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PubMed2000

Benign prostatic hyperplasia and prostate carcinoma in native Africans.

OBJECTIVE: To study the factors associated with morbidity and mortality in benign prostatic hyperplasia (BPH) and carcinoma of the prostate in native Africans. PATIENTS AND METHODS: A prospective study was conducted from 1993 to 1998 at the Ahmadu Bello University Teaching Hospitals, Zaria, Nigeria. During this 5-year period 686 patients were investigated and treated for symptoms and signs of prostatism. They were followed up for a mean (range) of 19.5 (1-60) months. RESULTS: BPH was found in 588 and clinical carcinoma in 98 patients. Adequate results, including a histological diagnosis, were available for 640 patients; there were 545 patients with BPH and 95 patients with histologically diagnosed prostate cancer. Treatment consisted of open prostatectomy for BPH, and subcapsular orchidectomy and/or open bladder-neck wedge resection for patients with prostate cancer and bladder neck obstruction. Within 6 months of surgery, four of 545 (0.7%) patients with BPH and 25 of 95 (26. 3%) with prostate cancer had died. Two-thirds of the patients with cancer presented with paraparesis or paraplegia. CONCLUSIONS: BPH and prostate cancer cause significant morbidity and mortality in African men. There is a need for health education about the early recognition of symptoms. Provision of facilities for transurethral prostatectomy would minimize the complications of surgery and ensure better use of the meagre resources available for health care.

Africa↗
PubMed1995

Prostate-specific antigen density: correlation with histological diagnosis of prostate cancer, benign prostatic hyperplasia and prostatitis.

OBJECTIVE: To assess the additional value of prostate-specific antigen density in the diagnosis of prostate cancer in patients who undergo prostate biopsies. PATIENTS AND METHODS: The study comprised 376 patients with symptoms of prostatism who were undergoing prostate biopsy. Digital rectal examination (DRE) and transrectal ultrasonography (TRUS) were performed and the prostate specific antigen level (PSA) and density (PSAD) were determined for each patient. RESULTS: Both PSA and PSAD significantly differentiated (P < 0.001) between benign and malignant histology. Of the 376 patients, 91 (24%) had a PSA level in the intermediate range (4.0-10.0 ng/mL). In these patients PSAD was significantly better than PSA in differentiating between benign and malignant histology (P = 0.027 vs 0.316). With a PSAD limit of 0.15 ng/mL/cm3 in these patients, the sensitivity was 92% and the specificity was 54% for the diagnosis of prostate cancer. No patient with a positive biopsy had a PSAD < 0.11 ng/mL/cm3. No limiting value could be found for PSAD that combined both an acceptable sensitivity and specificity. Of the patients with a malignancy detected by the biopsy, 92% also had a suspect DRE. CONCLUSION: In patients with intermediate PSA levels, PSAD is of limited additional value when compared to DRE in correctly diagnosing prostate cancer. Acute prostatitis is also a possible cause of elevated PSA. Both PSA and PSAD had no additional value in differentiating between benign prostatic hyperplasia (BPH) and histologically proven extensive prostatitis.

Aged↗
PubMed1994

Differentiation of benign prostatic hyperplasia and prostate cancer employing prostatic-specific antigen density.

To enhance the ability of prostate-specific antigen (PSA) to distinguish benign prostatic hyperplasia (BPH) from cancer of the prostate (CaP) Benson et al. defined a new parameter, PSA density (PSAD), which is the ratio of the serum PSA concentration to the volume of the prostate. We have employed this parameter in a prospective study of 28 patients with clinically localised CaP and 57 patients with BPH. Mean PSAD was 0.116 for the BPH patients and 0.46 for the CaP patients (p < 0.005). The authors conclude that the information provided by PSAD is superior to absolute PSA values in the differentiation between BPH and CaP.

Biomarkers, Tumor↗
PubMed1994

Responses to the antagonistic analog of LH-RH (SB-75, Cetrorelix) in patients with benign prostatic hyperplasia and prostatic cancer.

