Article
Differential expression of interleukin-8 and its receptors in the neuroendocrine and non-neuroendocrine compartments of prostate cancer.
Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Ave., Box 626, Rochester, NY 14642, USA.
American Journal Of Pathology (impact factor:
4.89).
07/2005;
166(6):1807-15.
DOI:10.1016/S0002-9440(10)62490-X
Source: PubMed
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Article: Activation of mitogen-activated protein kinase pathway by the antiandrogen hydroxyflutamide in androgen receptor-negative prostate cancer cells.
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ABSTRACT: Whereas hydroxyflutamide (HF) has been used as an antiandrogen to block androgen-stimulated prostate tumor growth, the antiandrogen withdrawal syndrome that allows antiandrogens to stimulate prostate tumor growth still occurs in many patients treated with androgen ablation therapy. This was previously explained by mutations in the androgen receptor (AR) and/or modulation from AR coregulators, so that HF becomes an AR agonist. Using immunohistochemical analysis, we analyzed four prostate cancer patients undergoing androgen ablation therapy with flutamide and compared their phospho-extracellular signal-regulated kinase 1/2 levels in prostate cancer biopsies before receiving HF and after experiencing disease progression while taking HF. We found a significant increase of activated mitogen-activated protein (MAP) kinase in prostate tumors from patients receiving HF during androgen ablation therapy. In vitro studies showed that HF induced a rapid activation of the Ras/MAP kinase pathway in human prostate cancer DU145 cells which lack the AR, as well as in PC-3AR2 and CWR22 cells which express the AR. Cycloheximide failed to inhibit this activation, but both AG1478, an inhibitor of the epidermal growth factor receptor (EGF-R), and an EGF-R-neutralizing antibody blocked this HF-mediated activation of MAP kinase, which suggests that the activation of Ras/MAP kinase by HF is a membrane-initiated, non-AR-mediated, and nongenomic action. The consequence of this activation may result in increasing cell proliferation and cyclin D1 expression. This raises a concern for using HF in the complete-androgen-ablation therapy in prostate cancer treatment and provides a possible pathway that might contribute to the HF withdrawal syndrome.Cancer Research 12/2002; 62(21):6039-44. · 7.86 Impact Factor -
Article: Androgen receptor as a target in androgen-independent prostate cancer.
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ABSTRACT: Prostate cancer is dependent on androgen stimulation mediated by the androgen receptor (AR), a member of the steroid hormone receptor family of ligand-dependent nuclear receptors. Most patients respond to standard androgen ablation therapies, but virtually all patients eventually relapse with disease that has been termed hormone-refractory or androgen-independent disease. Efforts to use AR antagonists, such as flutamide or bicalutamide, to enhance responses to primary androgen ablation therapy or to treat androgen-independent prostate cancer have been disappointing, which has diminished enthusiasm for more aggressive or alternative methods to block AR function. However, many lines of evidence indicate that AR function contributes to tumor cell survival after androgen ablation and to growth of androgen-independent prostate cancer. This article outlines a number of mechanisms that may contribute to AR activity in androgen-independent prostate cancer, including AR amplification, AR mutation, altered expression of AR coactivator and corepressor proteins, and activation of other pathways that can enhance AR function. Understanding the mechanisms responsible for AR function in androgen-independent prostate cancer should allow the more rational development of antagonists that can enhance the efficacy of androgen ablation therapies.Urology 10/2002; 60(3 Suppl 1):132-8; discussion 138-9. · 2.43 Impact Factor -
Article: Evaluation of HER-2/neu immunohistochemical assay sensitivity and scoring on formalin-fixed and paraffin-processed cell lines and breast tumors: a comparative study involving results from laboratories in 21 countries.
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ABSTRACT: Variation in assay sensitivity was studied in more than 90 laboratories that assayed 4formalin-fixed, paraffin-processed breast and ovarian carcinoma cell lines with graded levels of HER-2/neu protein overexpression and known levels of HER-2/neu gene amplification, in addition to breast carcinomas fixed and processed in the laboratories. Main methods were the HercepTest (DAKO, Ely, England) and individualized protocols using a polyclonal antibody and the CB11 clone. While the proportion of laboratories achieving appropriate results with the HercepTest was significantly higher than for participants using other assays, laboratories using other assays showed significant improvement in the second assessment run. The level of agreement in evaluations by 26 laboratories using the HercepTest was excellent on cell lines and tumors and was significantly greater than that achieved by the remaining 41 laboratories using other immunohistochemical methods. While laboratories using the DAKO HercepTest had the highest level of reproducibility in assay sensitivity and evaluation, the significant improvement in results by laboratories using other antibodies in the second assessment run suggests that stringent quality control and an ongoing quality assurance program using a standard reference material have the potential to improve the reliability of immunohistochemical assays for HER-2/neu, regardless of the antibody used.American Journal of Clinical Pathology 10/2002; 118(3):408-17. · 2.60 Impact Factor
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Keywords
androgen-independent growth
androgen-independent state
autocrine mechanism
benign prostatic tissue
Hormonal therapy
human prostate cancer tissue
initial response
interleukin-8 receptor
interleukin-8 receptor CXCR1
interleukin-8 regulates
interleukin-8 signaling
malignant cells
neuroendocrine cells
neuroendocrine differentiation
neuroendocrine tumor cells
neuroendocrine tumor cells stimulates androgen-independent proliferation
paracrine mechanism
prostate
prostate cancer
Recent studies
