Download Animal Models of Human Disease, Volume 100 (Molecular by Min Kyung-Tai, Karen Chang PDF

By Min Kyung-Tai, Karen Chang

Animal experiments have contributed a lot to our knowing of mechanisms of sickness and are important for settling on new treatments. This quantity studies the most recent study and advancements during this box. * Discusses new discoveries, methods, and concepts * Contributions from top students and specialists * Reference advisor for researchers desirous about molecular biology and similar fields

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Extra info for Animal Models of Human Disease, Volume 100 (Molecular Biology and Translational Science)

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Interestingly, ARR2PBi-caFGFR1 transgenic mice that express caFGFR1 at high levels with the ARR2PB promoter develop high-grade PIN within 8 months (Fig. 4). Foci with cribriform structures in acini lumen and epithelial cells pushing through stromal compartments are common features throughout the ARR2PBi-caFGFR1 prostate. Most epithelial cells in high-grade PIN foci fail to express cytokeratins that are differentiation markers of luminal epithelial cells of the prostate. In high-grade PIN foci, stromal cells surrounding the epithelial cells also fail to express a-actin, a characteristic marker associated with differentiated SMCs.

VI. Androgen Signaling Disruption Models A. AR Mutant Models The prostate is an androgen-dependent organ; androgen deprivation induces massive apoptosis in the epithelium within 2 days, and the prostate atrophies in 2 weeks. Androgen replenishment quickly induces prostate epithelial cells to undergo proliferation, and the atrophied prostate regenerates and recovers to its original volume and morphology within 2 weeks. Like a normal prostate, prostate cancers at early stages are also androgen responsive.

85 Interestingly, ablation of the AR in both epithelial MOUSE MODELS OF HUMAN PROSTATE CANCER 27 and stromal compartments of the TRAMP prostate results in smaller primary prostate tumors with lower proliferation rates,85 which is in contrast to the epithelial AR ablation that results in larger primary prostate tumors with higher proliferation rates. The results suggest that stromal AR play a more dominant role than epithelial AR to promote tumor cell proliferation. Similar to AR knockout in the epithelium, AR knockout in both stroma and epithelium significantly increases intermediate cell populations in the tumors, suggesting AR signals in the epithelium promotes epithelial cell differentiation.

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