Cancer you invited two large clinical studies to investigate the e r m resembled the 5AR inhibitors in the prevention of prostate cancer Pr: The Prostate Cancer Prevention Trial and the reduction of dutasteride of prostate cancer events. The CPP was a multicenter, randomized, double-blind, controlled clinical trial against placebo TKI258 Dovitinib Fi nasteride compared with placebo in the prevention of prostate adenocarcinoma. 18 882 M Men over 55 with a PSA of 3.0 ng / ml or less and a normal DRE at age were randomized to receive seven years nasteride fi t Possible or placebo. The study participants were measured with a J Hrlichen PSA and digital rectal examination followed. TRUS-guided biopsies were performed for gr He performed than or equal to 4 ng / ml PSA or abnormal DRE.
In addition, all M Men for biopsy study end after seven years of treatment recommended are passed. Included among the 9060 M Nnern in the statistical analysis of internal fi, 18.4% of the men in the group fi nasteride with adenocarcinoma of the prostate were diagnosed, compared with 24.4% in the placebo group, a lower risk of 24.8%. A significant difference was analyzed in all subgroups, and about 98% of cancers in both groups were organized, denied the trust. Despite the drastic reduction in the risk of 24.8% compared to the diagnosis of prostate cancer in the PCPT study population, different topics to a broad acceptance of the fi nasteride as a preventive treatment for prostate cancer have been prevented. Zun Highest nasteride if the treatment was poor with an increased Hten rate of diagnosis of prostate cancer associated differentiated from placebo.
In addition, rates of prostate cancer diagnosis much h Ago were as expected in both study groups. Closing Lich, almost half of the H All positive diagnoses of cancer in the study were biopsies, tumors with a clinically significant EndOf Cancer is unknown. The PPC has had with immediate skepticism from some researchers and clinicians, from fears that fi nasteride weight Hlt and accelerates the growth of high-grade tumors fueled fulfilled. The subsequent Analysis of the PCPT data provide an alternative hypothesis, which is slightly h Recognized herer percentage of high-grade tumors in the treatment group explained Ren. Rst Of the green was-Run difference in the proportion of cancers of high or low quality T between treatment and placebo groups demonstrated in these subjects w Observed during biopsies for cause, such as biopsies to study to find.
The hazard ratio for the detection of prostate cancer degrees in of the treated group erh Ht themselves not w During of the clinical study to erh hen. In fact, the number of the men with prostate cancer with high w During the end-point biopsies diagnosed Similar in both study groups. The subsequent End analysis showed that fi nasteride infl uence the properties of the PSA as a screening test, which increased its sensitivity Ht in all types of prostate cancer in general and the high quality t prostate cancer in particular. In addition, the PSA is more sensitive for prostate cancer in high-quality cut-off PSA levels between 1.1 ng / ml to 10.1 ng / ml, which reduced the rate of false negative and increased The rate of diagnosis of high grade tumors hen . Is why assumes the combination of cancer-Chemopr Vention, the lowering of the PSA and PSA sensitivity for the gro Ec