Disease relevance of GDEP

• GDEP, a new gene differentially expressed in normal prostate and prostate cancer [1].
• A new human retrovirus associated with prostate cancer [2].
• In similar populations, the PHE may serve as a clinically important forum for the promotion of evidence-based colorectal cancer and breast cancer screening and of screening with relatively less empirical support, such as prostate cancer screening [3].
• We conducted a Phase I study of in situ herpes simplex virus thymidine kinase (HSV-tk) plus ganciclovir (GCV) gene therapy, which was approved by the Japanese government as the first prostate cancer gene therapy trial [4].
• PURPOSE: To retrospectively determine the magnetic resonance (MR) and MR spectroscopic imaging features of high-grade prostatic intraepithelial neoplasia (HGPIN) in patients with prostate cancer [5].

Psychiatry related information on GDEP

• Environmental factors, such as dietary habits, may play a major role in the causation of prostate cancer [6].
• This pilot study explored the feasibility and efficacy of coping skills training (CST), an intervention developed to enhance coping with treatment side effects in a sample of African American prostate cancer survivors and their intimate partners [7].
• PATIENTS AND METHODS: In all, 121 men undergoing RRP for clinically localized prostate cancer were prospectively evaluated for short-term HRQoL using an acute Short Form-12 version-2 Physical and Mental Health Survey Acute Form before and serially each week from 1 to 6 weeks after RRP [8].
• PURPOSE: Many clinicians lack resources to engage patients in shared decision making for prostate cancer screening [9].
• METHODS: Statistical tools from classical measurement theory and factor analytic methods were used to evaluate the psychometric properties of the Prostate Cancer Outcomes Study disease-specific scales [10].

High impact information on GDEP

• Peroxisome Proliferator-Activated Receptor {gamma} Regulates E-Cadherin Expression and Inhibits Growth and Invasion of Prostate Cancer [11].
• Overexpression of both genes has been reported in high-grade, androgen-resistant prostate cancer [12].
• These results indicate that SOX9 in prostate basal cells supports the development and maintenance of the luminal epithelium and that a subset of prostate cancer cells may escape basal cell requirements through SOX9 expression [13].
• However, AR-mediated transcriptional activity in stromal cells isolated from prostate cancer was reduced compared with stromal cells isolated from benign prostate and continued to be reduced when cocultured with tumor-derived prostate epithelial cells [14].
• Thus, the ability of epithelial cells to modulate coregulator recruitment to the AR transcriptional complex on androgen-responsive genes seems altered in the stromal microenvironment of prostate cancer [14].

Chemical compound and disease context of GDEP

• Prostate cancer (PCa) is the most common cancer for men in Europe, North America, and some parts of Africa. Initially, growth of prostate cancer is usually androgen-dependent, but often it becomes androgen-independent after androgen-deprivation therapy [15].
• In this study, the sulforhodamine B assays showed that ilimaquinone induced a concentration-dependent anti-proliferative effect in several types of cancer cell lines, including prostate cancer PC-3 and LNCaP, non-small cell lung cancer A549 and hepatocellular carcinoma Hep3B cells [16].
• Testosterone replacement for hypogonadism after treatment of early prostate cancer with brachytherapy [17].
• The preferred primary treatment of patients with advanced, androgen-dependent prostate cancer is based on the periodic administration of depot preparations of LHRH agonists; these agonists can be likewise used to treat estrogen-sensitive breast cancer in premenopausal women [18].
• Parenteral estrogens for prostate cancer: can a new route of administration overcome old toxicities [19]?

Biological context of GDEP

• The GDEP gene was mapped to chromosome 4q21.1 by radiation hybrid mapping [1].
• Stromal-epithelial cell interactions and androgen receptor-coregulator recruitment is altered in the tissue microenvironment of prostate cancer [14].
• The consumption of diets containing 5 to 10 servings of fruits and vegetables daily is the foundation of public health recommendations for cancer prevention, yet this concept has not been tested in experimental models of prostate cancer [20].
• Localized prostate cancer or BPH showed no gene amplification or topoIIalpha overexpression [12].
• Recent in vitro studies in our laboratory have shown that garlic-derived organosulfur compound S-allylmercaptocysteine suppresses invasion and cell motility of androgen-independent prostate cancer cells via the up-regulation of cell-adhesion molecule E-cadherin [21].

Anatomical context of GDEP

• We further characterize PCAN1 expression in the prostate cell lines RWPE1, RWPE2, and LnCAP FGC [22].
• In addition, normal prostate epithelial cells co-cultured with normal prostate stromal cells did not exhibit PCAN1 expression at any time [22].
• Tolerization of tumor-specific T cells despite efficient initial priming in a primary murine model of prostate cancer [23].
• On the basis of this knowledge, the isolation and characterization of prostate cancer stem cells may now be possible and could provide an explanation for the known clinical and molecular heterogeneity of human prostate cancer [24].
• Optimized coverage of high-risk adjuvant lymph node areas in prostate cancer using a sentinel node-based, intensity-modulated radiation therapy technique [25].

Associations of GDEP with chemical compounds

• Testosterone was not found to increase PCAN1 expression in this culture system [22].
• Localization of a Prostate Cancer Predisposition Gene to an 880-kb Region on Chromosome 22q12.3 in Utah High-Risk Pedigrees [26].
• The occupancy of AR and coregulators on target genes showed that androgen-bound AR in prostate cancer stromal cells was associated with the corepressor silencing mediator for retinoid and thyroid hormone receptor [14].
• Nitric oxide-mediated inhibition of androgen receptor activity: possible implications for prostate cancer progression [27].
• Re: Zoledronic acid initiated during the first year of androgen deprivation therapy increases bone mineral density in patients with prostate cancer: C. W. Ryan, D. Huo, L. M. Demers, T. M. Beer and L. V. Lacerna. J Urol 2006; 176: 972-978 [28].
• The presence of human NME and glyceraldehyde-3-phosphate dehydrogenase in the serum of PC339-bearing mice was confirmed by Western blotting [29].

Other interactions of GDEP

• BACKGROUND: Prostate cancer gene 3 (PCA3) encodes a prostate-specific mRNA that has shown promise as a prostate cancer diagnostic tool [30].
• We evaluated the potential utility of the investigational prostate cancer gene 3 (PCA3) urine assay to predict the repeat biopsy outcome [31].

Analytical, diagnostic and therapeutic context of GDEP

• A total of 11 htSNPs (including COMT Val(158)Met) were selected based on the resequencing and dense genotyping approach of the Breast and Prostate Cancer Cohort Consortium. htSNPs were genotyped in a population-based, case-control study in Poland (1,995 cases and 2,296 controls) [32].
• METHODS: In a retrospective cohort study, we determined the association between receipt of a PHE and cancer testing in a population-based sample of enrollees in a Washington State health plan who were aged 52 to 78 years and eligible for colorectal, breast, or prostate cancer screening in 2002-2003 (N = 64 288) [3].
• Analysing prostate cancer biopsies by immunohistochemistry we found iNOS protein expression in tumor cells strongly paralleled by nitrotyrosine suggesting that iNOS is fully active [27].
• Cooperative effects of adenoviral vector-mediated interleukin 12 gene therapy with radiotherapy in a preclinical model of metastatic prostate cancer [33].
• Furthermore, WA potently inhibits the chymotrypsin-like activity of a purified rabbit 20S proteasome (IC50=4.5 microM) and 26S proteasome in human prostate cancer cultures (at 5-10 microM) and xenografts (4-8 mg/kg/day) [34].

References