Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/48422
Title: Transition to androgen-independence in prostate cancer
Authors: Navarro Bosch, Domingo 
Luzardo, Octavio P. 
Fernández, Leandro 
Chesa, Nicolás
Díaz-Chico, Bonifacio N. 
UNESCO Clasification: 32 Ciencias médicas
320101 Oncología
Keywords: Receptor Gene Amplification
In-Situ Hybridization
Rat Liver-Microsomes
Therapy Failure
Antiandrogen Withdrawal, et al
Issue Date: 2002
Journal: Journal of Steroid Biochemistry and Molecular Biology 
Abstract: Prostate carcinoma is the most frequently diagnosed malignancy and the second leading cause of death as a result of cancer in men in the western countries. Withdrawal of androgens or the peripheral blockage of androgen action remain the critical therapeutic options for the treatment of advanced prostate cancer. However. after initial regression, most of the prostate cancers become androgen-independent and progress further with eventual fatal outcome. Understanding the mechanisms of transition to androgen independence and tumor progression in prostate cancer is critical to finding new ways to treat aged patients that are ineligible for conventional chemotherapy. A large number of different molecular mechanisms might be responsible for the transition to androgen-independence. Many of these involve the androgen receptor (AR) and its signalling pathways. but they might also include genetic chances that affect several genes, which results in the activation of oncogenes or the inactivation of tumor suppressor genes. Here. we discuss the Most recent and relevant findings on androgen resistance in prostate cancer in order provide a comprehensive interpretation of the clinical behaviour of tumors at molecular levels.
URI: http://hdl.handle.net/10553/48422
ISSN: 0960-0760
DOI: 10.1016/S0960-0760(02)00064-X
Source: Journal of Steroid Biochemistry and Molecular Biology[ISSN 0960-0760],v. 81, p. 191-201
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