By Min Kyung-Tai, Karen Chang
Animal experiments have contributed a lot to our figuring out of mechanisms of ailment and are important for identifying new treatments. This quantity studies the most recent examine and advancements during this box. * Discusses new discoveries, methods, and ideas * Contributions from major students and specialists * Reference consultant for researchers excited about molecular biology and comparable fields
Read Online or Download Animal Models of Human Disease, Volume 100 (Molecular Biology and Translational Science) PDF
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Additional info for Animal Models of Human Disease, Volume 100 (Molecular Biology and Translational Science)
The prostates expressing c-Myc exhibit a high rate of proliferation and apoptosis. However, c-Myc induced high rate proliferation overcomes the apoptosis and results in rapid development of PIN. In addition, expression of c-Myc also increases angiogenesis; increased vascular density has been detected in the prostate as early as in 2-month-old transgenic animals. The PIN lesions progress to invasive adenocarcinomas by 3–6 months in the Hi-Myc mice and by 10–12 months in the Lo-Myc mice, suggesting that 16 FEN WANG progression of the disease is c-Myc expression level dependent.
Docking of FGF releases FGFR from negative restrictions imposed by interaction with heparan sulfate chains of heparan sulfate proteoglycans (HSPG) resulting in an active conformation where adjacent kinases maintain an enzymesubstrate relationship. Positions of the four major tyrosine phosphorylation sites on the FGFR are indicated. II, Ig-loop II; III, Ig-loop III; F, FGF; K, kinase domain; circles, monosaccharides of heparan sulfate chains; solid bar, plasma membrane. MOUSE MODELS OF HUMAN PROSTATE CANCER 29 Four highly conserved genes (Fgfr1, Fgfr2, Fgfr3, and Fgfr4) encode the FGFR.
60 The mice develop tumors within VP and DP at first, rapidly grow in the pelvic region, and then metastasis to lymph nodes and distant sites. About 75% of heterozygous and 100% of homozygous transgenic males develop prostate tumors. The tumorigenesis and progression is androgen independent, since castration shortly after prostate morphogenesis does not prevent tumor development. The advanced tumors exhibit both NE and epithelial phenotypes, but the epithelial differentiation markers are often lost early in tumorigenesis.