Research In Alimentary Tract Surgery
Susan E Waltz, Associate Professor
University Of Cincinnati Sponsored Research Services Cincinnati, Oh 45221
Grant 5T32DK064581-05 from National Institute Of Diabetes And Digestive And Kidney Diseases IRG: ZDK1
Abstract: The goal of this T32 program, entitled Research in Alimentary Tract Surgery, is to enhance the professional development and research capabilities of new surgeon-scientists and postgraduate-level PhDs, with a specific interest in academic careers related to the study of digestive disease. This unique program will take advantage of three already-established research focus groups (RFGs) that straddle the Departments of Surgery, Molecular Genetics, Molecular and Cellular Physiology, Pathology and Developmental Biology at the University of Cincinnati College of Medicine and the Cincinnati Children s Hospital Medical Center. These RFGs cover the thematic core areas of Epithelial Pathobiology, GI Oncology, and Adaptation/Developmental Biology. Each RFG is led by an NIH-funded surgeon-scientist in the Department of Surgery as well as an independent NIH-funded basic investigator who share responsibility for creating the structured environment in which the intellectual rigor of laboratory investigation is enriched by the clinical perspective of surgical practice, thus providing both a broad and deep training experience that emphasizes translational potential and scholarly achievement. The training program centers on a supervised laboratory research project directed by a core or adjunct preceptor with oversight by the RFG co-directors. The research is supplemented by didactic coursework commensurate with the trainee s prior experience, and an organized program of seminars and research conferences that will enhance core knowledge base as well as skills in hypothesis formation, experimental design, grant preparation, and oral/written presentation of results. Extensive resources and core facilities are available for trainees, and special efforts are made to attract candidates from underrepresented minorities. Trainees receive instruction in the responsible conduct of research. At the completion of the program, surgeons-scientists will be strongly prepared for academic positions from which they will launch their investigative careers, while postdoctoral Ph.D. trainees should be competitive for entry-level independent funding.
Project start date: 2003-07-01
Project end date: 2008-06-30
5T32DK064581-05 (2007): $223470
Sponsored Links Excellgen http://Excellgen.com
Grants awarded to Susan E Waltz
TRAINING PROGRAM IN CANCER THERAPEUTICS
Susan E Waltz
University Of Cincinnati, Sponsored Research Services, Cincinnati, Oh 45221
Grant 5T32CA117846-05 from National Cancer Institute
Abstract: To improve cancer therapy, it is increasingly critical that advances in basic cancer research be translated to the clinic. In the Training Program in Cancer Therapeutics, the goal is to provide training to cancer researchers in the action of therapeutic agents used in the treatment of cancer. This Training Program will be multi-disciplinary and expose the trainees to both basic research involving cancer therapeutic agents and the clinical utilization of therapeutics. A particular emphasis will be placed on the mechanisms through which basic scientific discovery is brought into the clinic through clinical trials. To facilitate this training, a team of mentoring faculty and ancillary clinical faculty has been recruited into the Training Program from the University of Cincinnati and Cincinnati Children´s Hospital Medical Center. All mentors on this training program are independently funded, have experience in mentoring, and work on projects related to cancer therapy. The