Journal
DIFFERENTIATION
Volume 76, Issue 6, Pages 606-623Publisher
ELSEVIER SCI LTD
DOI: 10.1111/j.1432-0436.2008.00273.x
Keywords
prostate; stroma or stromal; mesenchymal; bone; osteoblasts; tissue recombination xenografting; transgenic mice; conditional knock-out
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Funding
- NCI NIH HHS [R01 CA108646, CA126505, U54 CA126505, R01 CA108646-04, CA108646] Funding Source: Medline
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Stromal-epithelial interactions mediated by paracrine signaling mechanisms dictate prostate development and progression of prostate cancer. The regulatory role of androgens in both the prostate stromal and epithelial compartments set the prostate apart from many other organs and tissues with regard to gene targeting. The identification of androgen-dependent prostate epithelial promoters has allowed successful gene targeting to the prostate epithelial compartment. Currently, there are no transgenic mouse models available to specifically alter gene expression within the prostate stromal compartment. As a primary metastatic site for prostate cancer is bone, the functional dissection of the bone stromal compartment is important for understanding stromal-epithelial interactions associated with metastatic tumor growth. Use of currently available methodologies for the expression or deletion of gene expression in recent research studies has advanced our understanding of the stroma. However, the complexity of stromal heterogeneity within the prostate remains a challenge to obtaining compartment or cell-lineage-specific in vivo models necessary for furthering our understanding of prostatic developmental, benign, tumorigenic, and metastatic growth.
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