Carcinogenesis Advance Access originally published online on September 29, 2005
Carcinogenesis 2006 27(1):1-22; doi:10.1093/carcin/bgi229
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Carcinogenesis vol.27 no.1 © Oxford University Press 2005; all rights reserved.
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Recent advances on multiple tumorigenic cascades involved in prostatic cancer progression and targeting therapies
Department of Biochemistry and Molecular Biology, Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198, USA
* To whom correspondence should be addressed at: Department of Biochemistry and Molecular Biology, 985870 University of Nebraska Medical Center, 7052 DRC, Omaha, NE 68198-5870, USA. Tel: +1 402 559 5455; Fax: +1 402 559 6650; Email: sbatra{at}unmc.edu
Recent advances on differently-expressed gene products and their functions during the progression from localized androgen-dependent states into androgen-independent and metastatic forms of prostate cancer are reported. The expression levels of numerous oncogenes and tumor suppressor genes in distinct prostatic cancer epithelial cell lines and tissues relative to normal prostate cells are described. This is carried out to identify the signaling elements that are altered during the initiation, progression and metastatic process of prostate cancer. Additional information on the interactions between certain deregulated signaling pathways such as androgen receptor (AR), estrogen receptors, epidermal growth factor receptor (EGFR), hedgehog and Wnt/ß-catenin cascades in controlling the proliferation, survival and invasion of tumor prostate epithelial cells during the disease progression is described. The emphasis is on the critical functions of the AR and EGF–EGFR systems at all stages during prostate carcinogenesis. Of therapeutic interest, new strategies for the diagnosis and treatment of localized and metastatic forms of prostate cancer by targeting multiple tumorigenic signaling elements are also reported.
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