ancillary faculty are clinical partners on this proposal, who will educate on the clinical utilization of specific therapeutic modalities. Together, the mentors and ancillary faculty will provide training both through direct interactions and through specialized educational activities and course work for the Training Program. This Program will provide outstanding career development for trainees, as more emphasis is placed on translating basic scientific discovery into improved patient care. Logistically, the Training Program in Cancer Therapeutics has 19 mentors and 6 ancillary faculty. It is administered by the Principal Investigator and Administrative Committees, which are directed at training excellence and providing an ethnically and scientifically diverse group of trainees. The Training Program requests support for 6 postdoctoral and 2 predoctoral trainees. The program will be evaluated regularly through both internal and external review to ensure that the trainees are receiving the best possible training
Keywords: Cancers; Malignant Neoplasms; Malignant Tumor; Therapeutic; Training Programs; malignancy; neoplasm/cancer
Project start date: 2006-09-01
Project end date: 2011-08-31
Budget start date: 1-SEP-2010
Budget end date: 31-AUG-2011
5T32CA117846-05 (2010): $395220
5T32CA117846-04 (2009): $316191
5T32CA117846-03 (2008): $346294
THE RON RECEPTOR IN MAMMARY GLAND BIOLOGY
Susan E Waltz, Associate Professor
University Of Cincinnati, Sponsored Research Services, Cincinnati, Oh 45221
Grant 5R01CA100002-05 from National Cancer Institute
Abstract: The long-term objective of my research is to define the in vivo role of the receptor tyrosine kinase Ron in mammary gland biology. Virtually nothing is known regarding the function of Ron in the breast. However, recent studies have shown that Ron is over-expressed and highly phosphorylated in a large number of human and feline breast cancers. In order to define the in vivo significance of this receptor, my laboratory generated mice with a targeted ablation of the tyrosine kinase (TK) domain of Ron. Preliminary analysis of breast development in these mice lacking Ron signaling has pointed to a major, and largely unappreciated, role for the receptor tyrosine kinase Ron in mammary gland biology. Our preliminary studies indicate that Ron is required for the normal growth control of the mammary gland both during development and during tumorigenesis. The studies in this proposal are aimed at examining in greater detail, the role of this relatively unknown receptor in mammary development and tumorigenesis. The proposed studies will take the initial steps toward defining the underlying mechanism by which Ron influences mammary gland development and tumor biology in vivo. Our goal is to rigorously explore the following specific hypotheses i) Ron is an influential determinant in mammary gland development; ii) Ron signaling augments mammary gland tumorigenesis and metastasis; and iii) Ron over-expression in vivo leads to mammary transformation. In order to test these hypotheses, we have proposed three Specific Aims. Aim I is to define the contribution of Ron signaling in mammary gland development by localizing the sites of Ron synthesis and Ron action (stromal, epithelial or systemic). Aim II is to use a genetic approach to examine the in vivo impact of Ron signaling in the pathogenesis of oncogene-induced mammary gland tumors. For this aim we will analyze the role of Ron signaling and activation in mammary tumor formation and metastatic dissemination. In Aim III we will focus on understanding the role of Ron over-expression observed in human cancer by generating mouse models that mimic this conditions. In total, we hope to understand the role of a potentially important and unknown receptor in mammary biology with the hopes of ultimately impacting the treatment of human breast cancer
