J
Joseph Negri
Researcher at Broad Institute
Publications - 59
Citations - 1988
Joseph Negri is an academic researcher from Broad Institute. The author has contributed to research in topics: Bortezomib & Stromal cell. The author has an hindex of 21, co-authored 57 publications receiving 1790 citations. Previous affiliations of Joseph Negri include Harvard University & Bristol-Myers Squibb.
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The role of tumour-stromal interactions in modifying drug response: challenges and opportunities.
TL;DR: Progress in in vitro screening platforms as well as orthotopic and 'orthometastatic' xenograft mouse models has enabled comprehensive characterization of the impact of the tumour microenvironment on therapeutic efficacy, which can hopefully bridge the gap between preclinical studies and clinical trials of anticancer agents.
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Tumor cell-specific bioluminescence platform to identify stroma-induced changes to anticancer drug activity
Douglas W. McMillin,Jake Delmore,Jake Delmore,Ellen Weisberg,Ellen Weisberg,Joseph Negri,Joseph Negri,D. Corey Geer,D. Corey Geer,Steffen Klippel,Steffen Klippel,Nicholas Mitsiades,Robert L. Schlossman,Robert L. Schlossman,Nikhil C. Munshi,Andrew L. Kung,James D. Griffin,James D. Griffin,Paul G. Richardson,Paul G. Richardson,Kenneth C. Anderson,Kenneth C. Anderson,Constantine S. Mitsiades,Constantine S. Mitsiades +23 more
TL;DR: In this paper, a tumor cell-specific in vitro bioluminescence imaging (CS-BLI) assay was developed to identify stroma-induced chemoresistance in diverse malignancies, including imatinib resistance in leukemic cells.
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Antimyeloma Activity of the Orally Bioavailable Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235
Douglas W. McMillin,Melissa G. Ooi,Jake Delmore,Joseph Negri,Patrick Hayden,N. Mitsiades,Jana Jakubikova,Sauveur-Michel Maira,Carlos Garcia-Echeverria,Robert L. Schlossman,Nikhil C. Munshi,Paul G. Richardson,Kenneth C. Anderson,Constantine S. Mitsiades +13 more
TL;DR: BEZ235 treatment decreased the amplitude of transcriptional signatures previously associated with myc, ribosome, and proteasome function, as well as high-risk MM and undifferentiated human embryonic stem cells, and indicates that BEZ235 merits clinical testing, alone and in combination with other agents, in multiple myeloma.
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Antitumor effects of the proteasome inhibitor bortezomib in medullary and anaplastic thyroid carcinoma cells in vitro.
Constantine S. Mitsiades,Douglas W. McMillin,Vassiliki Kotoula,Vassiliki Poulaki,Ciaran J. McMullan,Joseph Negri,Galinos Fanourakis,Galinos Fanourakis,Sophia Tseleni-Balafouta,Kenneth B. Ain,Kenneth B. Ain,Nicholas Mitsiades +11 more
TL;DR: These data provide both insights into the molecular mechanisms of antitumor activity of proteasome inhibitors and the rationale for future clinical trials of bortezomib, alone or in combination with conventional chemotherapy, to improve patient outcome in medullary and anaplastic thyroid carcinomas.
Journal ArticleDOI
Niche-based screening identifies small-molecule inhibitors of leukemia stem cells
Kimberly A. Hartwell,Kimberly A. Hartwell,Kimberly A. Hartwell,Peter Miller,Peter Miller,Siddhartha Mukherjee,Alissa R. Kahn,Alison L. Stewart,David J. Logan,Joseph Negri,Mildred Duvet,Mildred Duvet,Marcus Järås,Rishi V. Puram,Rishi V. Puram,Vlado Dančík,Fatima Al-Shahrour,Fatima Al-Shahrour,Thomas Kindler,Zuzana Tothova,Zuzana Tothova,Shrikanta Chattopadhyay,Shrikanta Chattopadhyay,Thomas P. Hasaka,Rajiv Narayan,Mingji Dai,Mingji Dai,Christina Huang,Sebastian Shterental,Lisa P. Chu,J. Erika Haydu,Jae Hung Shieh,David P. Steensma,Benito Munoz,Joshua A. Bittker,Alykhan F. Shamji,Paul A. Clemons,Nicola Tolliday,Anne E. Carpenter,D. Gary Gilliland,Andrew M. Stern,Malcolm A.S. Moore,David T. Scadden,David T. Scadden,Stuart L. Schreiber,Stuart L. Schreiber,Stuart L. Schreiber,Benjamin L. Ebert,Todd R. Golub +48 more
TL;DR: The cholesterol-lowering drug lovastatin showed anti-LSC activity in vitro and in an in vivo bone marrow transplantation model, and Mechanistic studies demonstrated that the effect was on target, via inhibition of HMG-CoA reductase.