Among new highly potent antagonistic analogs of luteinizing hormone-releasing hormone (LH-RH), containing neutral hydrophilic D-ureidoalkyl amino acids such as D-Cit and D-Hci at position 6 and free of edematogenic and anaphylactoid reactions, Ac-D-Nal(2)1, D-Ph(4Cl)2, D-Pal(3)3, D-Cit6, D-Ala10 (LH-RH) (SB-75; Cetrorelix) was shown to be one of the most powerful. In this trial, we evaluated the response to 500 micrograms SB-75 given every 12 hr subcutaneously (sc) for 4 weeks in 11 patients with benign prostatic hyperplasia (BPH), and 6 weeks in 6 prostatic cancer patients (2 stage C, 4 stage D2). In patients with BPH presenting with prostatism and urinary outflow obstruction, there was a noticeable clinical improvement after the first week of SB-75 administration. This improvement continued during the course of treatment. Before therapy with SB-75, the serum levels of prostate-specific antigen (PSA) (6.73 +/- 1.46 ng/ml), acid phosphatases, total (12.67 +/- 1.15 U/l), and prostatic (2.27 +/- 0.34 U/l), were mildly elevated, but declined to normal values at 4 weeks: (2.13 +/- 0.59 ng/ml; P < 0.01), (7.68 +/- 0.89 U/l; P < 0.01), and (1.39 +/- 0.18 U/l; P < 0.01), respectively. Mean prostatic volume assessed by ultrasonography showed a significant decrease in all patients from 67.84 +/- 8.86 to 37.92 +/- 8.52 cm3; P < 0.01, which represents a reduction of 44%. In patients with prostate cancer, after the first week of therapy with SB-75, we observed a significant decrease in bone pain, relief in urinary outflow obstruction, and reversal of the signs of prostatism. Subjective improvement continued during the following weeks of treatment, so that the patients no longer needed analgesics. PSA, acid, and alkaline phosphatases gradually fell, achieving nearly normal values at 6 weeks. Initial serum testosterone levels in BPH and prostatic cancer patients were within normal limits, but during treatment with the antagonistic analog SB-75, fell to castration values. A major fall in free testosterone levels was observed after the first dose; the maximal inhibition was seen after 6-12 hr, with a simultaneous decrease in levels of both gonadotropins. Our results show that antagonist SB-75 can be safely administered for prolonged periods of time. The rapid shrinkage of the prostate and concomitant improvement in obstructive symptoms of prostatism obtained with antagonistic analog SB-75 in patients with BPH may decrease the morbidity of prostatic surgery and offer a therapeutic alternative in men who are considered poor surgical risks.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid Phosphatase↗
PubMed1998

Detection of human papillomavirus (HPV) DNA in archival specimens of benign prostatic hyperplasia and prostatic cancer using a highly sensitive nested PCR method.

Human papillomavirus is thought to be an etiological factor for urological tumors such as penile cancer. However, there is much conflicting data surrounding prostatic cancer. We recently established a highly sensitive nested PCR method with consensus human papillomavirus (HPV) primers for the detection of many high-risk HPV types. HPV DNA from the long-control region (LCR) to E7 open reading frame was amplified with first primer pairs and subsequently amplified with second internal E6-E7 primers. Our nested PCR method could detect HPV16, 18, 31, 33, 35, 52, 58 and some undetermined HPV DNAs. Using this method, we investigated the existence of HPV DNA in formalin-fixed paraffin-embedded tissue of the prostate. We found HPV DNA in three of 71 specimens of benign prostatic hyperplasia (BPH) and in none of 38 prostatic carcinomas. These three samples were infected with HPV 16. These results suggest that HPV is not a causal factor for prostatic cancer and BPH.

Base Sequence↗
PubMed2004

Phytoestrogen tissue levels in benign prostatic hyperplasia and prostate cancer and their association with prostatic diseases.