Keywords: (2, 6)-sialyl T antigen; ATP[{..}]protein-tyrosine O-phosphotransferase; Ablation; Autoregulation; Biology; Body Tissues; Breast; Breast Carcinoma; Breast Neoplasms; Breast Tumors; Cancer Genes; Cancer Induction; Cancer of Breast; Cancer-Promoting Gene; Cancers; Cell Communication and Signaling; Cell Signaling; Characteristics; Condition; Coupled; Development; Ductal; EPH- and ELK-Related Tyrosine Kinase; EPH-and ELK-Related Kinase; EPHA8; EphA8 Protein; Ephrin Type-A Receptor 8; Ephrin Type-A Receptor 8 Precursor; Epithelial; Epithelium; Event; Family Felidae; Felidae; Felids; Generalized Growth; Genetic; Genetically Engineered Mouse; Goals; Growth; Growth and Development; Growth and Development function; HEK3; Homeostasis; Human; Human, General; In Vitro; Influentials; Intracellular Communication and Signaling; Kinetic; Kinetics; Laboratories; Localized; Lung; Malignant Neoplasms; Malignant Tumor; Malignant Tumor of the Breast; Malignant neoplasm of breast; Mammals, Mice; Mammary Cancer; Mammary Carcinoma; Mammary Glands, Human; Mammary Neoplasms; Mammary Tumorigenesis; Mammary gland; Man (Taxonomy); Man, Modern; Metastasis; Metastasize; Metastatic Neoplasm; Metastatic Tumor; Mice; Mice, Transgenic; Morbidity; Morbidity - disease rate; Morphogenesis; Mortality; Mortality Vital Statistics; Murine; Mus; Neoplasm Metastasis; Numbers; Oncogenes; Oncogenesis; Organ; Organoids; PTK; PTK Receptors; PYMT; Pathogenesis; Pathway interactions; Phosphorylation; Physiological Homeostasis; Play; Polyoma Virus Middle T; Polyoma Virus Middle T Staining Method; Process; Protein Phosphorylation; Protein Tyrosine Kinase; Protein Tyrosine Kinase EEK; Purpose; RTK; Receptor Protein; Receptor Protein-Tyrosine Kinases; Receptor Signaling; Research; Respiratory System, Lung; Role; ST antigen; Secondary Neoplasm; Secondary Tumor; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Site; T Antigens; Testing; Therapeutic Intervention; Tissue Growth; Tissues; Transforming Genes; Transgenic Mice; Transmembrane Receptor Protein Tyrosine Kinase; Tumor Biology; Tumor Cell Migration; Tyrosine Kinase; Tyrosine Kinase Domain; Tyrosine Kinase Growth Factor Receptor; Tyrosine Kinase Linked Receptors; Tyrosine Kinase Receptors; Tyrosine-Protein Kinase Receptor EEK; Tyrosine-Specific Protein Kinase; Tyrosylprotein Kinase; Viral T Antigens; Viral Tumor Antigens; Virus Transforming Antigens; biological signal transduction; cancer metastasis; cancer progression; carcinogenesis; cell type; defined contribution; feline; hydroxyaryl protein kinase; in vivo; intervention therapy; malignancy; malignant breast neoplasm; mammary; mammary tumor; mouse model; neoplasm progression; neoplasm/cancer; neoplastic progression; ontogeny; pathway; pulmonary; receptor; receptor function; s-T antigen; sialosyl-T antigen; social role; tumor; tumor progression; tumorigenesis; tyrosyl protein kinase
Project start date: 2004-06-07
Project end date: 2010-04-30
Budget start date: 1-MAY-2008
Budget end date: 30-APR-2010
5R01CA100002-05 (2008): $0
5R01CA100002-04 (2007): $268531
5R01CA100002-03 (2006): $276552
5R01CA100002-02 (2005): $283208
1R01CA100002-01A1 (2004): $283208
3R01CA100002-01A1S1 (2004): $76036
HEPATOCYTE GROWTH FACTOR-LIKE PROTEIN RECEPTOR
Susan E Waltz, Associate Professor
University Of Cincinnati, Sponsored Research Services, Cincinnati, Oh 45221
Grant 5R01DK073552-10 from National Institute Of Diabetes And Digestive And Kidney Diseases
