By Min Kyung-Tai, Karen Chang
Animal experiments have contributed a lot to our realizing of mechanisms of sickness and are very important for picking new cures. Animal types of Human sickness reviews the newest learn and advancements during this field.
- Discusses new discoveries, methods, and ideas
- Contributions from major students and experts
- Reference advisor for researchers thinking about molecular biology and comparable fields
Read or Download Animal Models of Human Disease, Volume 100 (Progress in Molecular Biology and Translational Science) PDF
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Extra info for Animal Models of Human Disease, Volume 100 (Progress in Molecular Biology and Translational Science)
4). At the age of 20 months or older, the transgenic mice have a prostate that is MOUSE MODELS OF HUMAN PROSTATE CANCER A B C D E F 33 FIG. 4. Dosage-dependent activity of ectopic FGFR1 in induction of prostatic intraepithelial neoplasia. Paraffin sections prepared from the indicated wild-type or transgenic mice expressing constitutively active FGFR1 in the prostate epithelium were H&E stained to demonstrate tissue structures. (A) 30-week-old wild-type mouse; 30-week-old PB-caFGFR1 transgenic mouse; C&D, 25-month-old PB-caFGFR1 transgenic mice; E&F, 30-week-old ARR2PBi-caFGFR1 mice.
The affected stroma consists primarily of the SMC component. The epithelial cells exhibit papillary hyperplasia with atypia displayed in the FGF8b transgenic mice. 122 In addition to late age-related development of typical adenocarcinoma, the FGF8b/Ptenþ/À mice also displays a low incidence of mucinous adenocarcinoma, a rare variant type of human prostatic adenocarcinoma. Thus, the results demonstrate the cooperation between FGF8b overexpression and Pten deficiency in prostate tumorigenesis. 124,125 Forced expression of FGFR1 in premalignant rat prostate tumor cells, DT3 from the Dunning 3327 tumors, accelerates progression of the cells to malignancy in a time-dependent manner.
118 Furthermore, inactivation of one Fgf2 allele also significantly suppresses TRAMP tumorigenesis and progression, suggesting that FGF2 promotes prostate tumorigenesis and progression in a gene dosage-dependent manner. 119 The FGF3 transgenic mice develop extensive prostate hyperplasia; all prostatic lobes exhibit epithelial stratification, cribriform structures, and papillary tufts. The cell proliferation activity in the epithelial compartment is significantly increased. The luminal epithelial cells display increased nuclear-to-cytoplasmic ratios but retain relatively uniform nuclear AR and the tumor suppressor C-CAM1 staining.