Newswire (Published: Monday, January 9, 2017, Received: Saturday, January 7, 2017, 3:09:43 AM CST)

Word Count: 495

Washington State University Reports Findings in Prostate Cancer (Lentiviral Vector-Mediated Insertional Mutagenesis Screen Identifies Genes That Influence Androgen Independent Prostate Cancer Progression and Predict Clinical Outcome)

By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Current study results on Oncology - Prostate Cancer have been published. According to news reporting originating from Pullman, Washington, by NewsRx correspondents, research stated, "Prostate cancer (PC) is the second leading cause of cancer related deaths in US men. Androgen deprivation therapy (ADT) improves clinical outcome, but tumors often recur and progress to androgen independent prostate cancer (AIPC) which no longer responds to ADT."

Our news editors obtained a quote from the research from Washington State University, "The progression to AIPC is due to genetic alterations that allow PC cancer cells to grow in the absence of androgen. Here we performed an insertional mutagenesis screen using a replication-incompetent lentiviral vector (LV) to identify the genes that promote AIPC in an orthotopic mouse model. Androgen sensitive PC cells, LNCaP, were mutagenized with LV and injected into the prostate of male mice. After tumor development, mice were castrated to select for cells that proliferate in the absence of androgen. Proviral integration sites and nearby dysregulated genes were identified in tumors developed in an androgen deficient environment. Using publically available datasets, the expression of these candidate androgen independence genes in human PC tissues were analyzed. A total of 11 promising candidate AIPC genes were identified: GLYATL1, FLNA, OBSCN, STRA13, WHSC1, ARFGAP3, KDM2A, FAM83H, CLDN7, CNOT6, and B3GNT9. Seven out the 11 candidate genes; GLYATL1, OBSCN, STRA13, KDM2A, FAM83H, CNOT6, and B3GNT6, have not been previously implicated in PC. An in vitro clonogenic assay showed that knockdown of KDM2A, FAM83H, and GLYATL1 genes significantly inhibited the colony forming ability of LNCaP cells."

According to the news editors, the research concluded: "Additionally, we showed that a combination of four genes, OBSCN, FAM83H, CLDN7, and ARFGAP3 could significantly predicted the recurrence risk in PC patients after prostatectomy (P = 5.3 x 10(-5))."

For more information on this research see: Lentiviral Vector-Mediated Insertional Mutagenesis Screen Identifies Genes That Influence Androgen Independent Prostate Cancer Progression and Predict Clinical Outcome. Molecular Carcinogenesis, 2016;55(11):1761-1771. Molecular Carcinogenesis can be contacted at: Wiley-Blackwell, 111 River St, Hoboken 07030-5774, NJ, USA. (Wiley-Blackwell - www.wiley.com/; Molecular Carcinogenesis - onlinelibrary.wiley.com/journal/10.1002/(ISSN)1098-2744)

The news editors report that additional information may be obtained by contacting G.D. Trobridge, Washington State University, Sch Mol Biosci, Pullman, WA 99164, United States. Additional authors for this research include T.F. Williams, C.P. Collins, D.T. Rae and G.D. Trobridge (see also Oncology - Prostate Cancer).

Keywords for this news article include: Pullman, Washington, United States, North and Central America, Mutagenesis, Genetics, Drugs and Therapies, Cancer Gene Therapy, Prostatic Neoplasms, Prostate Cancer, Bioengineering, Biotechnology, Androgens, Oncology, Washington State University.

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