Prostate cancer is the leading cause of cancer-related deaths in men. Androgen 
ablation is the mainstay of treatment for advanced prostate cancer. This therapy 
is very effective in androgen-dependent cancer; however, these cancers 
eventually become androgen independent, rendering anti-androgen therapy 
ineffective. The exploration of novel modalities of treatment is therefore 
essential to improve the prognosis of this neoplasia. Telomeres are specialized 
heterochromatin structures that act as protective caps at the ends of 
chromosomes. Telomere maintenance in the majority of tumor cells is achieved by 
telomerase, a reverse transcriptase enzyme that catalyzes the synthesis of 
further telomeric DNA. Telomerase is detected in the majority of prostate 
cancers, but not in normal or benign prostatic hyperplasia tissue. Moreover, the 
human telomerase reverse transcriptase (hTERT) gene, the catalytic subunit of 
telomerase, is regulated by androgens as well as by different oncogenes 
including Her-2, Ras, c-Myc and Bcl-2, which seem to play an important role in 
prostate cancer progression. Thus, telomerase may represent a very good 
candidate for targeted therapy in prostate tumors. To inhibit telomere 
maintenance by telomerase, approaches that directly target either telomerase and 
telomeres or the telomerase regulatory mechanisms have been used. Moreover, 
strategies targeting telomerase-positive cells as a means to directly kill the 
tumor cells have been tested. This review summarizes the most promising results 
achieved by anti-telomerase strategy in different solid tumors. Most of the 
telomerase-associated therapies described here have proved very promising for 
the treatment of prostate cancer. On the basis of the good results obtained and 
considering the multigenic defects of human tumors, including prostate cancer, 
the combination of anti-telomerase strategies with conventional drugs and/or 
molecules capable of interfering with oncogenic pathways could efficiently 
improve the response of this neoplasia.