Subprojects involve the development of therapy of AML and the analysis of the molecular and biological changes which occur during the evolution of response or resistance to myeloid growth factors and phase specific chemotherapeutic agents and bone marrow transplantation.This Core has the responsibility for handling all patient samples for clinical and research use. In component 1 of this Core, peripheral blood cells and marrow cells are to be collected at predetermined intervals from AML patients in the outpatient department throughout several sequential therapeutic interventions. Aliquots of samples are stored, and distributed to the appropriate project investigators. Dr. Steven Kornblau is the director of this effort. In Component 2, selected AML and normal bone marrow samples are separated into fractions enriched in early and late stages of maturation or enriched in normal versus leukemic cells. Engrafting doses of peripheral blood mononuclear cells or bone marrow cells manipulated by in vitro separation and/or growth are also collected and samples distributed to investigators or stored for reinfusion into patients undergoing autologous or allogeneic bone marrow transplantation. Dr. Richard Champlin is the director of this effort. In Component 3, progenitor cells are grown in culture systems which identify AML versus normal, various lineages of mature progenitors, stem cells versus mature progenitors or proliferating versus differentiating cells. Dr. Zeev Estrov is the director of this core. This core is designed to provide for the collection, processing, separation, culture and analysis of patient samples.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
3P01CA055164-09S1
Application #
6417633
Study Section
Project Start
2000-08-04
Project End
2001-06-30
Budget Start
Budget End
Support Year
9
Fiscal Year
2001
Total Cost
Indirect Cost
Name
University of Texas MD Anderson Cancer Center
Department
Type
DUNS #
001910777
City
Houston
State
TX
Country
United States
Zip Code
77030
Ruvolo, Peter P; Ruvolo, Vivian R; Burks, Jared K et al. (2018) Role of MSC-derived galectin 3 in the AML microenvironment. Biochim Biophys Acta Mol Cell Res 1865:959-969
Ngankeu, Apollinaire; Ranganathan, Parvathi; Havelange, Violaine et al. (2018) Discovery and functional implications of a miR-29b-1/miR-29a cluster polymorphism in acute myeloid leukemia. Oncotarget 9:4354-4365
Le, Phuong M; Andreeff, Michael; Battula, Venkata Lokesh (2018) Osteogenic niche in the regulation of normal hematopoiesis and leukemogenesis. Haematologica :
Jiang, Xuejie; Mak, Po Yee; Mu, Hong et al. (2018) Disruption of Wnt/?-Catenin Exerts Antileukemia Activity and Synergizes with FLT3 Inhibition in FLT3-Mutant Acute Myeloid Leukemia. Clin Cancer Res 24:2417-2429
Ishizawa, Jo; Nakamaru, Kenji; Seki, Takahiko et al. (2018) Predictive Gene Signatures Determine Tumor Sensitivity to MDM2 Inhibition. Cancer Res 78:2721-2731
Sekihara, Kazumasa; Saitoh, Kaori; Han, Lina et al. (2017) Targeting mantle cell lymphoma metabolism and survival through simultaneous blockade of mTOR and nuclear transporter exportin-1. Oncotarget 8:34552-34564
Carter, Bing Z; Mak, Po Yee; Wang, Xiangmeng et al. (2017) Focal Adhesion Kinase as a Potential Target in AML and MDS. Mol Cancer Ther 16:1133-1144
Zeng, Zhihong; Liu, Wenbin; Tsao, Twee et al. (2017) High-throughput profiling of signaling networks identifies mechanism-based combination therapy to eliminate microenvironmental resistance in acute myeloid leukemia. Haematologica 102:1537-1548
Pan, Rongqing; Ruvolo, Vivian; Mu, Hong et al. (2017) Synthetic Lethality of Combined Bcl-2 Inhibition and p53 Activation in AML: Mechanisms and Superior Antileukemic Efficacy. Cancer Cell 32:748-760.e6
Jacamo, Rodrigo; Davis, R Eric; Ling, Xiaoyang et al. (2017) Tumor Trp53 status and genotype affect the bone marrow microenvironment in acute myeloid leukemia. Oncotarget 8:83354-83369

Showing the most recent 10 out of 422 publications