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IntroductionProstate cancer (PCa) is one of the most commonly diagnosed neoplasms in elderly men. The precancerous lesion of PCa is considered a high-grade prostate intraepithelial neoplasm (HG-PIN), while atypical small acinar proliferation (ASAP) is commonly considered as an under-diagnosed cancer. The aim of the study was to establish the impact of ASAP and extensive HG-PIN on pre-biopsy prostate-specific antigen (PSA) levels and the risk of cancer development in subsequent biopseis.Material and methodsThe 1,010 men suspected for PCa were included in the study based on elevated PSA, and/or positive rectal examination. Transrectal ultrasound (TRUS) guided 10 core biopsy was performed. In those with extensive HG-PIN or ASAP on the first biopsy, and/or elevated PSA value, a second biopsy was performed.ResultsIn the second biopsy, PCa was diagnosed in 6 of 19 patients (31.57%) with extensive HG-PIN, in four of 40 (10%) with BPH, and in 4 of 18 (22.22%) with ASAP.There was a statistically significant difference between the values of PSA in the group of patients with ASAP in comparison to those with benign prostate hyperplasia (BPH) (p = 0.005) as well as in patients with HG-PIN in comparison to BPH (p = 0.02).ConclusionsA precancerous lesion diagnosed upon biopsy causes a statistically significant increase in the values of PSA in relation to BPH, as well as in the case of ASAP and extensive HG-PIN.The estimate of risk of PCa diagnosis in patients with ASAP and those with extensive HG-PIN in the first biopsy is comparable, which is why there are no reasons for different treatment of patients with the above-mentioned diagnoses. Both should be subjected to urgent second biopsy in around the 4-6 weeks following the initial biopsy.

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Doxazosin triggers apoptosis via an imprecisely defined receptor mechanism that is related to tumor necrosis factor receptors (TNFRs). The aim of this study was to determine CD95, TNFR-1, TNFR-2, CD40 expression in primary prostate epithelial cultures incubated with doxazosin. Epithelial cultures were cultivated from 10 benign prostate hyperplasia patients. The cells were incubated with 20, 50 and 80 lM of doxazosin. Apoptosis was confirmed by fluorescence microscopy and flow cytometry. The cells were analyzed for expression of FAS, CD40, TNFR-1 and TNFR-2 by flow cytometry. Early apoptotic cells were present in all groups. A positive correlation was noticed between doxazosin dose and TNFR-1-, -2-positive cells. A decrease of CD40-positive cell population was observed in the lowest concentration. A decrease of mean fluorescence intensity signal of CD40 and CD95 was observed in the lowest concentration. Doxazosin-triggered apoptosis was doseindependent. The initiation of apoptosis was a result of receptors 'crosstalk' rather than a single receptor pathway activation. TNF receptor self-assembly process should be checked as a potential mechanism leading to apoptosis after doxazosin treatment.