The Friday news reports: January 9, 2009


There are a number of rather technical reports in the news today, and we summarize these briefly below, providing the usual links to the abstracts for readers who are interested. In a separate report we have addressed the development of a new nomogram that can be used to predict risk for early disease progression following radical prostatectomy for localized disease.

Wiklund et al. have reported an association between the presence of known prostate cancer risk alleles and PSA levels among men with no diagnosis of prostate cancer. This is a “dense” scientific paper with implications for understanding how genetic profiling may be used to address risk for prostate cancer.

Saito et al. have shown that epigenetic changes in cancer cells (including prostate cancer cells specifically) may be able to  control the expression of tumor suppressor “micro-RNAs” by directly controlling their host genes. Thus, epigenetic therapy may not only directly activate micro-RNAs from their own promoters, but may also activate intronic micro-RNAs and with their host genes. (The term “epigenetics” refers to inheritable changes in the phenotype or physical expression of a specific gene caused by mechanisms other than changes in the underlying DNA sequence.)

Antunes et al. have analyzed the prognostic value of six specific genes in the tissues of 50 patients with localized prostate cancer who underwent radical prostatectomy. Analysis of malignant prostatic tissue demonstrated that prostate specific membrane antigen was overexpressed (mean 9 times) and pepsinogen C was underexpressed (mean 1.3 x 10-4) times) in all cases compared to benign prostatic hyperplasia. The authors suggest that tissue expression of pepsinogen C may have value in the identification of men at risk for progression following radical prostatectomy.

Cohen and Rokhlin have reviewed underlying biologic data related to the  molecular changes required for driving prostate cancer cells from an androgen-dependent to an androgen-independent or androgen depletion-independent state. Their review focuses primarily on mechanisms of prostate cancer cell survival after inhibition of androgen receptor activity by androgen depletion or by targeting the expression of androgen resistance by “small interfering RNA” (siRNA). Based on evolving information about the mechanisms of androgen resistance and depletion, the authors suggest that there may be a need for re-evaluation of the therapeutic approaches to human prostate cancer. The “New” Prostate Cancer InfoLink is of the opinion that the current clinical understanding of the molecular basis for androgen deprivation therapy is at best crude, and that better therapies with fewer side effects will be possible as we develop a more sophisticated appreciation of how to manage the complexities of this disease.

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