RETINOBLASTOMA GENE IN INFLAMMATION AND CANCER

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project proposes to examine the signaling pathways that drive inflammation-mediated carcinogenesis. It has been shown that hyperphosphorylation and inactivation of the retinoblastoma protein (pRb) is associated with nitric oxide-induced inflammation and tumorigenesis. The functional significance of this process will be examined in cultured cells. Furthermore, the sites of hyperphosphorylation on the pRb polypeptide will be determined, and the physiological role of pRb hyperphosphorylation on the colitis-to-cancer sequence will be assessed in mouse models in vivo. Dr. Hofseths studies will generate important mechanistic insights into how pro-inflammatory factors, such as nitric oxide, promote tumorigenesis.