Sentence examples for mouse prostate results from inspiring English sources

Wang et al. showed that targeted disruption of FoxP3 (a gene that is critical to the development of regulatory T cells) in the mouse prostate results in the overexpression of Myc, prostatic hyperplasia, and PIN[86].

It has been shown that ETK overexpression can increase proliferation in mouse prostate epithelium and result in development of prostatic intraepithelial neoplasia (PIN) partly by increasing AKT and STAT3 activity [13].

Genetic disruption of PPARγ or PPARγ2 signaling in mouse prostate epithelial cells resulted in dysregulated expression patterns of peroxisomal and mitochondrial genes whose products are involved in lipid transportation and oxidation pathways.

The results obtained indicate that putative mouse prostate stem cells are likely to reside in the basal layer.

Histopathologic characterization indicates that PPARγ is a regulator of mouse prostate epithelial cell differentiation and that its loss results in generally progressive mPIN.

Autophagy accompanied the altered cellular proliferation and differentiation that resulted from PPARγ-deficiency in mouse prostate models.

The loss of TGF-β responsiveness in fibroblasts resulted in intraepithelial neoplasia in mouse prostate and invasive squamous cell carcinoma of the forestomach (Bhowmick et al. 2004).

The results showed restoration of PPAR γ2 rescues and drives mouse prostate benign epithelial cell differentiation associated with AR activation.

These results suggest that iASPP deficiency is unlikely to grossly affect mouse prostate development.

We employed the murine transgenic adenocarcinoma of the mouse prostate (TRAMP) model, in which prostate-specific expression of SV40 large T antigen results in prostate cancer (Greenberg et al., 1995), to evaluate the role of NR2F6 in cancer immunity.

These results suggest that PTEN is required for TRAIL-induced apoptosis in mouse prostate epithelial cells.