetts Institute of Technology & Northwestern University.
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Journal ArticleDOI
Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
Ross L. Levine,Ross L. Levine,Martha Wadleigh,Jan Cools,Benjamin L. Ebert,Benjamin L. Ebert,Gerlinde Wernig,Brian J. P. Huntly,Titus J. Boggon,Iwona Wlodarska,Jennifer J. Clark,Sandra A. Moore,Jennifer Adelsperger,Sumin Koo,Jeffrey C. Lee,Stacey Gabriel,Thomas Mercher,Alan D. D'Andrea,Stefan Fröhling,Konstanze Döhner,Peter Marynen,Peter Vandenberghe,Ruben A. Mesa,Ayalew Tefferi,James D. Griffin,Michael J. Eck,William R. Sellers,William R. Sellers,Matthew Meyerson,Matthew Meyerson,Todd R. Golub,Todd R. Golub,Todd R. Golub,Stephanie J. Lee,D. Gary Gilliland,D. Gary Gilliland,D. Gary Gilliland +36 more
TL;DR: High-throughput DNA resequencing identified a recurrent somatic missense mutation JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations.
Journal ArticleDOI
A Tyrosine Kinase Created by Fusion of the PDGFRA and FIP1L1 Genes as a Therapeutic Target of Imatinib in Idiopathic Hypereosinophilic Syndrome
Jan Cools,Jan Cools,Daniel J. DeAngelo,Jason Gotlib,Elizabeth H. Stover,Robert D. Legare,Robert D. Legare,J. E. Cortes,Jeffrey L. Kutok,Jennifer J. Clark,Ilene Galinsky,James D. Griffin,Nicholas C.P. Cross,Ayalew Tefferi,James M. Malone,Rafeul Alam,Stanley L. Schrier,Janet L. Schmid,Michal G. Rose,Peter Vandenberghe,Gregor Verhoef,Marc Boogaerts,Iwona Wlodarska,Hagop M. Kantarjian,Peter Marynen,Steven Coutre,Richard Stone,D. Gary Gilliland +27 more
TL;DR: The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib, and data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.
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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
MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.
Yana Pikman,Benjamin H. Lee,Thomas Mercher,Elizabeth McDowell,Benjamin L. Ebert,Benjamin L. Ebert,Maricel Gozo,Adam Cuker,Gerlinde Wernig,Sandra A. Moore,Ilene Galinsky,Daniel J. DeAngelo,Jennifer J. Clark,Stephanie J. Lee,Todd R. Golub,Todd R. Golub,Todd R. Golub,Martha Wadleigh,D. Gary Gilliland,D. Gary Gilliland,D. Gary Gilliland,Ross L. Levine,Ross L. Levine +22 more
TL;DR: The JAK2V617F allele has been identified in patients with polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis with myeloid metaplasia (MF).
Journal ArticleDOI
JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis.
Linda M. Scott,Wei Tong,Ross L. Levine,Michael A. Scott,Philip A. Beer,Michael R. Stratton,P. Andrew Futreal,Wendy N. Erber,Mary Frances McMullin,Claire N. Harrison,Alan J. Warren,Alan J. Warren,D. Gary Gilliland,D. Gary Gilliland,Harvey F. Lodish,Anthony R. Green,Anthony R. Green +16 more
TL;DR: Four somatic gain-of-function mutations affecting JAK2 exon 12 define a distinctive myeloproliferative syndrome that affects patients who currently receive a diagnosis of polycythemia vera or idiopathic erythrocytosis.