This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.In this project, Dr. Baudino will follow up on his recent observation that haplo-insufficiency of c-MYC leads to a profound decrease in tumorigenesis in the ApcMin/+ mouse. Furthermore, this decrease is associated with altered expression of angiogenic factors in tumors, suggesting that c-MYC is a central regulator of factors responsible for cell proliferation, angiogenesis, and tumorigenesis. Dr. Baudino will examine and compare expression of both pro- and anti-angiogenic regulators (e.g., HuR, VEGF, Ang-2, ephrin-A2, Eph-A2, and Eph-B2) in ApcMin/+ c-myc+/+ vs. ApcMin/+ c-myc+/- mice, and determine the mechanisms involved. Furthermore, he will define the physiological impact of c-myc regulation of these factors and assess the roles of both the c-myc and N-myc genes in neoplasia of the intestinal tract.
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