Hematopoietic Stem Cells for Transplantation View Homepage


Ontology type: schema:MonetaryGrant     


Grant Info

YEARS

1998-2014

FUNDING AMOUNT

23674144 USD

ABSTRACT

DESCRIPTION (provided by applicant): This grant proposal focuses our sustained laboratory and clinical research experience in animal and human stem cell biology and leukemia to extend exciting new investigations on normal tissue-specific and cancer stem cells. The investigators in this PPG look forward to discovering key information about the defining characteristics of cancer stem cells. This knowledge will enable us to develop new methods to better identify and isolate these rare cells for further study. In addition, this PPG seeks increased understanding of the pathophysiologic mechanisms of cancer stem cells, particularly the signaling pathways that these cells depend on for their persistence and other malignant behavior. This basic information will suggest new clinical cancer stem cell targets, which we will proceed to attack via pharmacologic and biologic approaches. Both within the Projects and in interactions among the Projects and Cores, clinical research and laboratory inquiries will proceed in parallel, so that insights generated in one sphere will translate to, and promote progress in the other. We believe that our highly interactive, closely integrated, translational approach is the best way to determine mechanisms of normal and malignant stem cell biology, and simultaneously to develop new treatments utilizing normal stem cells and targeting malignant stem cells in human diseases. Relevance: There is growing evidence suggesting that many cancers originate in early (stem or progenitor) cells and that the mature cancers continue to be maintained by a stem-progenitor cell hierarchy. Our group has provided important evidence demonstrating the existence of discrete populations of cancer stem cells in human diseases, and our results support the prediction that cancer recurrence in patients after chemotherapy may be due to failure to eradicate the rare, sustaining cancer stem cell population, despite massive reduction of the predominant bulk population of mature cancer cells. The investigators in this PPG look forward to discovering key information about the defining characteristics and molecular mechanisms of cancer stem cells that will provide new ways to identify and attack cancer stem cells therapeutically. More... »

URL

http://projectreporter.nih.gov/project_info_description.cfm?aid=8213672

Related SciGraph Publications

  • 2013-01. Mutations of FLT3/ITD confer resistance to multiple tyrosine kinase inhibitors in LEUKEMIA
  • 2011-09. Further activation of FLT3 mutants by FLT3 ligand in ONCOGENE
  • 2010-11. High frequencies of leukemia stem cells in poor-outcome childhood precursor-B acute lymphoblastic leukemias in LEUKEMIA
  • 2010-07. High-dose cyclophosphamide for autoimmunity and alloimmunity in IMMUNOLOGIC RESEARCH
  • 2008-01. Enhancement of antitumor activity of cisplatin in human lung cancer cells by tumor suppressor FUS1 in CANCER GENE THERAPY
  • 2007-09. Induction of acute lymphocytic leukemia differentiation by maintenance therapy in LEUKEMIA
  • 2007-04. Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease in LEUKEMIA
  • 2007-01. Enhancement of adenoviral MDA-7-mediated cell killing in human lung cancer cells by geldanamycin and its 17-allyl- amino-17-demethoxy analogue in CANCER GENE THERAPY
  • 2006-11. Identification of a region on the outer surface of the CBFβ-SMMHC myeloid oncoprotein assembly competence domain critical for multimerization in ONCOGENE
  • 2006-08. Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner in LEUKEMIA
  • 2006-08. Induction of apoptosis in human lung cancer cells following treatment with amifostine and an adenoviral vector containing wild-type p53 in CANCER GENE THERAPY
  • 2006-03. Quantitative analysis of bone marrow CD34 cells in aplastic anemia and hypoplastic myelodysplastic syndromes in LEUKEMIA
  • 2004-11. Liposomal vector mediated delivery of the 3p FUS1 gene demonstrates potent antitumor activity against human lung cancer in vivo in CANCER GENE THERAPY
  • 2004-09. 5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells in ONCOGENE
  • 2004-02. Induction of p53-regulated genes in lung cancer cells: implications of the mechanism for adenoviral p53-mediated apoptosis in ONCOGENE
  • 2003-09. FLT3: ITDoes matter in leukemia in LEUKEMIA
  • 2002-10. Inhibition of the transforming activity of FLT3 internal tandem duplication mutants from AML patients by a tyrosine kinase inhibitor in LEUKEMIA
  • 2002-09. Human AML cells in NOD/SCID mice: engraftment potential and gene expression in LEUKEMIA
  • 2002-08. Bis(1H-2-indolyl)-1-methanones as inhibitors of the hematopoietic tyrosine kinase Flt3 in LEUKEMIA
  • 2002-07. A novel single tetracycline-regulative adenoviral vector for tumor-specific Bax gene expression and cell killing in vitro and in vivo in ONCOGENE
  • 2002-04. Multiple lysine mutations in the C-terminus of p53 make it resistant to degradation mediated by MDM2 but not by human papillomavirus E6 and induce growth inhibition in MDM2-overexpressing cells in ONCOGENE
  • 2002-03. Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells in ONCOGENE
  • 2002-03. C-terminus of p53 is required for G2 arrest in ONCOGENE
  • 2001-07. Inhibition of FLT3-mediated transformation by use of a tyrosine kinase inhibitor in LEUKEMIA
  • 2000-10. Constitutive activation of FLT3 stimulates multiple intracellular signal transducers and results in transformation in LEUKEMIA
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