Prostate Cancer

Prostate cancer is a neoplasm of the male reproductive gland with a high mortality rate. This cancer presents primarily after the age of fifty. The molecular cause of prostate cancer is still unclear, but it is often associated with dysregulated androgen signaling and aberrant metabolism of macromolecules such as fatty acids. Indeed, androgen ablation therapy causes regression of primary and metastatic androgen-dependent prostate cancer. Androgen receptor expression seems to promote prostate cancer cell survival, but inhibiting the androgen receptor has been clinically less effective than predicted. Androgen-independent prostate cancer is more aggressive. This form of prostate cancer continues androgen signaling, but avoids the need for androgen ligands through a variety of mechanisms, some of which have been identified. Polyunsaturated fatty acids cause prostate tumor progression and increased mortality, while diets rich in omega-3 fatty acids seem to benefit prostate cancer patients. Prostate cancer progression involves androgen, PI3K/AKT, and PTEN signaling, as well as cell cycle and apoptotic pathways. Research directed at these pathways may yield insights into the molecular mechanisms behind prostate oncogenesis. Prostate cancers also tend to metastasize, highlighting the need to analyze metastatic potential. Dysregulated gene expression, mutations, and differentially methylated promoters are routinely detected in molecular analyses of prostate cancer samples.

QIAGEN provides a broad range of assay technologies for prostate cancer research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for prostate cancer studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.