New Evidence Links Inflammation and Increased Prostate Cancer Risk

UCLA researchers, and collaborators, have discovered a previously unrecognized type of progenitor cell that, though rare in most regions of the human prostate, is found in uncommonly high numbers in inflamed areas of the gland. These progenitor cells have the ability to initiate prostate cancer in response to genetic changes. The study results suggest inflammation increases overall risk for the disease by increasing the available pool of progenitor cells that can develop into prostate cancer. Scientists have known that one of the risk factors for high-grade prostate cancer is chronic inflammation of the prostate (a process in which cells from the immune system have taken up residence in the gland), but they have been unsure how this process led to cancer. UCLA-led research previously showed that two different types of cells, known as basal and luminal cells, represented potential progenitor cells and, with varying degrees of aggressiveness, could initiate prostate cancer. Further research by colleagues at Johns Hopkins Medical Center observed that prostate cells in the proximity of inflammation appeared different under the microscope and expressed different genes, leading to the hypothesis that they were more likely to proliferate than prostate cells from areas without inflammation. The UCLA-led team was able to test this hypothesis in human cells and found that cells from areas with inflammation are progenitor cells that can initiate aggressive tumors, validating their previous hypothesis and laying the foundation for the new study. Led by Dr. Andrew Goldstein, an Assistant Professor of Molecular Biology, the UCLA researchers investigated the CD38 gene, which is expressed by most (but not all) luminal cells in the human prostate.
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