OBJECTIVES: To compare phytoestrogen tissue levels in men with small-volume benign prostatic hyperplasia (BPH), large-volume BPH, and prostate cancer (PCa). METHODS: Prostatic tissue samples of men consuming a Western diet who underwent surgery for BPH (n = 63) or PCa (n = 31) were collected and frozen at -40 degrees C. In the tissue samples, the enterolactone and genistein levels were determined in duplicate by monoclonal antibody-based immunoassays. We subsequently compared the tissue levels in patients with BPH and PCa and studied the impact of enterolactone and genistein on prostate volume. RESULTS: The enterolactone tissue levels were comparable in patients with BPH and PCa and revealed no correlation to prostate volume. The genistein tissue levels tended to be lower in patients with PCa (median 8.4 ng/g dry weight) compared with the entire BPH group (11.0 ng/g dry weight; P = 0.072). In addition, the genistein tissue levels were significantly greater in men with small-volume BPH (median 20.9 ng/g dry weight) compared with those with large-volume BPH (8.8 ng/g dry weight; P = 0.023). CONCLUSIONS: Our data suggest an involvement of genistein in the pathogenesis of BPH and, possibly, of PCa. The impact of enterolactone is currently unknown.

4-Butyrolactone↗
PubMed2002

Alterations in gap junction protein expression in human benign prostatic hyperplasia and prostate cancer.

PURPOSE: Gap junctions composed of connexin proteins have an essential role in intercellular communication and differentiation. Dysregulation of connexin expression is believed to have a role in carcinogenesis. The human prostate has been reported to express connexin 32 and 43. However, the expression pattern in prostate cancer is controversial, while to our knowledge connexin expression has not been reported in benign prostatic hyperplasia (BPH). To understand the potential involvement in prostate disease connexin 32 and 43 expression was evaluated in a series of normal prostate, BPH and prostate cancer specimens that were surgically removed due to bladder outlet obstruction. MATERIALS AND METHODS: Frozen sections of 23 normal, 43 BPH and 40 cancer involved prostates were evaluated for the presence, staining intensity and pattern of connexin 32 and 43 by immunocytochemical testing. RESULTS: In all specimens examined connexin 43 stain was punctate along the borders of the basal epithelial cells, whereas connexin 32 immunolocalized to luminal epithelial cells. In normal prostate connexin 43 and 32 were present in 87% and 65% of specimens, respectively, at low to moderate stain intensity. Importantly none of the normal samples were negative foreach connexin. In BPH specimens there was a marked increase in the incidence and intensity of connexin 43 and 32 immunostaining within epithelial cells. In addition, 23% of BPH samples showed strong connexin 43 expression in stromal cells. In contrast, connexin was decreased in prostate cancer specimens, of which 65% and 38% were negative for connexin 43 and 32, respectively, and 28% were negative for each type. In poorly differentiated tumors connexin 43 and 32 were present in only 10% and 40% of tumors, respectively, at low immunostaining intensity. CONCLUSIONS: In normal human prostate basal cells communicate via connexin 43 gap junctions, whereas luminal cells communicate via connexin 32 gap junctions. In BPH gap junctional intercellular communication is increased in epithelial and stromal cells, which may have a role in BPH pathogenesis. In prostate cancer gap junctional intercellular communication is decreased, is as indicated by decreased expression of connexin 43 and 32 with severe loss in poorly differentiated prostate cancer. These alterations in connexin expression may have a role in dedifferentiation and tumor progression.

Adenocarcinoma↗
PubMed2001

Alterations in gap junction protein expression in human benign prostatic hyperplasia and prostate cancer.

