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A critical feature of tumor development is the ability of tumor cells to undergo autocrine and/or paracrine growth factor stimulation. This phenomenon allows tumors to grow progressively and causes them to become resistant to conventional treatments such as radiation therapy and chemotherapy. Moreover, once a tumor becomes resistant to these treatments it may become invasive and metastasize, leading to tumor progression and death. Most solid tumors contain varying degrees of neovascularization and a subpopulation of tumor cells often proliferate in association with and in response to the angiogenic phenotype. Therefore, understanding the molecular mechanisms underlying the regulation of tumor cell growth in the context of the tumor microenvironment would lead to new therapeutic strategies for the treatment of cancer. In previous years the PI has discovered and characterized several proteins that are expressed in cancer cells that regulate the angiogenic phenotype and tumor growth. These include the co-amplification of the transcriptional activation domains of myc and ras in hematopoietic malignancies that result in overexpression of the myc and ras genes and the upregulation of genes that are implicated in angiogenesis and cell adhesion. More recently, the PI has identified the Aurora-A kinase as an additional transcriptional co-activator that regulates gene expression involved in tumorigenesis. Based on these studies, the PI hypothesizes that ras-associated kinases regulate gene expression in tumor cells and are required for tumor growth and angiogenesis. In the next grant period, the PI will continue to test the hypothesis that ras-associated kinases regulate gene expression in tumor cells and are required for tumor growth and angiogenesis. In addition, the PI hypothesizes that the ras-related GTP-binding protein, HRas, is required for normal hematopoietic cell function and that the ras-related GTP-binding protein, HRas, is required for normal hematopoietic cell function. Specifically, she proposes to (1) characterize the function of HRas in hematopoietic cells and its effect on the hematopoietic stem cell niche, (2) d