D
D. Gary Gilliland
Researcher at Brigham and Women's Hospital
Publications - 178
Citations - 33138
D. Gary Gilliland is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Leukemia & Tyrosine kinase. The author has an hindex of 83, co-authored 177 publications receiving 30852 citations. Previous affiliations of D. Gary Gilliland include University of Pennsylvania & University of North Carolina at Chapel Hill.
Papers
More filters
Journal ArticleDOI
Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1
David A. Barbie,Pablo Tamayo,Jesse S. Boehm,So Young Kim,Susan Moody,Ian F. Dunn,Anna C. Schinzel,Peter Sandy,Etienne Meylan,Claudia Scholl,Stefan Fröhling,Edmond M. Chan,Martin L. Sos,Kathrin Michel,Craig H. Mermel,Serena J. Silver,Barbara A. Weir,Jan H. Reiling,Qing Sheng,Piyush Gupta,Raymond C. Wadlow,Raymond C. Wadlow,Hanh Le,Sebastian Hoersch,Ben S. Wittner,Ben S. Wittner,Sridhar Ramaswamy,Sridhar Ramaswamy,David M. Livingston,David M. Sabatini,Matthew Meyerson,Matthew Meyerson,Roman K. Thomas,Eric S. Lander,Jill P. Mesirov,David E. Root,D. Gary Gilliland,Tyler Jacks,William C. Hahn +38 more
TL;DR: Observations indicate that TBK1 and NF-κB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.
Journal ArticleDOI
Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
Ellen Weisberg,Paul W. Manley,Werner Breitenstein,Josef Brüggen,Sandra W. Cowan-Jacob,Arghya Ray,Brian J. P. Huntly,Doriano Fabbro,Gabriele Fendrich,Elizabeth Hall-Meyers,Andrew L. Kung,Andrew L. Kung,Jürgen Mestan,George Q. Daley,Linda Callahan,Laurie Catley,Cara Cavazza,Azam Mohammed,Donna Neuberg,Renee D. Wright,D. Gary Gilliland,James D. Griffin +21 more
TL;DR: AMN107 prolonged survival of mice injected with Bcr-Abl-transformed hematopoietic cell lines or primary marrow cells, and prolonged survival in imatinib-resistant CML mouse models, suggests this is a promising new inhibitor for the therapy of CML and Ph+ ALL.
Journal ArticleDOI
The roles of FLT3 in hematopoiesis and leukemia.
TL;DR: Results suggest that FLT3 is an attractive therapeutic target for kinase inhibitors or other approaches for patients with mutations of this gene, and preliminary studies suggest that mutantFLT3 cooperates with other leukemia oncogenes to confer a more aggressive phenotype.
Journal ArticleDOI
Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.
Andrei V. Krivtsov,David Twomey,David Twomey,Zhaohui Feng,Matthew C. Stubbs,Yingzi Wang,Joerg Faber,Jason E. Levine,Jing Wang,William C. Hahn,William C. Hahn,D. Gary Gilliland,D. Gary Gilliland,Todd R. Golub,Todd R. Golub,Scott A. Armstrong +15 more
TL;DR: It is shown that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme.
MPLW515L Is a Novel Somatic Activating Mutation in Myelofibrosis with Myeloid
Metaplasia Pikman,Benjamin H. Lee,Thomas Mercher,Elizabeth McDowell,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,Martha Wadleigh,D. Gary Gilliland,Ross L. Levine +16 more
TL;DR: Activation of JAK-STAT signaling via MPLW515L is an important pathogenetic event in patients with JAK2V617F-negative MF, including extramedullary hematopoiesis, splenomegaly, and megakaryocytic proliferation.