PURPOSE: Gap junctions composed of connexin proteins have an essential role in intercellular communication and differentiation. Dysregulation of connexin expression is believed to have a role in carcinogenesis. The human prostate has been reported to express connexin 32 and 43. However, the expression pattern in prostate cancer is controversial, while to our knowledge connexin expression has not been reported in benign prostatic hyperplasia (BPH). To understand the potential involvement in prostate disease connexin 32 and 43 expression was evaluated in a series of normal prostate, BPH and prostate cancer specimens that were surgically removed due to bladder outlet obstruction. MATERIALS AND METHODS: Frozen sections of 23 normal, 43 BPH and 40 cancer involved prostates were evaluated for the presence, staining intensity and pattern of connexin 32 and 43 by immunocytochemical testing. RESULTS: In all specimens examined connexin 43 stain was punctate along the borders of the basal epithelial cells, whereas connexin 32 immunolocalized to luminal epithelial cells. In normal prostate connexin 43 and 32 were present in 87% and 65% of specimens, respectively, at low to moderate stain intensity. Importantly none of the normal samples were negative foreach connexin. In BPH specimens there was a marked increase in the incidence and intensity of connexin 43 and 32 immunostaining within epithelial cells. In addition, 23% of BPH samples showed strong connexin 43 expression in stromal cells. In contrast, connexin was decreased in prostate cancer specimens, of which 65% and 38% were negative for connexin 43 and 32, respectively, and 28% were negative for each type. In poorly differentiated tumors connexin 43 and 32 were present in only 10% and 40% of tumors, respectively, at low immunostaining intensity. CONCLUSIONS: In normal human prostate basal cells communicate via connexin 43 gap junctions, whereas luminal cells communicate via connexin 32 gap junctions. In BPH gap junctional intercellular communication is increased in epithelial and stromal cells, which may have a role in BPH pathogenesis. In prostate cancer gap junctional intercellular communication is decreased, is as indicated by decreased expression of connexin 43 and 32 with severe loss in poorly differentiated prostate cancer. These alterations in connexin expression may have a role in dedifferentiation and tumor progression.

Adenocarcinoma↗
PubMed1993

Evaluation of PAP and PSA gene expression in prostatic hyperplasia and prostatic carcinoma using northern-blot analyses, in situ hybridization and immunohistochemical stainings with monoclonal and bispecific antibodies.

In this report we have investigated levels of prostatic acid phosphatase (PAP) and prostate-specific antigen (PSA) gene expression in prostatic carcinoma (Ca) and benign prostatic hyperplasia (BPH) specimens. Northern-blot analyses of total prostatic mRNA indicated that there was a tendency towards lower amounts of PAP mRNA and PSA mRNA in the Ca specimens than in the BPH specimens, although, because of the great variation in the expression levels of both mRNAs, these differences were not statistically significant. In situ hybridization analyses clearly showed that both PAP and PSA mRNAs were confined to the columnar epithelial cells and that stromal cells were devoid of these mRNAs. In addition, PAP and PSA mRNAs were more abundant in BPH tissue than in adjacent Ca tissue within the same specimen. The levels of PAP and PSA enzymes were analyzed immunohistochemically using a bispecific antibody having high affinity for both PAP and PSA, and the results were compared with those obtained using monoclonal anti-PAP and anti-PSA antibodies. All 3 antibodies stained only epithelial cells and BPH tissue consistently gave more intense staining than Ca tissue. Furthermore, the anti-PSA and the bispecific anti-PAP-PSA antibodies stained well or moderately differentiated Ca tissues more strongly than poorly differentiated Ca tissues. No PSA staining was detected in 3 and no PAP staining in 5 of the moderately or poorly differentiated carcinomas (grades II or III). Our results show that, in comparison with BPH tissue, prostatic Ca tissue is associated with significantly lower levels of mRNAs coding for the prostatic marker enzymes PAP and PSA, as well as with lower concentrations of these enzymes. Furthermore, dedifferentiation of prostate Ca is associated with a decrease in the level of intraprostatic PSA.

Acid Phosphatase↗
PubMed1992

Inter-relation between measurement of serum prostatic specific antigen and transrectal ultrasound in the diagnosis of benign prostatic hyperplasia and prostatic cancer.

