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High-probability grants
According to our matching algorithm, Noel P. Bouck is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 — 1992 |
Bouck, Noel P |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Genetic Analysis of Malignant Transformation @ Northwestern University
It is the long term goal of these experiments to define, eventually at the molecular level, the mechanisms by which malignant transformation is induced and the mechanisms by which it is suppressed. Direct induction of transformation in hamster cells by methylating agents which are carcinogenic but not mutagenic will be measured and correlated with alterations in cellular DNA methylation levels and with tumorigenicity to determine if methylation-associated changes in gene regulation can be responsible for carcinogenesis. Cell fusions will be performed among hamster cells and between hamster and human cells which have been treated to induce tetraploidy in order to determine if the suppression of neoplastic transformation observed in fusions between normal and transformed diploid cells can be overcome by increased dosage of transformed cell chromosomes. DNA from tumor cell lines will be transfected into an unusual BHK hamster cell line which is unable to suppress transformation in order to attempt to detect and identify human oncogenes which are distinct from those isolated to date from human cells either in the way in which they are regulated or in their primary sequence. A dominant selective marker will be introduced to normal human chromosome #1 and used as a marker in cell fusions designed to test whether or not this human chromosome can suppress the malignancy of human tumor cell lines.
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1 |
1990 — 1999 |
Bouck, Noel P |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Tumor Suppressor Genes and Angiogenesis @ Northwestern University
As normal cells progress towards tumorigenicity they must switch to an angiogenic phenotype in order to attract the nourishing new blood vessels on which their progressive growth depends. In human cells of glial or fibroblast origin this essential shift to an angiogenic phenotype requires loss of a tumor suppressor gene and results from a decrease in the secretion of an inhibitor of angiogenesis, thrombospondin-1 (TSP-1). Small peptides derived from the large TSP-l molecule are also potent inhibitors of neovascularization. This proposal outlines experiments designed to (l) test the in vivo efficacy of TSP-1 by examining its ability to slow tumor growth and angiogenesis when over and under expressed in human glioblastoma lines and by testing the effect of high levels of circulating TSP-1 on the growth of lung metastases; (2) use substituted peptides to define the specific amino acid residues that are necessary to the inhibitory activity of TSP-l peptides; (3) examine hallmarks of endothelial cell activation at the cell surface and in the nucleus to determine if TSP-1 and its peptides make endothelial cells unable to respond to angiogenic factors by blocking the propagation of positive signals; and (4) isolate another naturally occurring protein that inhibits angiogenesis and whose production depends on the retinoblastoma tumor suppressor gene. It is our hope that these experiments will increase our understanding of endothelial cell activation and its inhibition, prepare TSP-1 and its peptides for development as clinical anti-tumor agents and identify additional antiangiogenic proteins that will shed light on the function of tumor suppressor genes and may be of eventual clinical utility.
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1 |
1994 — 1998 |
Bouck, Noel P |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Switching On of Angiogenesis During Tumor Progression @ Northwestern University
neoplastic process; thrombospondins; neoplasm /cancer genetics; tumor suppressor genes; angiogenesis; fibrosarcoma; phenotype; molecular genetics; alleles; genetic promoter element; genetic regulation; reporter genes; human tissue; laboratory mouse; genetically modified animals; transfection; fibroblasts; nuclear runoff assay;
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1 |
1999 — 2000 |
Bouck, Noel P |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Antiangiogenic Barriers to Tumor Development @ Northwestern University
DESCRIPTION (Adapted from investigators abstract): All tumors must overcome an angiogenic barrier as they progress to malignancy. This barrier is maintained by a variety of molecules that are natural inhibitors of angiogenesis and serve to block the sprouting of new blood vessels in most normal adult tissues. The PI has recently discovered a new and exceptionally potent natural inhibitor of angiogenesis that is highly expressed in the normal retina , but lost in several pediatric tumors and identified it as a 50 kDa protein that had been previously cloned in another context. This proposal outlines experiments designed to understand how this inhibitor works, how it is regulated during tumor progression and what role it plays in the angiogenesis associated with childhood malignancies and in eye diseases. The mechanism by which the new inhibitor blocks angiogenesis will be identified along with the site on the protein that mediates its anti-angiogenic activity. This new inhibitor is unique among the previously identified inhibitors in that its production by cells is inhibited by hypoxia, so the mechanism underlying this suppression will be studied to determine if it is widespread, if it is dependent on an oxygen sensor and to learn the molecular level at which control is exerted. To determine the general function of this protein, a mouse expressing beta-galactosidase in its place is being produced and will be used to investigate expression patterns and effects of loss of the inhibitor on gross and microscopic anatomy, on normal vascular development, and on tumorigenesis. Finally the expression of the anti-angiogenic protein will be examined in a murine model of retinopathy and in neuroblastoma tumors and its ability to control the angiogenic phenotype of primary tumors, their explants and tumor cell lines determined. These experiments will enhance our understanding of how tumors develop and maintain their essential angiogenic phenotype. They have the exciting possibility of defining a new anti-angiogenic agent capable of controlling the growth of vessels that feed malignant tumors and cause the devastating ocular angiogenesis that is a leading cause of blindness.
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1 |