Abstract: The long-term objective of my research is to define the in vivo role of the receptor tyrosine kinase Ron in liver pathophysiology. Virtually nothing is known regarding the function of Ron in the liver. However, recent studies have shown that Ron signaling modulates hepatic responses in vivo. In order to define the in vivo significance of this receptor, my laboratory generated mice with a targeted ablation of the tyrosine kinase (TK) domain of Ron. These mice, referred to as TK-/- mice, display marked protection compared to control mice in a well characterized model of endotoxin (lipopolysaccharide, LPS) induced acute liver failure in galactosamine (GalN)-sensitized mice. In response to LPS/GalN, control mice exhibit profound hepatocellular injury evaluated by increases in serum aminotransferase levels and hemorrhagic necrosis of the liver. In contrast, the TK-/- mice have mild aminotransferase levels and relatively normal liver histology. The TK-/- mice also display a significant reduction in hepatocyte apoptosis compared to controls. Our preliminary data show that LPS/GalN treatment of TK-/- mice results in diminished levels of IFN-gamma an essential mediator of this injury model, as well as reduced amounts of select chemokines. The reduction in cytokine and chemokine production is associated with a decrease in the number of infiltrating neutrophils into the liver. Based on our preliminary data, this proposal will test the central hypothesis that Ron receptor signaling promotes the progression of acute liver failure by augmenting IFN-( and select chemokine production, leading to an increase in neutrophil recruitment, hepatocyte apoptosis and acute liver failure. In order to test this hypothesis, three specific aims are proposed. Aim I will delineate the Ron-dependent cell type-specific mechanism responsible for augmenting IFN-( levels. Aim II will define the Ron-dependent Kupffer cell-mediated mechanism required for promoting hepatocyte apoptosis. Aim III will establish the requirement for Ron-dependent chemokine production in neutrophil mobilization to the liver. In total, we hope to understand the role of a potentially important receptor in liver biology with the hopes of impacting the treatment of human liver disease
Keywords: ATP[{..}]protein-tyrosine O-phosphotransferase; Ablation; Acute Liver Failure; Alcoholic Liver Diseases; Aminotransferases; Animals; Apoptosis; Apoptosis Pathway; Biology; Blood Neutrophil; Blood Polymorphonuclear Neutrophil; Blood Segmented Neutrophil; Blood Serum; Blood leukocyte; Blood monocyte; Body Tissues; CXCL12; CXCL12 gene; CXCL12 protein; Cell Communication and Signaling; Cell Death, Programmed; Cell Function; Cell Process; Cell Signaling; Cell physiology; Cells; Cellular Function; Cellular Physiology; Cellular Process; Chemokine (C-X-C Motif) Ligand 12; Conditioned Culture Media; Conditioned Medium; Culture Media, Conditioned; Cytokines, Chemotactic; Cytotoxic cell; D-Galactose, 2-amino-2-deoxy-; Data; Development; Disease; Disorder; Dysfunction; EC 2.6.1; EPH- and ELK-Related Tyrosine Kinase; EPH-and ELK-Related Kinase; EPHA8; Edodekin Alfa; Endotoxins; EphA8 Protein; Ephrin Type-A Receptor 8; Ephrin Type-A Receptor 8 Precursor; Event; Exhibits; Fulminating Hepatic Failure; Fulminating Liver Failure; Functional disorder; Funding; Galactosamine; Gamma interferon; Genes; HEK3; HGF-like protein receptor; HLP receptor; Hepatic; Hepatic Cells; Hepatic Disorder; Hepatic Failure, Acute; Hepatic Failure, Fulminant; Hepatic Parenchymal Cell; Hepatocyte; Heterophil Granulocyte; Histology; Homologous Chemotactic Cytokines; Human; Human, General; IFN; IFN-Gamma; IFN-g; IFN-gamma-Inducing Factor; IFNG; IGIF; IL-1 Gamma; IL-12; IL-18; IL-1g; IL12; IL18 Protein; IL1F4; Injury; Intercrines; Interferon Gamma; Interferon Type II; Interferon gamma (human lymphocyte protein moiety