Serum prostatic specific antigen (PSA) and ultrasound-determined prostatic volume (UPV) were measured in 50 patients with histologically proven benign prostatic hyperplasia (BPH) and in 40 patients with histologically proven prostatic cancer of whom 17 had evidence of distant metastases (M1) and 23 did not (M0). A good correlation between log PSA and UPV was demonstrated in the BPH group and rearrangement of the linear regression equation allowed calculation of a single variable--the log PSA corrected to a standard prostate volume for any given individual. A volume-corrected PSA correctly identified all patients with M1 disease and greatly improved but did not eliminate overlap of M0 disease with BPH. Reduction of serum PSA to a single volume-corrected variable will allow the introduction of practical and optimum protocols for the management of patients with prostatic enlargement.

Aged↗
PubMed2004

A system for studying epithelial-stromal interactions reveals distinct inductive abilities of stromal cells from benign prostatic hyperplasia and prostate cancer.

The development of normal and abnormal glandular structures in the prostate is controlled at the endocrine and paracrine levels by reciprocal interactions between epithelium and stroma. To study these processes, it is useful to have an efficient method of tissue acquisition for reproducible isolation of cells from defined histologies. Here we assessed the utility of a standardized system for acquisition and growth of prostatic cells from different regions of the prostate with different pathologies, and we compared the abilities of stromal cells from normal peripheral zone, benign prostatic hyperplasia (BPH-S), and cancer to induce the growth of a human prostatic epithelial cell line (BPH-1) in vivo. Using the tissue recombination method, we showed that grafting stromal cells (from any histology) alone or BPH-1 epithelial cells alone produced no visible grafts. Recombining stromal cells from normal peripheral zone with BPH-1 cells also produced no visible grafts (n = 15). Recombining BPH-S with BPH-1 cells generated small, well-organized, and sharply demarcated grafts approximately 3-4 mm in diameter (n = 9), demonstrating a moderate inductive ability of BPH-S. Recombining stromal cells from cancer with BPH-1 cells generated highly disorganized grafts that completely surrounded the host kidney and invaded into adjacent renal tissue, demonstrating induction of an aggressive phenotype. We conclude that acquisition of tissue from toluidine blue dye-stained specimens is an efficient method to generate high-quality epithelial and/or stromal cultures. Stromal cells derived by this method from areas of BPH and cancer induce epithelial cell growth in vivo, which mimics the natural history of these diseases.

Cell Communication↗
PubMed2002

Expression, localization and activity of neutral endopeptidase in cultured cells of benign prostatic hyperplasia and prostate cancer.

PURPOSE: Neutral endopeptidase is a cell surface enzyme that cleaves and inactivates neuropeptides. Neutral endopeptidase is expressed by prostatic epithelial cells and is thought to have a key role in the growth of androgen independent prostate cancer. In contrast to the encouraging data dealing with neutral endopeptidase and prostate cancer progression, only few studies are available of the significance of neutral endopeptidase in prostatic stromal cells and benign prostatic hyperplasia (BPH). We report the expression and activity of neutral endopeptidase in human prostatic stromal cells. MATERIALS AND METHODS: We recently established and characterized human prostatic stromal cells from BPH tissue. Reverse transcriptase-polymerase chain reaction, Western blot experiments and immunohistochemistry were performed to investigate the expression levels of neutral endopeptidase and show the cellular localization of the enzyme in these cells. Enzymatic neutral endopeptidase activity was evaluated using a colorimetric assay in nonstimulated cells, and after androgen and estrogen application. RESULTS: Stromal BPH cells showed strong expression of the neutral endopeptidase messenger RNA and protein, equaling the neutral endopeptidase expression level in prostate cancer cells. The neutral endopeptidase protein located in the plasma membrane of the cells showed a mean enzymatic activity plus or minus standard deviation of 75% +/- 2.5% compared with LNCaP prostate cancer cells. Interestingly enzymatic activity of the membrane bound neutral endopeptidase in stromal cells was not regulated by androgen and estrogen. CONCLUSIONS: These data suggest that neutral endopeptidase is expressed by prostatic stromal cells. In addition to its role in the progression of prostate cancer, it may also be involved in regulatory processes in the stroma, namely the degradation of neuropeptides released from prostatic neuroendocrine cells.

