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Carcinogenesis Advance Access published online on September 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi229
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received July 21, 2005
Revised September 10, 2005
Accepted September 17, 2005

REVIEW

Recent advances on multiple tumorigenic cascades involved in prostatic cancer progression and targeting therapies

Murielle Mimeault 1 and Surinder K Batra 1*

1 Department of Biochemistry and Molecular Biology, Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198

* To whom correspondence should be addressed.
Surinder K Batra, E-mail: sbatra{at}unmc.edu


  Abstract

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 done 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/{beta}-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.

Keywords: Prostate carcinogenesis; Prostatic stem cells; Oncogene; Androgenic and estrogenic signaling; EGF-EGFR system; Targeting therapies.
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