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Prostate Cancer
Volume 2013, Article ID 920612, 23 pages
Review Article

Dissecting Major Signaling Pathways throughout the Development of Prostate Cancer

1Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Avenida Prof. Lineu Prestes 1730, 05508-900 São Paulo, SP, Brazil
2Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida Prof. Lineu Prestes 580, 05508-000 São Paulo, SP, Brazil
3Departamento de Genética e Biologia Evolutiva, Instituto de Biociências, Universidade de São Paulo, Rua do Matão 277, 05508-900 São Paulo, SP, Brazil
4Instituto Israelita de Ensino e Pesquisa Albert Einstein, Avenida Albert Einstein 627/701, 05652-000 São Paulo, SP, Brazil
5International Center for Genetic Engineering & Biotechnology (ICGEB), Cancer Genomics Group and Division of Medical Biochemistry, University of Cape Town, Cape Town 7925, South Africa
6Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA

Received 30 November 2012; Revised 25 March 2013; Accepted 28 March 2013

Academic Editor: Craig Robson

Copyright © 2013 Henrique B. da Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Prostate cancer (PCa) is one of the most common malignancies found in males. The development of PCa involves several mutations in prostate epithelial cells, usually linked to developmental changes, such as enhanced resistance to apoptotic death, constitutive proliferation, and, in some cases, to differentiation into an androgen deprivation-resistant phenotype, leading to the appearance of castration-resistant PCa (CRPCa), which leads to a poor prognosis in patients. In this review, we summarize recent findings concerning the main deregulations into signaling pathways that will lead to the development of PCa and/or CRPCa. Key mutations in some pathway molecules are often linked to a higher prevalence of PCa, by directly affecting the respective cascade and, in some cases, by deregulating a cross-talk node or junction along the pathways. We also discuss the possible environmental and nonenvironmental inducers for these mutations, as well as the potential therapeutic strategies targeting these signaling pathways. A better understanding of how some risk factors induce deregulation of these signaling pathways, as well as how these deregulated pathways affect the development of PCa and CRPCa, will further help in the development of new treatments and prevention strategies for this disease.