Cells, Cultured↗
PubMed1988

Prolactin and luteinizing hormone-releasing hormone receptors in human benign prostatic hyperplasia and prostate cancer.

Using a sensitive micromethod for the determination of prolactin (PRL) binding sites based on 125I-human PRL ligand, PRL receptor levels in specimens of benign prostatic hyperplasia (BPH) and human prostate cancer were estimated by the one-point assay system. Ten of 19 BPH specimens (53%), showed significant PRL binding, four being in the 9-12 fmol/mg range. All ten of these cases had an histological diagnosis of nodular glandular hyperplasia. Of ten adenocarcinomas examined, four samples (40%) exhibited positive PRL binding, the highest receptor levels being 10.2 fmol/mg protein. To characterize the receptors from BPH membranes, samples were then separately pooled according to the results obtained in one-point assays. In the PRL-negative pool no displacement could be detected. In the PRL-positive pool, the Scatchard analysis revealed one class of receptors with an average affinity Kd = 1.1 X 10(-9) M and capacity Bmax = 287 fmol/mg protein. In the prostate cancer specimens, luteinizing hormone-releasing hormone receptors with a high affinity and a low capacity were also found. The results indicate the presence of prolactin receptors in prostate cancer and in BPH. The clinical implications of such findings are not clear, but it is possible that a certain proportion of BPH and prostate cancers might be in part PRL dependent. Further studies are necessary to ascertain this hypothesis in an attempt to improve the treatment of BPH and prostate cancer.

Gonadotropin-Releasing Hormone↗
PubMed2002

Assessing the vascular-stromal coefficient in patients with benign prostatic hyperplasia or prostate cancer using transrectal ultrasonography and power Doppler analysis.

OBJECTIVES: To assess a coefficient of the prostatic blood supply in patients with prostate cancer or benign prostatic hyperplasia (BPH), and thus improve the diagnostic and prognostic variables needed to evaluate patients with prostate cancer. PATIENTS AND METHODS: The vascular-stromal coefficient was defined as the ratio of the blood vessel surface area and the surface area of the prostate, using power Doppler functions and transrectal ultrasonography. The index was calculated for the plane of the prostatic surface from the apex to the widest points of the peripheral zone, and for the plane across the highest density of blood vessels in the transition zone. A micobubble contrast agent was used to intensify the acoustic signals from prostatic vessels. The images were reconstructed in three dimensions. In all, 61 patients with BPH and 32 with confirmed prostate cancer were examined, and compared with a control group of young men. RESULTS: In the horizontal plane crossing the apex of the prostate, the vascular-stromal coefficient was 0.0054 for the controls, 0.0072 for BPH and 0.0067 for cancer. At the level of the highest density of blood vessels the respective values were 0.0083, 0.038 and 0.029. The respective values for the first plane after using the contrast agent were 0.025, 0.092 and 0.0365, and in the second level 0.04, 0.15 and 0.14. CONCLUSION: The vascular-stromal coefficient measured at both levels was higher in patients with BPH than in those with cancer or than in the controls. The prostatic vascular system can be computer-reconstructed in three dimensions, allowing an evaluation of asymmetry and other vascular abnormalities. The contrast agent effectively increases the vascular acoustic signals from the prostate, enhancing by a factor of five the visualization of blood vessels when using the power Doppler option.

Aged↗
PubMed2006

Prostate tissue and leukocyte levels of n-3 polyunsaturated fatty acids in men with benign prostate hyperplasia or prostate cancer.

