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Role of MSC-derived galectin 3 in the AML microenvironment.

Autor: Ruvolo PP; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States. Electronic address: pruvolo@mdanderson.org., Ruvolo VR; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Burks JK; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Qiu Y; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Wang RY; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Shpall EJ; Department of Stem Cell Transplantation, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Mirandola L; Kiromic Biopharma, Houston, TX, United States., Hail N Jr; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Zeng Z; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., McQueen T; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Daver N; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Post SM; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Chiriva-Internati M; Kiromic Biopharma, Houston, TX, United States; Department of Lymphoma and Myeloma, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Kornblau SM; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States., Andreeff M; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, United States; Section of Molecular Hematology, University of Texas MD Anderson Cancer Center, Houston, TX, United States.

Publikováno v: Biochimica et biophysica acta. Molecular cell research [Biochim Biophys Acta Mol Cell Res] 2018 Jul; Vol. 1865 (7), pp. 959-969. Date of Electronic Publication: 2018 Apr 12.

Bone Marrow Adipocytes Facilitate Fatty Acid Oxidation Activating AMPK and a Transcriptional Network Supporting Survival of Acute Monocytic Leukemia Cells.

Autor: Tabe Y; Department of Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan.; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.; Department of Next Generation Hematology Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan., Yamamoto S; Department of Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan.; Leading Center for the Development and Research of Cancer Medicine, Juntendo University School of Medicine, Tokyo, Japan., Saitoh K; Department of Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan., Sekihara K; Department of Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan., Monma N; Center for Information Biology, National Institute of Genetics, Sizuoka, Japan., Ikeo K; Center for Information Biology, National Institute of Genetics, Sizuoka, Japan., Mogushi K; Center for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan., Shikami M; Department of Hematology, Aichi Medical University, Aichi, Japan., Ruvolo V; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas., Ishizawa J; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas., Hail N Jr; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas., Kazuno S; Division of Proteomics and BioMolecular Science, Juntendo University School of Medicine, Tokyo, Japan., Igarashi M; Department of Host Defense and Biochemical Research, Juntendo University School of Medicine, Tokyo, Japan., Matsushita H; Department of Laboratory Medicine, Tokai University School of Medicine, Kanagawa, Japan., Yamanaka Y; Preventive Medicine and Diagnosis Innovation Program, RIKEN, Kanagawa, Japan., Arai H; Division of Proteomics and BioMolecular Science, Juntendo University School of Medicine, Tokyo, Japan., Nagaoka I; Department of Host Defense and Biochemical Research, Juntendo University School of Medicine, Tokyo, Japan., Miida T; Department of Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan., Hayashizaki Y; Preventive Medicine and Diagnosis Innovation Program, RIKEN, Kanagawa, Japan., Konopleva M; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas., Andreeff M; Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas. mandreef@mdanderson.org.

Publikováno v: Cancer research [Cancer Res] 2017 Mar 15; Vol. 77 (6), pp. 1453-1464. Date of Electronic Publication: 2017 Jan 20.

Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.

Autor: Ruvolo PP; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: pruvolo@mdanderson.org., Ruvolo VR; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Benton CB; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., AlRawi A; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Burks JK; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Schober W; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Rolke J; La Jolla Pharmaceutical Company, San Diego, CA, USA., Tidmarsh G; La Jolla Pharmaceutical Company, San Diego, CA, USA., Hail N Jr; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Davis RE; Department of Lymphoma/Myeloma, The University of Texas M.D. Anderson Cancer Center, Houston, USA., Andreeff M; Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Publikováno v: Biochimica et biophysica acta [Biochim Biophys Acta] 2016 Apr; Vol. 1863 (4), pp. 562-71. Date of Electronic Publication: 2015 Dec 17.