reduced); Interferon, Immune; Interferon-gamma; Interferon-gamma-Inducing Factor; Interferons; Interleukin 18 (Interferon-Gamma-Inducing Factor); Interleukin 18 Proprotein; Interleukin-1 Gamma; Interleukin-12; Interleukin-18; Interleukin-18 Precursor; Intracellular Communication and Signaling; Investigation; K lymphocyte; Knowledge; Kupffer Cells; LPS; Laboratories; Leukocytes; Ligands; Lipopolysaccharides; Liver; Liver Cells; Liver Failure, Acute; Liver Failure, Fulminant; Liver diseases; Liver necrosis; MGC12320; MSP Receptor; MST1R; MST1R protein, human; Macrophage Stimulating 1 Receptor; Macrophage Stimulating Protein Receptor; Mammals, Mice; Man (Taxonomy); Man, Modern; Marrow Neutrophil; Marrow leukocyte; Marrow monocyte; Mediating; Mediator; Mediator of Activation; Mediator of activation protein; Mice; Modeling; Mononuclear; Morbidity; Morbidity - disease rate; Mortality; Mortality Vital Statistics; Murine; Mus; Myelogenous; Myeloid; Myeloid Cells; NK Cells; NKSF; Natural Killer Cell Stimulatory Factor; Natural Killer Cells; Necrosis hepatocellular; Neutrophil Infiltration; Neutrophil Recruitment; Neutrophilic Granulocyte; Neutrophilic Leukocyte; Obesity; PBSF; PTK; PTK Receptors; Phenotype; Physiopathology; Polymorph; Polymorphonuclear Cell; Polymorphonuclear Leukocytes; Polymorphonuclear Neutrophils; Pre-B Cell Growth Stimulating Factor; Principal Investigator; Process; Production; Programs (PT); Programs [Publication Type]; Protein Tyrosine Kinase; Protein Tyrosine Kinase EEK; Proteins; RON; RON protein; RON receptor protein tyrosine kinase; RTK; Receptor Protein; Receptor Protein-Tyrosine Kinases; Receptor Signaling; Regulation; Research; Reticuloendothelial System, Leukocytes; Role; SCYB12; SDF-1; SDF-1A; SDF-1B; SDF-1alpha; SDF1; SDF1A; SDF1B; SIS cytokines; STK protein tyrosine kinase; Sdf1 protein; Serum; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Steatohepatitis; Stellate Sinusoidal Macrophage; Stromal Cell-Derived Factor 1; Subcellular Process; System; System, LOINC Axis 4; T-Cells; T-Lymphocyte; TLSF-A; TLSF-B; TPAR1; Testing; Therapeutic Intervention; Thymus-Dependent Lymphocytes; Tissues; Transaminases; Transmembrane Receptor Protein Tyrosine Kinase; Tyrosine Kinase; Tyrosine Kinase Domain; Tyrosine Kinase Growth Factor Receptor; Tyrosine Kinase Linked Receptors; Tyrosine Kinase Receptors; Tyrosine-Protein Kinase Receptor EEK; Tyrosine-Specific Protein Kinase; Tyrosylprotein Kinase; Up-Regulation; Up-Regulation (Physiology); Upregulation; White Blood Cells; White Cell; adiposity; alcohol induced hepatic injury; alcohol induced liver disorder; alcohol induced liver injury; alcohol-induced hepatic dysfunction; alcohol-induced liver disease; alcohol-induced liver dysfunction; alcohol-mediated liver dysfunction; alcohol-mediated liver injury; base; biological signal transduction; body system, hepatic; c-Met-related Tyrosine Kinase; cell type; chemoattractant cytokine; chemokine; corpulence; corpulency; corpulentia; cytokine; disease/disorder; ethanol induced hepatic injury; ethanol induced liver disorder; ethanol induced liver injury; ethanol-induced hepatic dysfunction; ethanol-induced liver disease; ethanol-induced liver dysfunction; ethanol-mediated liver dysfunction; ethanol-mediated liver injury; expectation; fulminant hepatic failure; gene product; hIRH; hepatic necrosis; hepatocyte growth factor-like protein receptor; hepatopathy; human MST1R protein; human morbidity; hydroxyaryl protein kinase; in vivo; intervention therapy; lFN-Gamma; liver disorder; liver macrophage; macrophage; monocyte; mouse model; neutrophil; obese; obese people; obese person; obese population; organ system, hepatic; pathophysiology; programs; protective effect; recepteur d`origine nantais; recepteur d`origine nantais receptor; receptor; response; social role; stem cell-derived tyrosine kinase; stromal cell-derived factor-1alpha; thymus derived lymphocyte; tyrosyl protein kinase; white blood cell; white blood corpuscle
