Functional-genetic dissection of HDAC dependencies in mouse lymphoid and myeloid malignancies
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- Geoffrey M. Matthews
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
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- Parinaz Mehdipour
- Department of Experimental Oncology, European Institute of Oncology, Milan, Italy;
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- Leonie A. Cluse
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
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- Katrina J. Falkenberg
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
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- Eric Wang
- Cold Spring Harbor Laboratory, Cold Spring Harbor, NY;
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- Mareike Roth
- Research Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria;
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- Fabio Santoro
- Department of Experimental Oncology, European Institute of Oncology, Milan, Italy;
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- Eva Vidacs
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
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- Kym Stanley
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
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- Colin M. House
- Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia;
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- James R. Rusche
- Repligen Corporation, Waltham, MA;
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- Christopher R. Vakoc
- Cold Spring Harbor Laboratory, Cold Spring Harbor, NY;
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- Johannes Zuber
- Research Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria;
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- Saverio Minucci
- Department of Experimental Oncology, European Institute of Oncology, Milan, Italy;
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- Ricky W. Johnstone
- Cancer Therapeutics Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia;
説明
<jats:title>Key Points</jats:title> <jats:p>Genetic studies suggest HDAC3-selective suppression may prove useful for treatment of hematological tumors but will not induce apoptosis. Genetic and pharmacological cosuppression of HDAC1 with HDAC2 induces a potent pro-apoptotic response of tumor cells.</jats:p>
収録刊行物
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- Blood
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Blood 126 (21), 2392-2403, 2015-11-19
American Society of Hematology