Genome Scanning and Tissue Microarrays for the Analysis of Molecular Mechanisms Underlying Hormone Therapy Failure in Prostate Cancer
Prostate cancer (PC) is the most frequent cancer among men in western countries (1). There is a considerable discrepancy between the prevalence of histological and clinical prostate cancer. More than 30% of all males over fifty have been shown to harbor histological (incidental) PC, but only 9% develop clinical disease during their life-time (2). Therefore, most of the histologically detectable early PCs do not progress to clinically detectable disease. Increased use of the serum PSA assays in screening and early diagnosis has caused a dramatic increase of newly detected prostate cancers during the early 1990’s (http://www-seer.ims.nci.nih.gov). Most tumors are now diagnosed at an early stage. However, up to 30% of of the patients still present with locally advanced or metastatic disease at the time of diagnosis (1). PC also remains the second most common cause of cancer deaths in men. This illustrates the inherent lethal nature of this disease, and the fact that advanced PC will remain a significant health problem. Androgen deprivation therapy can initially relieve symptoms in a large proportion of patients with advanced prostate cancer, but long-term cure is rarely achieved because the tumors eventually become hormone-refractory (after a few months or years), and efficient alternative systemic therapies are not yet available.
KeywordsAgar Paraffin Androgen eDNA
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