Normally growth suppressive in epithelial cells, the transforming growth factor beta superfamily has been shown to be disrupted in many types of cancers. Bone Morphogenetic Protein (BMP), a member of the transforming growth factor beta superfamily has been found to be intact and growth suppressive in a variety of cancers, but it has been found to be targeted for mutation in the colon cancer predisposition syndrome Juvenile Polyposis, and little is known about its role in colon cancer. In this dissertation, we attempt to understand what role the BMP signaling pathway plays in colon cancer. We aimed to do this by: a) determining if the BMP pathway is intact in microsatellite stable and unstable colon cancer cell lines and tissues, b) determining if the Ras pathway affects BMP signaling, and c) examining SMAD4-independent means of BMP signaling. We found that while the BMP pathway was intact in many of the colon cancer cell lines examined, the RAS pathway interfered with transmission of SMAD signaling to the nucleus. BMP2 was shown to increase the stability of p21, and the RAS/ERK pathway acts to dull the growth suppressiveness and decrease the stability of p21. Additionally, we found that in the absence of SMAD4, which is targeted for mutation in Juvenile Polyposis and some types of colon cancers, that BMP treatment becomes growth proliferative over time by decreasing cellular levels of PTEN through the RAS/ERK pathway. Our results suggest that while the BMP pathway is often intact in colon cancer cell lines, its effects are modulated by other signaling pathways