Project start date: 1999-07-01
Project end date: 2011-06-30
Budget start date: 1-JUL-2009
Budget end date: 30-JUN-2011
5R01DK073552-10 (2009): $288835
Sponsored Links Excellgen http://Excellgen.com
5R01DK073552-09 (2008): $288835
5R01DK073552-08 (2007): $294731
5R01DK073552-07 (2006): $303532
9R01DK073552-06A1 (2005): $310838
HEPATOCYTE GROWTH FACTOR LIKE PROTEIN RECEPTOR
Susan E Waltz, Associate Professor
Children´s Hospital Med Ctr (cincinnati)
3333 Burnet Ave
cincinnati, Oh 452293039
Grant 5R01HD036888-03 from Eunice Kennedy Shriver National Institute Of Child Health & Human Development IRG: MEP
Abstract: The long term goal of this proposal is to determine the in vivo function of the tyrosine kinase receptor known as Ron. Based on in vitro analyses, Ron has been postulated to have a critical role in cellular proliferation, dissociation and migration-processes important for normal organ function and regeneration following trauma. Additionally, Ron is thought be involved in liver function and in hematopoiesis, particularly in the development of macrophage, osteoclasts and megakaryocytes as well as in many aspects of the immune response including macrophage activation, antigen presentation and nitric oxide regulation. An association with Ron in the wound healing process has also been inferred by virtue of this receptor´s involvement in keratinocyte migration and proliferation. In an initial attempt to determine the function of Ron in vivo, mice were generated containing a targeted deletion of this gene. These mice however, die early during embryonic development. To circumvent the early embryonic lethality and to study the later functional significance of Ron in individual organs, a conditional knockout strategy involving the bacterial Cre/loxP recombinase system will be employed. By generating mice containing a tissue-restricted deletion of Ron in the liver, the role of this protein in the growth, development and regenerative processes of this organ will be directly accessed. Furthermore, the mice produced in these experiments will be used to examine the function of Ron in macrophage activation, inflammation and hematopoiesis. Secondly, the role of Ron in skin morphology and wound healing processes will be evaluated by producing a deletion of this receptor specifically in this organ. Finally, experiments are proposed to examine the consequences of a constitutively activated form of Ron on the normal growth and development of mice in vivo. These experiments should significantly aid in our understanding of the in vivo importance of this receptor tyrosine kinase in many of the processes outlined above
Keywords: cell growth regulation, growth factor receptor, hepatocyte growth factor, protein tyrosine kinase cell proliferation, developmental genetics, disease /disorder model, liver disorder, liver function, liver regeneration, macrophage, receptor expression, recombinase, skin, wound healing embryonic stem cell, gene targeting, laboratory mouse, transgenic animal
Project start date: 1999-07-01
Project end date: 2004-06-30
5R01HD036888-03 (2001): $188014
5R01HD036888-02 (2000): $182536
1R01HD036888-01A1 (1999): $177219
7R01HD036888-05 (2003): $211153
THE RON RECEPTOR/CHEMOKINE AXIS IN PROSTATE CANCER
Susan E Waltz
University Of Cincinnati, Sponsored Research Services, Cincinnati, Oh 45221
Grant 5R01CA125379-03 from National Cancer Institute
