G
Gary Gilliland
Researcher at Brigham and Women's Hospital
Publications - 15
Citations - 2545
Gary Gilliland is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Leukemia & Haematopoiesis. The author has an hindex of 9, co-authored 15 publications receiving 2491 citations. Previous affiliations of Gary Gilliland include Howard Hughes Medical Institute.
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Journal ArticleDOI
Analysis of cytokine mRNA and DNA: detection and quantitation by competitive polymerase chain reaction
TL;DR: An adaptation of the polymerase chain reaction (PCR) for highly accurate quantitation of mRNA or DNA from a small number of cells for expression of two cytokines and the copy number of the human GM-CSF gene in normal human cells is described.
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MOZ-TIF2, but Not BCR-ABL, Confers Properties of Leukemic Stem Cells to Committed Murine Hematopoietic Progenitors.
Brian J. P. Huntly,Hirokazu Shigematzu,Kenji Deguchi,Benjamin H. Lee,Shinichi Mizuno,Nicky Duclos,Rebecca Rowan,Sonia M Amaral,David P. Curley,Ifor R. Williams,Koichi Akashi,Gary Gilliland +11 more
TL;DR: In this article, the authors tested the ability of representative leukemia oncogenes to transform committed myeloid progenitor cells that lack the capacity for self-renewal, and showed that an active MOZ-TIF2, but not BCR-ABL, can collaborate with mutations induced by retroviral mutagenesis to confer properties of leukemic stem cells to committed progenitors.
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FLT3-ITD up-regulates MCL-1 to promote survival of stem cells in acute myeloid leukemia via FLT3-ITD–specific STAT5 activation
Goichi Yoshimoto,Toshihiro Miyamoto,Siamak Jabbarzadeh-Tabrizi,Tadafumi Iino,Jennifer Rocnik,Yoshikane Kikushige,Yasuo Mori,Takahiro Shima,Hiromi Iwasaki,Katsuto Takenaka,Koji Nagafuji,Shinichi Mizuno,Hiroaki Niiro,Gary Gilliland,Koichi Akashi,Koichi Akashi +15 more
TL;DR: The acquisition of FLT3-ITD ensures LSC survival by up-regulating MCL-1 via constitutive STAT5 activation that is independent of wild-typeFLT3 signaling.
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Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
Ellen Weisberg,Andrew L. Kung,Renee D. Wright,Daisy Moreno,Laurie Catley,Arghya Ray,Leigh Zawel,Mary Ann Tran,Jan Cools,Gary Gilliland,Constantine S. Mitsiades,Douglas W. McMillin,Jingrui Jiang,Elizabeth Hall-Meyers,James D. Griffin +14 more
TL;DR: The proapoptotic IAP inhibitor, LBW242, was shown in proliferation studies done in vitro to enhance the killing of PKC412-sensitive and PKC 412-resistant cell lines expressing mutant FLT3 when combined with either PKC512 or standard cytotoxic agents (doxorubicin and Ara-c).