Benigner Prostatahyperplasie, 1 EL

RöFo März 2015 Behandlung benigne Prostatahyperplasie

Wie wird man von Prostatitis Volksmittel befreien

BPH is associated with various lower urinary tract symptoms, which affect their day-to-day benigner Prostatahyperplasie. The patients underwent transurethral prostate benigner Prostatahyperplasie to address their primary urological problem.

All patients were evaluated by use of a comprehensive medical history and rectal digital examination. The preoperative evaluation also included serum prostate specific antigen PSA measurement and ultrasonographic benigner Prostatahyperplasie of prostate volume.

The mean PSA value of the patients was 9. The mean prostate volume was Conclusion: In this study, 1 EL discussed important genetic markers in benign prostatic hyperplasia patients which may, in the future, be used as markers for diagnosis and prognosis, as well as targets for therapeutic intervention.

Bei den Patienten wurde eine transurethrale Prostataresektion durchgeführt, um ihr primäres urologisches Problem zu behandeln.

Alle Patienten wurden benigner Prostatahyperplasie einer umfassenden Anamnese und einer rektalen digitalen Untersuchung beurteilt. Fazit: In dieser Studie wurden wichtige genetische Benigner Prostatahyperplasie bei benigner Prostatahyperplasie diskutiert, die möglicherweise in Zukunft als Marker für Diagnose und Prognose sowie als Ansatzpunkte für therapeutische Intervention dienen können.

Benign prostatic hyperplasia BPH is one of the most common diseases found in adult men [1]. BPH is characterized by the proliferation of smooth muscle cells and epithelial cells 1 EL the prostatic transition zone [1]. The exact etiology benigner Prostatahyperplasie mechanisms underlying BPH development and progression are not fully understood [1][2]. Benign prostatic hyperplasia mostly develops in a small region, the transition zone, close to the urethra [3].

Prostatic cancer and benign prostatic hyperplasia are often found at the same time in elderly men; however, the relation between the two has been controversial since their benigner Prostatahyperplasie descriptions [4]. The American Urological Association Symptom Index AUASI score is a self-administered questionnaire, used to assess the severity of three storage symptoms frequency, nocturia, urgency and four voiding symptoms feeling of incomplete emptying, intermittency, straining, and a weak stream and to help diagnose BPH.

How benigner Prostatahyperplasie the patient experiences each symptom is rated on a scale of 1 to 5 [5]. Cytogenetic information on malignant and benign prostatic 1 EL is limited because of the difficulties benigner Prostatahyperplasie culturing prostatic epithelial cells. Few studies have been conducted on chromosomal abnormalities and gene polymorphisms in patients with BPH [8][9][10][11]therefore information regarding cytogenetic changes in these patients is scarce. The age of the patients ranged from benigner Prostatahyperplasie to 89 years.

The patients were preoperatively considered to have BPH and underwent surgery for their primary urological 1 EL. Preoperative evaluation consisted of rectal examination, transrectal sonography, prostate specific antigen PSA determination, and prostate biopsies, if warranted.

Benign hyperplastic 1 EL tissue samples were obtained from adenomectomy A and transurethral resection of prostate TURP or from cystoprostatectomy CP for invasive bladder cancer. Three slides were set for each case, and benigner Prostatahyperplasie slide was used for hybridization with a probe cocktail, one probe specific for the gene under investigation and the other specific benigner Prostatahyperplasie the chromosome containing the gene. Ten microliters of the denatured probe were placed on each slide, covered with a glass coverslip, and sealed with rubber cement.

Only intact, non-overlapping nuclei were evaluated; positive signals 1 EL required to be bright and of approximately equal intensity benigner Prostatahyperplasie the nuclei. Ratio under 2. For p53, we also defined the FISH score as the percentage of cells for which the nuclei had lost at least one signal. The specificity of the probes and the validity of this method were checked by dual-color FISH using normal prostate sections from five individuals and normal human male peripheral lymphocytes.

Data were analyzed using SPSS version Proportions were compared using chi-squared test. Two-tailed p -values were considered statistically significant if they were less than 0. To determine the efficiency of in situ hybridization, normal prostate sections from five individuals 1 EL peripheral lymphocytes from normal human male were hybridized with the three probe cocktails. Table 1 [ Tab. A total of 45 benign prostate tumor patients were included. The mean age was PSA level was 9.

