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Dr. Ratliff’s laboratory focuses on understanding immune regulation and the development of alternative approaches to treating urologic cancers, primarily bladder and prostate cancers, through the modulation of anti-cancer immunity. Current studies focus on prostate inflammation, its immune regulation and its impact on prostate stem cells, gene expression in prostate tissue, and cancer development. The intent is to develop a better understanding of the inflammatory factors contributing to cancer development and to use the information gained to develop novel approaches to treating prostate cancer through modulation of the immune response. Genetically modified mouse models are used to probe inflammation, immune regulation, the development of autoimmunity and anticancer effector mechanisms. Regulatory cells termed myeloid-derived suppressor cells have been linked to regulation of prostate inflammation and are observed early in genetically modified mouse spontaneous prostate tumor models. Determining how to control myeloid-derived suppressor cell function is a focus that is anticipated to provide a new approach to augmenting antitumor immunity. Likewise, understanding the impact of inflammation on prostate stem cells is anticipated to advance knowledge about the mechanisms of prostate growth and cancer development.
Studies to understand aspects of cholesterol metabolism on prostate cancer growth are an active component of our research activities. Cholesterol sulfate is an important metabolite of cholesterol in prostate cancer. Cholesterol is converted to cholesterol sulfate by the sulfotransferase enzyme, SULT2B1b. We observe the induction of apoptosis if SULT2B1b is eliminated from prostate cancer cells. The apoptotic cascade appears to be initiated through the androgen receptor. Current studies are focused on understanding the mechanisms by which elimination of SULT2B1b initiates apoptosis.
Studies to improve the treatment of bladder cancer through the development of nano-delivery approaches for intravesical therapy are in progress. The fibronectin binding protein, previously identified as an important attachment protein for mycobacteria, was observed to mediate antitumor activity in a bladder tumor model and alter the bladder inflammatory process. The fibronectin binding protein has the capacity to deliver nanoparticles to bladder cancer cells is being tested as a new approach for delivery of therapeutic agents for the treatment of superficial bladder cancer. The approach has the potential to not only treat superficial bladder cancer but also to treat a bladder inflammatory condition termed interstitial cystitis.
More basic studies focus on the impact of platelet-derived immunomodulatory molecules on the adaptive immune response. Precursor frequency of antigen specific T and B lymphocytes is very low prior to antigenic recognition and clonal expansion of the reactive cells. Control of pathogenic microbes early in the infection period is linked to innate immunity prior to clonal expansion of antigen specific adaptive immunity. Studies in the Ratliff laboratory implicate platelet-derived ligands as mediators of the early amplification of the adaptive immune compartment. Ratliff’s team hypothesizes that platelet-derived ligands are the earliest signals to the adaptive immune compartment that enables rapid and ultimately optimal expansion of the adaptive immune response to the invading microbe. Studies are in progress to fully characterize the role of platelets in the modulation of adaptive immunity.
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Frontiers in Immunology (2024): 1354735-1354735
Soonbum Kwon,Fanfei Meng,Hassan Tamam,Hytham H Gadalla,Jianping Wang, Boyang Dong, Amber S Hopf Jannasch,Timothy L Ratliff,Yoon Yeo
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