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The study was published online in the journal Disease Models & Mechanisms and will appear in the November 2012 print edition in an articletitled, "Initiation of prostate cancer in mice by Tp53R270H:Evidence for an alternate molecular progression." "Our team found a molecular pathway to prostate cancer thatdiffers from the current conventional wisdom of how the diseasedevelops," said Alexander Borowsky, associate professor ofpathology and laboratory medicine and principal investigator of thestudy. "With this new understanding, research can go in newdirections to possibly develop new diagnostics and refinetherapy." Prostate cancer is the leading cancer diagnosis in men in theUnited States. Although it is curable in about 80 percent of menwith localized disease, the rate is much lower if the cancer ishighly virulent and has spread beyond the prostate gland. The investigators developed a mouse model genetically engineered tohave a mutation in the "tumor suppressor" gene, p53,specifically in the cells of the prostate gland. These mice weresignificantly more likely to develop prostate cancer than controlmice without the mutation, and provided the first indication thatthe p53 mutation could be involved in the initiation of prostatecancer. They also note that the mutation of p53 in the prostatediffers from loss or "knock-out" of the gene, whichsuggests that the mechanism is more complicated than simply a"loss of tumor suppression" and appears to involve anactively oncogenic function of the mutant gene. The p53 gene encodes for a protein that normally acts as a tumorsuppressor, preventing the replication of cells that have sufferedDNA damage. Mutation of the gene, which can occur throughchemicals, radiation or viruses, causes cells to undergouncontrolled cell division. The p53 mutation has been implicated inthe initiation of other malignancies, including breast, lung andesophageal cancers. Other studies have associated p53 mutation with disease progressionin prostate cancer, but this is the first to find that it can havea role in the early initiation of prostate cancer, as well. Until now, understanding of the role of p53 was that mutationoccurred exclusively as a late event in the course of prostatecancer. Based on the findings in the new mouse model that theresearchers developed, p53 mutation not only can initiate prostatecancer but might also be associated with early progression towardmore aggressive forms of the disease. Genetic mutations can initiate cancers in a variety of ways. Thoseinclude promotion of uncontrolled cell growth and loss of thegene's normal cell growth-suppressor functions. Exactly how the p53mutation promotes the initiation and progression of prostate cancerremains to be clarified and is a focus of current research by theUC Davis team. They also are trying to gain an understanding of howthe p53 mutation affects the effectiveness of standard treatmentsfor prostate cancer, such as radiation and hormone therapy. Another application of the discovery could be the development of anew diagnostic test for prostate cancer based on the presence ofthe p53 mutation as a biomarker. "Knowing that prostate cancer can develop via p53 mutationopens new opportunities for researchers in the field," saidBorowsky. "This is a game-changer in the understanding ofprostate cancer." Other UC Davis study authors were Ralph de Vere White and RuthVinall of the Department of Urology, and Jane Qian Chen, N.E.Hubbard and Shola Sulaimon of the Center for Comparative Medicine.Borowsky is also affiliated with the UC Davis Center forComparative Medicine. I am an expert from skf16.com, while we provides the quality product, such as China Combined Roller Bearing , China Thrust Roller Bearing , Spherical Roller Bearing,and more.
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