The volume of prostate was The PSAD, prostate specific antigen density, was 0. With respect to surgery techniques, 26 patients With respect to the previous treatments, 33 out of 45 Three cases out of 45 6. Using FISH analysis, we found that 38 of 45 cases Thirty-nine out of 45 patients Out of the 45 patients, 4 8.

Also, out of the 45 patients, 5 For the p53 gene, 20 patients Table 4 [ Tab. For chromosome 17, loss or gain was detected in 6 out of 11 For chromosome 8, the proportion of abnormal cases in patients treated was For p53 and c-myc copy numbers, no significant difference could be detected.

Table 5 [ Tab. Univariate analysis revealed no association between benigner Prostatahyperplasie and clinicopathological characteristics of patients. Univariate analysis failed to reveal any significant association between the oncogene copy number and clinicopathologic variables examined. Chromosomal changes in normal prostatic tissue and in BPH tissue 1 EL been investigated in few studies in contrast to prostate cancer tissues.

Miyauchi et al. Trisomy of chromosomes 7 and 16 were observed in 2 BPH in the same study. Aly et al. Visakorpi et al. Balachandar et al. Deletions, translocations, inversions and mosaics were the major chromosomal aberrations observed in the patients regardless their age.

Chromosome 1, 7, 16 and Y were affected in BPH patients. InBalachandar et al. Recently, Altok et al. Loss of the Y chromosome was the most frequent chromosomal abnormality and was observed benigner Prostatahyperplasie three benigner Prostatahyperplasie 5.

In our study, we successfully investigated dual-color FISH cytogenetic analysis on 45 patients with histologically proven BPH using two oncogenes and one tumor suppressor gene. We wished to identify genetic alterations in BPH and to estimate their eventual correlations with the genetic alterations of prostatic adenocarcinoma. If the genetic alterations of the adenocarcinoma epithelial in origin are also present in nonmalignant BPH which usually do not evolve to benigner Prostatahyperplasie and 1 EL nonepithelial prostatic tissues, these changes cannot be considered relevant to benigner Prostatahyperplasie origin of prostatic adenocarcinoma.

Edwards et al. This is in contrast to Edwards et al. 1 EL c-myc oncogene is a transcription factor that has pleiotropic effects on cell growth and differentiation. Amplification or overexpression of c-myc was detected in many human cancers including prostate cancer. Specifically, c-myc mRNA levels were found to be significantly higher in malignant benigner Prostatahyperplasie compared to BPH [25] 1 EL, [26].

Amplification of the c-myc locus has been found in some primary prostate tumors and in lymph node metastases [27][28]. Other 1 EL reported no significant amplification of c-myc expression [29][30].

Fox et al. In our study, the c-myc oncogene was amplified in Bivariate analysis failed to reveal any significant association between oncogene amplification and the clinicopathologic variables examined. Thus, further study of c-myc gene is required to benigner Prostatahyperplasie the role of this oncogene in prostate cancer and in BPH. The main function of p53 gene is the prohibition of entrance into the synthetic phase of the cell cycle and the promotion of apoptosis in cells that are incompetent or have damaged DNA [32][33].

Abnormal p53 expression correlates with high histological grade, high stage and clinical progression of the disease [36] while, it is also correlated with reduced survival after radical prostatectomy [37] and disease onset modulation [38]. In our study, deletion of the p53 gene was the most significant finding. Twenty patients O'Leary et al. Roehrborn et al. This is the first report to demonstrate genetic alterations in Egyptian patients with BPH. The most important alteration detected is for p53; it showed abnormal copy number in the majority of our patients.

Consequently, deletion of p53, when evident in prostatic adenocarcinoma, cannot be considered specific of or relevant for the genesis of this tumor, but although the patients studied had no evidence of carcinoma, they may benigner Prostatahyperplasie develop prostate cancer or may have a latent disease that was not detected. Indeed, future studies including larger databases of patients, which integrate clinical, pathologic, and molecular oncogene parameters are strongly recommended to identify the possible genetic abnormalities underlying BPH etiopathogenesis.

The merging of these data may provide the clinician with an enhancement of prognostic information that accurately predicts the aggressive phenotype 1 EL benign prostatic hyperplasia. Genetic alterations in benign prostatic hyperplasia patients Genetische Veränderungen bei Patienten mit benigner Prostatahyperplasie Research Article Urology.

No previous reports have been obtained for genetic alterations studies performed on Egyptian BPH patients. We recorded The patients benigner Prostatahyperplasie had no evidence of carcinoma, they 1 EL develop prostate cancer. Future studies are recommended to identify the possible genetic abnormalities underlying BPH etiopathogenesis.