Genetics of Prostate Cancer

Abstract

Prostate cancer is the most frequently diagnosed visceral cancer of men, responsible for approximately 40,000 deaths in adult males per year. To identify the genetic causes of prostate cancer, we performed a whole genome scan of affected sib pairs, using DNA markers spaced evenly across the human genome. We demonstrated that regions on chromosomes 1,4,5,7,8,11,16 and 19 might harbor genes that predispose individuals to prostate cancer and may affect tumor growth rate and tumor aggressiveness. Here we present DNA sequence analysis of KIAA 0872 and 17-β hydroxysteroid dehydrogenase that are located on chromosome 16 within the mapped region, and we demonstrate that neither of these genes carries mutations in the protein coding region or their splice junction sites. These results suggest that these genes are less likely to be associated with the cause of familial prostate cancer. INTRODUCTIONProstate cancer is the second leading cause of cancer mortality for men in the U.S. with a rate of 26 deaths per 100,000. 1 Although prostate cancer is potentially curable in its early stages, treatment of advanced hormone-refractory prostate cancer is ineffective, making early detection and treatment of disease a necessity. 2 Unfortunately, approximately 30% of men with prostate cancer have tumor that has spread beyond the prostate gland at the time of diagnosis. Despite the impressive response of metastases to androgen hormone deprivation, the survival rate is dismal, with greater than 90% of these patients dying from their cancer. 3 Screening tests for prostate cancer include digital rectal examination, transrectal ultrasonography, and measurement of prostate-specific antigen. However, these tests often do not detect the tumors before they have spread. The development of additional tests for earlier identification of prostate tumors will be extremely important. 4,5

Bio-Docklets: virtualization containers for single-step execution of NGS pipelines

“…In addition, we analyzed the same datasets with Bio-Docklets on a compute server with larger computational capacity that we rented from the Amazon Web Services cloud, and we observed a reduction of the overall compute time (Table 1 ). In both cases, the CHIPseq output contained the same peaks ( P < 0.001) on chromosomes 1, 4, 5, 7, 8, 11, 16, and 19, which harbor histone interactions with an active role in tumor genesis, found in earlier studies [ 17 ], similar to RNAseq regarding the differentially expressed genes that are active regulators in cancer progression [ 18 ].…”

The Omega-3 Polyunsaturated Fatty Acid DHA Induces Simultaneous Apoptosis and Autophagy via Mitochondrial ROS-Mediated Akt-mTOR Signaling in Prostate Cancer Cells Expressing Mutant p53

“…Prostate cancer is the second leading cause of male cancer-related death in the USA [1], and migration-associated changes in risk have provided evidence that genetic and environmental factors, such as p53 alteration and dietary fat, contribute to the disease [2–4]. Epidemiological data suggest that while high intake of saturated fatty acids is positively associated with prostate cancer risk, certain omega-3 polyunsaturated fatty acids ( ω 3-PUFAs), in particular docosahexaenoic acid (DHA), seem to prevent this type of cancer [5, 6].…”

A Polycomb Repression Signature in Metastatic Prostate Cancer Predicts Cancer Outcome

“…) portion of our gene set is located at chromosomes 1q, 17q, 19q, and 20q, all of which have previously been associated with prostate cancer (11).…”