ABSTRACT
BACKGROUND: The antitumor and immunomodulating activities of melatonin are widely known. These activities are based upon the multifactorial mechanism of action on various links of carcinogenesis. In the present paper, the long-term results of the clinical use of melatonin in the combined treatment of patients with prostate cancer of various risk groups were evaluated. MATERIALS AND METHODS: A retrospective study included 955 patients of various stages of prostate cancer (PCa) who received combined hormone radiation treatment from 2000 to 2019. Comprehensive statistical methods were used to analyze the overall survival rate of PCa patients treated with melatonin in various prognosis groups. RESULTS: The overall survival rate of PCa patients with favorable and intermediate prognoses treated or not treated with melatonin was not statistically significantly different. In the poor prognosis group, the median overall survival in patients taking the drug was 153.5 months versus 64.0 months in patients not using it (p < 0.0001). The 5-year overall survival rates in the research and control groups were 66.8 ± 1.9 and 53.7 ± 2.6 (p < 0.0001) respectively. In a multivariate analysis, melatonin administration proved to be an independent prognostic factor and reduced the risk of death of PCa patients by more than twice (p < 0.0001). CONCLUSIONS: The multicomponent antitumor effect of melatonin is fully realized and clearly demonstrated in treatment of PCa patients with poor prognosis with a set of unfavorable factors of the tumor progression.
ABSTRACT
The goal of this paper was to estimate the predictive value of kinetic parameters of tumor growth in 109 prostatic cancer (PCa) patients with the morphologically verified diagnosis. Results: The cell loss factor, calculated on the basis of Ki-67 values, and the PSA doubling time, proved to be an important prognostic parameter. A cumulative comparative analysis of these criteria, depending on the prevalence of the tumor process, indicates that the level of cell loss significantly decreases with increasing tumor stage (p = 1*10-5), and the growth rate of the tumor significantly increases (p = 1*10-6). In the multivariate prognostic model, the CLF is an independent predictor of tumor-specific survival along with the stage of PCa. Materials and methods: For each patient of the study group were as follows. The level of Ki-67 expression in biopsies of adenocarcinoma of the prostate gland was estimated. Also, in the selected group of patients, based on the available data on the kinetics of the prostatic specific antigen (PSA), the initial time of doubling of PSA was determined. The obtained values of the actual tumor growth rate and the cell loss factor (CLF) were compared with the parameters characterizing the tumor state (stage, Gleason score, PSA level at diagnosis) and tumor-specific survival rates. Conclusion: Inclusion of proliferative activity factors in nomograms and prognostic models will increase their prognostic value and practical significance. Further prospective studies are needed to analyze the actual growth rate of PCa and evaluate its proliferative activity.
