Molecular alterations in prostate cancer.
Prostate tumors display a range of clinical phenotypes, from indolent to aggressively metastatic. Numerous gene expression profiling studies have been conducted toward the potential molecular staging of these pathologies, however the identification of genetic markers that predict aggressive disease has not yet been demonstrated in the clinical setting. A recent survey of the literature has shown that molecular alterations in prostate carcinomas can occur through a variety of different mechanisms, ranging from upstream epigenetic changes and genetic polymorphisms to downstream modulations through alternative splicing and other post-translational processes, some of which could involve noncoding RNAs. A summary of these results and recommendations for future work are the subject of this review.
Reynolds
Mark A
MA
Gen-Probe Incorporated, San Diego, CA 92121, USA. markr@gen-probe.com
D017398:Alternative Splicing; D044127:Epigenesis, Genetic; D020869:Gene Expression Profiling; D006801:Humans; D008297:Male; D009154:Mutation; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology; D012323:RNA Processing, Post-Transcriptional