Prostate Cancer Basic Research Session I - AUA 2006

UroToday.com - A Discussed Poster Session on Prostate Cancer Basic Research took place on Sunday May 21, 2006 at the annual AUA meeting in Atlanta. Many interesting posters on basic and potential translation science were presented. A few of these are described herein.

Dr. Stephen Freedland and colleagues, Baltimore MD compared gene expression patterns by microarray from obese and normal weight men. They found differences greater than expected by chance alone. 3-hydroxymethyl glutaryl coA, a rate limiting enzyme in ketone body production was significantly lower in obese men.

Dr. Eric Klein, Cleveland Clinic presented their work on a virus closely related to murine leukemia viruses that were identified in prostate tumors of men homozygous for the R462Q mutation in the HPC1 gene. This work suggests that there may be a link between viral infection and the development of CaP in men with a mutated gene.

A research group from Japan and California had their work on a biomarker in different ethnic cohorts presented by Dr. Enokida. They found that GSTP-1 gene hypermethylation was a biomarker for CaP in African-American as opposed to Caucasian or Asian men, but that it strongly influenced tumor progression in Asian men with CaP.

Dr. Ralf Herwig presented exciting work from Austrian collaborators regarding a new method to differentiate between benign and malignant prostate disease. To do this, they isolated peripheral blood mononuclear cells from 25 men with CaP and 10 healthy controls. Using cell surface antigens, the cells populations were separated by flow cytometry and intracellular PSA measured. Differentiation between malignant and benign disease was achieved using the CD14/PSA staining. PSA was only found in activated CD14 cells, and was much higher in metastatic compared to localized CaP.

Dr. Mark Rubin's group from Boston, MA characterized Metastasis-Associated Protein 1 (MTA1) in CaP cell lines. MTA-1 is overexpressed in several tumor types and facilitates cancer through transcription repression. MTA-1 overexpression in LNCaP cells resulted in significantly increased ability for migration and invasion. MTA-1 overexpression resulted in upregulation of several genes associated with CaP progression.

Work from Vancouver, Canada presented by Dr. Hayashi discussed how the anti-apoptotic survival gene Clusterin upregulates the transcription factor NFk-B. Androgen-withdrawal is shown to up-regulate Clusterin expression. Using microarray techniques combined with small interfering RNA inhibition experiments NFk-B was identified to be under Clusterin regulation. This suggests that the NFk-B pathway may be a potential downstream effector of clusterin-mediated cytoprotective function.

By Christopher P. Evans, M.D.

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