title: [Prostate cancer: update].
abstract: The study of mitotic transduction of the signal showed that overexpression of pAkt and reduction in pERK expression would be associated a biological relapse. For tumors T1-3 N0M0 at the high risk of local relapse after prostatectomy, an immediate radiotherapy compared with a differed radiotherapy (at the time of PSA relapse), showed a significant reduction in the rate of local relapse and an ameliorated progression free survival. The effectiveness of the docetaxel was confirmed in two phase III randomized clinical trials : TAX-327 with 3 arms compared docetaxel every 21 days, docetaxel every 7 days and mitoxantrone. All arms were prednisone-based. An increase in overall survival, PSA progression free survival, PSA response rate and a pain reduction were highlighted in the docetaxel arm every 21 days. Docetaxel obtained at the end of this study the marketing authorization in this indication and became the treatment of reference. The SWOG 99-16 study compared the docetaxel estramustine association with the same arm of reference, mitoxantrone and prednisone, with similar results. The addition of estramustine to the docetaxel seems to improve the PSA response rate and progression free survival, but with a greater embolic toxicity. The addition of an antiangiogenic agent, the thalidomide, to docetaxel, improves progression free survival and overall survival. PSA responses were observed with an inhibitor of the proteasome, the bortezomib, in monotherapy, contrary to the imatinib which in monotherapy didn't have any effectiveness. Studies in association with docetaxel are ongoing. Some biological responses were observed with a vaccine anti MUC-1 and must be confirmed on a greater series of patients. The docetaxel impact on localized disease is actually evaluated.
authors.affiliation: Département de cancérologie médicale, Hôpital européen Georges-Pompidou, 20, rue Leblanc, 75015 Paris. stephane.oudard@hop.egp.ap-hopparisfr>
authors.forename: Stéphane
authors.initials: S
authors.lastname: Oudard
authors.forename: Jacques
authors.initials: J
authors.lastname: Medioni
authors.forename: Florian
authors.initials: F
authors.lastname: Scotté
authors.forename: Eugénie
authors.initials: E
authors.lastname: Banu
mesh_terms: D000726:Androgen Antagonists / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D019496:Cancer Vaccines / Q000627:therapeutic use; D017326:Clinical Trials, Phase III as Topic; D000077143:Docetaxel; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D008297:Male; D009376:Neoplasms, Hormone-Dependent / Q000628:therapy; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000175:diagnosis / Q000378:metabolism / Q000628:therapy*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011878:Radiotherapy / Q000379:methods; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D043823:Taxoids / Q000627:therapeutic use
chemical_list: D000726:Androgen Antagonists; D000970:Antineoplastic Agents; D019496:Cancer Vaccines; D000077143:Docetaxel; D048049:Extracellular Signal-Regulated MAP Kinases; D017430:Prostate-Specific Antigen; D051057:Proto-Oncogene Proteins c-akt; D018719:Erb-b2 Receptor Tyrosine Kinases; D043823:Taxoids