Abstract: Prostate cancer is the most common cancer in men in North America and the second leading cause of cancer-related deaths in males. The high mortality rate of this disease is mainly due to the metastatic spread of malignant cells. Compelling evidence suggests that angiogenesis is a critical factor regulating the growth and spread of cancer. However, a significant gap exists in our understanding of the genes that impact these processes. Our preliminary data show that prostate cancer cell lines and tumors produce angiogenic CXC chemokines through a mechanism dependent on NF-kB activation. The angiogenic chemokines produced by these prostate cancer cells induce endothelial cell chemotaxis and this effect is dependent upon the angiogenic chemokine receptor CXCR2. Moreover, we also demonstrate that the Ron receptor tyrosine kinase is highly expressed in human prostate tumors and prostate cancer cell lines. In addition, we show that a blockade of Ron signaling in prostate cancer cells inhibits angiogenic CXC chemokine production and results in the stabilization of the NF-kB inhibitory protein IkB. Utilizing gene-targeted mice, we also show that a functional loss of Ron or CXCR2 significantly delays prostate tumor development in vivo. Based on our preliminary data, this proposal will test the central hypothesis that Ron signaling promotes prostate tumor growth by stimulating angiogenic chemokine production leading to CXCR2-mediated angiogenesis. The studies in this proposal will focus on the unique role of the Ron-chemokine axis in regulating prostate tumor growth by (i) delineating the mechanisms responsible for the Ron-dependent regulation of angiogenic chemokine production, (ii) determining the impact of Ron signaling in prostate tumor growth in vivo, (iii) by examining the functional significance of the chemokine receptor, CXCR2, in prostate tumor growth and angiogenesis, and (iv) by validating the significance of Ron-mediated angiogenic chemokine production in prostate cancer cells on CXCR2-regulated angiogenesis. In total, we hope to understand role of the novel Ron-chemokine axis in the development and spread of prostate cancer and provide a scientific rationale for new diagnostic or treatment modalities for this disease. The research in this application will focus on a novel signaling pathway, driven by a protein termed the Ron receptor tyrosine kinase, in regulating the growth of prostate tumors. The goal of this proposal is to provide the scientific rationale to design new treatment strategies targeting this pathway for patients with prostate cancer
Keywords: 4q Chemokine; ATP[{..}]protein-tyrosine O-phosphotransferase; Adenocarcinoma; Adenoma, Malignant; Blood Vessels; Body Tissues; Bone; Bone and Bones; Bones and Bone Tissue; C-X-C Chemokines; CDw128b; CDw128b Antigens; CMKAR2; CXC Chemokine Receptor 2; CXC Chemokines; CXCR2; CXCR2 Protein; Cancer Cause; Cancer Etiology; Cancer cell line; Cancer of Prostate; Cancers; Cell Communication and Signaling; Cell Locomotion; Cell Migration; Cell Movement; Cell Signaling; Cells; Cellular Migration; Cessation of life; Characteristics; Chemokine (C-X-C) Receptor 2; Chemotaxis; Cytokines, Chemotactic; Data; Death; Development; Disease; Disorder; EPH- and ELK-Related Tyrosine Kinase; EPH-and ELK-Related Kinase; EPHA8; Endothelial Cells; EphA8 Protein; Ephrin Type-A Receptor 8; Ephrin Type-A Receptor 8 Precursor; Epithelial; Epithelial Cells; Event; Extraprostatic; GRO/MGSA Receptor; Gene Targeting; Generalized Growth; Genes; Genital System, Male, Prostate; Goals; Growth; Growth Factor Receptors; Growth and Development; Growth and Development function; HEK3; High Affinity Interleukin 8 Receptor Type B; Homologous Chemotactic Cytokines; Human; Human Prostate; Human Prostate Gland; Human, General; IL-8RB; IL-8Rbeta; IL8 Receptor Type 