It is well-known that inflammation is commonly associated with cancer and may be a key trigger of carcinogenesis and tumor growth. It is also known that tumor cells exhibit many physical and molecular features of cells during organ development. We have found that inflammatory mediators are highly expressed during normal development and play a significant role in organogenesis by promoting proliferation. Second, the proliferative effect of interleukin is reiterated in the adult during inflammation. Finally, the mechanism by which IL-1 induces proliferation during prostate development and inflammatory repair is the paracrine production of bona fide developmental mediators, particularly the insulin-like growth factors (IGFs) and transforming growth factors (TGFs). These results demonstrate clear interplay between inflammatory and developmental signaling networks. We now seek to understand how these signaling interactions promote epithelial proliferation and allow damaged cells to escape cell death in the inflamed prostate. Currently, my lab has three main specific projects: The role of IGF-1 in inflammation-induced epithelial survival and proliferation; 2, investigating small heat-shock chaperones that promote apoptotic or autophagic escape during inflammatory reactive hyperplasia in the prostate; 3 investigating how androgen and IL-1 cooperatively promote prostatic growth by STAT-3 dependent IGF-1 signaling.
