RETINOBLASTOMA GENE IN INFLAMMATION AND CANCER

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 该项目建议检查驱动炎症介导的致癌的信号通路。研究表明，视网膜母细胞瘤蛋白(PRB)的过度磷酸化和失活与一氧化氮诱导的炎症和肿瘤的发生有关。这一过程的功能意义将在培养的细胞中进行检验。此外，将确定pRb多肽的过度磷酸化位置，并将在活体小鼠模型中评估pRb过度磷酸化对结肠炎到癌症序列的生理作用。霍塞斯博士的研究将对一氧化氮等促炎因子如何促进肿瘤的发生产生重要的机械论见解。

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.