2; IL8R2; IL8RB; IL8RB gene; Immunocompromised; Immunocompromised Host; Immunocompromised Patient; Immunoglobulin Enhancer-Binding Protein; Immunosuppressed Host; In Vitro; Intercrines; Interleukin 8 Receptor Beta; Interleukin 8 Receptor Type 2; Interleukin-8 Receptor Type B; Interleukin-8 Receptors B; Interleukin-8B Receptor; Intracellular Communication and Signaling; Kinetic; Kinetics; Literature; Lung; Malignant Cell; Malignant Neoplasms; Malignant Tumor; Malignant Tumor of the Prostate; Malignant neoplasm of prostate; Malignant prostatic tumor; Mammals, Mice; Man (Taxonomy); Man, Modern; Mediating; Membrane; Metastasis; Metastasize; Metastatic Neoplasm; Metastatic Tumor; Metastatic to; Mice; Modality; Modeling; Mortality; Mortality Vital Statistics; Motility; Motility, Cellular; Murine; Mus; NF-kB; NF-kappa B; NF-kappaB; NFKB; Neoplasm Metastasis; North America; Nuclear Factor kappa B; Nuclear Transcription Factor NF-kB; Organ; PC3 cell line; PTK; PTK Receptors; Pathogenesis; Pathway interactions; Patients; Peptides; Phosphorylation; Primary Neoplasm; Primary Tumor; Process; Production; Prostate; Prostate CA; Prostate Cancer; Prostate Gland; Prostate Neoplasms; Prostatic Cancer; Prostatic Gland; Prostatic Neoplasia; Prostatic Neoplasms; Prostatic Parenchyma; Prostatic Tissue; Protein Phosphorylation; Protein Tyrosine Kinase; Protein Tyrosine Kinase EEK; Proteins; Proto-Oncogene, Growth Factor Receptor; Publishing; RTK; Receptor Activation; Receptor Protein; Receptor Protein-Tyrosine Kinases; Receptor Signaling; Receptors, CXCR2; Regulation; Research; Respiratory System, Lung; Role; SIS cytokines; Secondary Neoplasm; Secondary Tumor; Severities; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Targetings, Gene; Testing; Therapeutic; Tissue Growth; Tissues; Transcription Factor NF-kB; Transgenic Organisms; Transmembrane Receptor Protein Tyrosine Kinase; Tumor Cell; Tumor Cell Migration; Tumor of the Prostate; Tyrosine Kinase; Tyrosine Kinase Growth Factor Receptor; Tyrosine Kinase Linked Receptors; Tyrosine Kinase Receptors; Tyrosine-Protein Kinase Receptor EEK; Tyrosine-Specific Protein Kinase; Tyrosylprotein Kinase; Vascularization; alpha-Chemokines; angiogenesis; base; biological signal transduction; bone; cancer cell; cancer metastasis; cancer progression; cancer type; cell motility; chemoattractant cytokine; chemokine; chemokine receptor; density; design; designing; disease/disorder; experiment; experimental research; experimental study; functional loss; gene product; hydroxyaryl protein kinase; immunosuppressed patient; in vivo; inhibitor; inhibitor/antagonist; kappa B Enhancer Binding Protein; male; malignancy; membrane structure; men; men`s; migration; neoplasm progression; neoplasm/cancer; neoplastic cell; neoplastic progression; neutralizing antibody; new diagnostics; next generation diagnostics; novel; novel diagnostics; nuclear factor kappa beta; ontogeny; overexpression; pathway; prostate cancer cell line; public health relevance; pulmonary; receptor; receptor binding; research study; social role; transgenic; treatment strategy; tumor; tumor growth; tumor progression; tyrosyl protein kinase; vascular
Project start date: 2008-09-01
Project end date: 2013-07-31
Budget start date: 27-AUG-2010
Budget end date: 31-JUL-2011
PFA/PA: PA-07-070
5R01CA125379-03 (2010): $1
5R01CA125379-02 (2009): $323700
Sponsored Links Excellgen http://Excellgen.com
1R01CA125379-01A2 (2008): $323700
BIOLOGY OF HEPATOCYTE GROWTH FACTOR-LIKE PROTEIN
Susan E Waltz, Associate Professor
Children s Hospital Med Ctr (cincinnati) 3333 Burnet Ave Cincinnati, Oh 452293039
Grant 1F32DK009466-01 from National Institute Of Diabetes And Digestive And Kidney Diseases IRG: MEP
1F32DK009466-01 (1996): $23700