PCa Saffron 100mg. 60 caps
I am pleased to announce that after months of trials on my inner circle of sufferers this stuff is working!
This Saffron is a special extract formulated in Italy specifically for Prostate Cancer. Here is a copy of the information from a Uro-Oncologist in Italy as I first read it.
As you know prostate cancer continues to be a leading cause of cancer death in males . Patients with localized prostate cancer possess a favorable 5-year survival rate, whereas patients with metastatic cancer have a median survival of only 12–15 months, which is an indication that PCa cell metastasis is the primary mediator of mortality for this disease. A variety of therapeutic strategies are utilized for the treatment of advanced metastatic PCa. However, despite advances in the understanding of PCa biology, these therapies rarely produce significant increases in survival time in metastatic PCa. Natural products like yours have long been used to prevent and treat diseases including cancers and might be good candidates for the development of anticancer drugs. Many herbs and spices are the subject of scientific investigations related to antioxidant properties and health. Saffron, a commonly used spice and food additive, is known for its anticancer and antitumor properties. CR and CCT, two carotenoid compounds derived from saffron, have shown a significant inhibitory effect on the growth of cancer cells .
Many mechanisms of action have been identified or supposed. Different hypotheses for antitumor effects of saffron and its ingredients have been proposed including inhibition of DNA and RNA synthesis, but not protein; ability to scavenge free radicals; involvement in the metabolic conversion of carotenoids to retinoids; mediation of interactions of carotenoids with topoisomerase II (an enzyme involved in cellular DNA-protein interaction) ; and downregulation of the expression of the catalytic subunit of the human telomerase (hTERT).
Here, we demonstrate that, although different phytochemicals in saffron extracts could have additive and synergistic effects enhancing its anticarcinogenic properties , only CR and CCT showed higher antitumor effects with respect to SE. The in vivo effects of these compounds were evident in in vivo models. SE, CR, and CCT inhibited tumor cell proliferation of aggressive models of PCa as shown by the reduced proliferating cell nuclear antigens, mitotic figure counts, tumor vessels, and tumor growth rate and increased apoptosis especially in the CCT-treated animal group. CCT showed the strongest antitumor effects since it resulted in a tumor weight reduction of 75% and 85% in PC3 and 22rv1 xenografts, with respect to control while CR and SE resulted in tumor weight reduction of 38% and 18%, and 54% and 39%, in PC3 and 22rv1 xenografts Additionally, CCT tumor xenografts had a reduction of 50% and 69% of proliferating index (PI) in PC3 and 22rv1 xenografts, while CR and SE decreased PI by 30% and 16% and 27 and 15%, respectively The induction of apoptosis and the decrease of the vessel count were once again mainly affected by CCT. The changes in biologically relevant markers were parallel with the increase in the time to progression as shown by the data concerning the time trend of tumor growth. Conversely, SE and CR induced stronger epithelial differentiation with increased E-cadherin and K18 expression levels and a decrease in EMT markers such as N-cadherin, β-catenin, and vimentin.
EMT phenotype is associated with the activation of the Wnt signaling pathway, in which its key component β-catenin plays critical roles in embryonic development as well as in human diseases, including cancer. The progression of carcinomas is associated with the loss of epithelial morphology and a concomitant acquisition of a more mesenchymal phenotype, which in turn is thought to contribute to the invasive and/or metastatic behavior of the malignant process. Loss of E-cadherin is reported to be associated with a poor prognosis . It has been demonstrated that N-cadherin was not expressed in normal prostate tissue; however, in prostatic cancer, N-cadherin was expressed in the poorly differentiated areas, which showed negative E-cadherin staining. Accumulated evidence has demonstrated a significant role for the Wnt pathway in the development and progression of human prostate cancer. Clearly, the mere loss of cell-cell contact and communication cannot be the sole explanation for the observed relationship between loss of E-cadherin-mediated adhesion and poor clinical outcome. Recently, a number of papers have been published that describe the inappropriate expression of nonepithelial cadherins by epithelial cells as a putative novel mechanism for promoting the interaction with the stroma, thereby facilitating invasion and metastasis . We showed that human prostate cancer cell lines, which lack expression of either E-cadherin or catenins and, therefore, lack an E-cadherin-mediated cell-cell adhesion, acquire cadherin expression .
In our previous report we noticed that SE and CR were effective in vitro in PCa tumor cells including PC3 cells used in the present report. Androgen sensitive PCa cells seem to be more affected by treatments of androgen insensitive ones. The lower efficacy of SE observed in vivo, especially for PC3 cells, could be due to the reduced blood levels (and thus reduced tumor levels) of carotenoids that were achieved after the oral administration of SE. It has been demonstrated that CR was absorbed in the intestinal tract in a minimal amount whereas, when we administered CCT could be, indeed, the major compound which can be found in the blood. Crocin shows intrinsic antiproliferative effects but the oral administration shows only the effects of CCT. In addition, not all crocin turns into crocetin. However the relative blood amounts and blood peaks are unknown. Further experiments are necessary to establish the amount of carotenoids found in the blood after oral administration of SE, CR, and CCT (paper in preparation). In addition, although CCT is more effective of CR, its tumor levels were probably not sufficient to determine antiproliferative/proapoptotic effects in our PCa xenografts.
In addition, as widely described in this paper, CCT showed higher effects on proliferation/apoptosis when compared to differentiative ones; therefore, although MMPs was reduced (whereas uPA was not modified) overall Matrigel degradation (and invasion) seems to be not influenced.
To our knowledge, this is the first report showing that saffron-induced antitumor effects may affect EMT processes. Specifically, we observed that the induction of epithelial differentiation was a time-dependent event and was evident from 4 days of treatment with SE and CR. Based on the current data, this special concentrated saffron and its ingredients could be considered as a promising candidate for clinical anticancer trials in aggressive prostate cancer with a high risk of metastases.