Molecular and Genetic Profiling of Prostate Cancer: Implications for Future Therapy

Abstract

Prostate cancer is predicted to be the most common cancer diagnosed in American men in 2006 with an estimated 230,000 new cases in the United States alone [1]. It is likely to result in over 27,000 deaths in 2006, and the average male will have a one in six chance of developing this malady in his lifetime [1]. These statistics illustrate the need to have screening and treatment systems in place that possess both a high degree of sensitivity as well as proven effectiveness. With the recent strides made in the field of molecular and cellular biology, it is now possible to analyze and tailor treatments to an individual's tumor. As the methods of analysis become more refined, researchers are better able to sift through the vast amounts of data and hone in on promising new targets. Molecular prognostic markers are already beginning to appear as a result of modern genomic analysis, and more are on the way. These markers are appearing in a variety of pathways including signal transduction, apoptosis, cell cycle regulation, angiogenesis, and cell adhesion. The emergence of viable prognostic markers indicative of specific tumor types holds the potential of greatly improving cancer screening methods as well as overall patient survival.

Mechanism of β-Catenin-mediated Transcriptional Regulation of Epidermal Growth Factor Receptor Expression in Glycogen Synthase Kinase 3 β-inactivated Prostate Cancer Cells

“…All of these results strongly suggest that activation of ␤-catenin signaling may be associated with the progression of the disease through signaling cross-talk. Thus, our study can open a new avenue in the combinatorial therapeutic approach which is currently under development in cancer treatment (42,51,52).…”

Cannabinoids, endocannabinoids, and cancer

“…Several studies have revealed that cannabinoids have an effect on the expression of VEGF, which is one of the major cancer cell-released chemoattractants in tumor neovascularization [100]. Met-F-AEA has been shown to decrease levels of VEGF and VEGFR-1 in K-ras-transformed thyroid cells and in experimental tumors of xenografted nude mice [90].…”

Antitumorigenic Effects of Cannabinoids beyond Apoptosis

“…at ASPET Journals on May 12, 2018 jpet.aspetjournals.org endothelial growth factor (VEGF), which is one of the major cancer cell-released chemoattractants in tumor neovascularization (for review, see Saia et al, 2007). Met-F-AEA was demonstrated to decrease levels of VEGF and VEGFR-1 in K-ras-transformed thyroid cells and in experimental tumors of nude mice xenografted with these cells (Portella et al, 2003).…”