Sentence examples for mouse prostate and from inspiring English sources

The treatment was found to have minimal or no effects on normal prostatic epithelial cells in the mouse prostate and on benign prostate epithelial cells (e.g. BPH-1) arrested in a growth-quiescent state, which is the state most normal epithelial cells are in in vivo (20, 21).

Furthermore, we found G-1 to have little or no effects (weight and histology) on mouse prostate and on growth-quiescent immortalized benign prostatic epithelial cells in cultures.

Interestingly, the sequence specificity of siRNA allowed here discriminating in vivo the closely related mouse and human AR mRNAs: treatment with hAR-siRNA silenced AR in tumor cells and inhibited the tumor growth while preserving AR expression in mouse prostate and testes.

Doll and colleagues reported that exogenous rPEDF protein induced tumor epithelial apoptosis in mouse prostate and pancreas [ 13].

It has been reported that the gene expression pattern is largely different between mouse prostate and human prostate [ 57].

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).

To our knowledge, this report provides the first demonstration for a role of Tyr-phosphorylated AKT in its compartmentalization, which allowed us to delineate its critical role in AKT kinase activation, its potential to initiate neoplasia in mouse prostates and promote disease progression in human breast cancers.

As shown in Fig 5A, we successfully isolated the PrSCs from Pten+/+ and Pten+/− mouse prostates and established the AR siRNA knockdown stromal cells.

RNA from microdissected mouse prostate stroma and epithelium, and human prostate fibroblast (PSC27) were used as template for qRT-PCR.

Mouse prostate lobes and tissue recombinants were dissected and fixed in 10% phosphate-buffered formalin overnight, transferred to 50% ethanol, then embedded in paraffin.

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].