OBJECTIVE: To compare the levels of n-3 polyunsaturated fatty acids (PUFAs) in leukocytes and prostate tissue in men with prostate cancer or benign prostatic hyperplasia (BPH), as dietary intake of n-3 PUFAs has been linked to the risk of prostate cancer; the prostate-specific antigen (PSA) level was also compared to prostate tissue levels of n-3 PUFAs. PATIENTS AND METHODS: Prostate tissue was obtained and leukocytes isolated from 20 men with prostate cancer and 35 with BPH. The n-3 PUFAs alpha-linolenic acid (ALA), eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) were measured in prostate tissue and in peripheral blood leukocytes using gas chromatography. PSA levels were measured in all of the men. RESULTS: There was a strong positive correlation between EPA and DHA in leukocytes and in prostate tissue (EPA: r = 0.80, DHA: r = 0.53, both P < 0.001) in all the men, whereas there was no association between the content of ALA in leukocytes and in prostate tissue (r = -0.15). Men with BPH had similar levels of ALA in leukocytes and in prostate tissue, but men with prostate cancer had more ALA in prostate tissue than in leukocytes. The PSA level was significantly positively correlated with ALA level in prostate tissue (r = 0.42, P < 0.01) but there was no significant correlation between PSA level and EPA and DHA levels. There were no significant correlations between PSA level and n-3 PUFA levels in leukocytes. CONCLUSION: Dietary intake of the marine n-3 PUFAs reflected in EPA and DHA levels in leukocytes are also reflected in EPA and DHA levels in prostate tissue in men with and without prostate cancer. However, there is a discrepancy between the levels of ALA in leukocytes and in prostate tissue, with higher levels in men with prostate cancer. This is in accordance with the strong positive association between PSA and ALA levels in prostate tissue. This study therefore does not support the hypothesis that intake of marine n-3 PUFAs might protect against prostate cancer, but lends support to the deleterious role of ALA in the development of prostate cancer.

Aged↗
PubMed2005

Serum interleukin-11 in patients with benign prostatic hyperplasia and prostate cancer.

To clarify whether serum levels of interleukin-11 (IL-11) could be a useful marker in patients with prostate cancer, serum IL-11 was determined in 73 and 23 men with prostate cancer and benign prostate hyperplasia (BPH), respectively, before treatment. There were no statistical differences of IL-11 levels between patients with prostate cancer and BPH. Patients with hormone-resistant prostate cancer had a significantly higher level of IL-11 than those with untreated cancer. Serum IL-11 levels may be a potential tumor marker for prostate cancer progression.

Aged↗
PubMed1998

The clinical utility of measuring free-to-total prostate-specific antigen (PSA) ratio and PSA density in differentiating between benign prostatic hyperplasia and prostate cancer.

OBJECTIVE: To evaluate the role of free-to-total prostate-specific antigen ratio (f/tPSA), prostate volume and PSA density in differentiating between men with prostate cancer and benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: The study comprised 51 patients who were assessed after transurethral electroresection of the prostate (16 with prostate cancer and 35 with BPH). Patients with a tPSA of < or = 4.0 ng/mL and > or = 30.0 ng/mL were excluded from the analysis. Total and fPSA were measured using an immunoradiometric assay and prostate volume was determined by transrectal ultrasonography. The incidence of prostate cancer and BPH was then compared with the PSA variables to determine specificity and predictive value. RESULTS: Most patients with BPH had a tPSA of 4.0-6.0 ng/mL; no patients with BPH had a tPSA of > 20.0 ng/mL. Most patients with prostate cancer had a f/tPSA of 6-10%. The area under the receiver operating characteristic curve for f/tPSA was significantly greater than that for tPSA (P < 0.003). CONCLUSIONS: The measurement of f/tPSA and PSA density increase the specificity of the differential diagnosis between BPH and prostate cancer.

Aged↗
PubMed1998

Endothelial cell proliferation activity in benign prostatic hyperplasia and prostate cancer: an in vitro model for assessment.

PURPOSE: Urinary excretion of several pro-angiogenic and antiangiogenic substances has been correlated with malignant tumor growth. The aim of this study was to assay angiogenic activity in urine from patients with cancer of the prostate and benign prostatic hyperplasia (BPH). MATERIALS AND METHODS: Urine specimens from 22 healthy male volunteers (control), 33 patients with BPH and 29 with organ confined prostate cancer were analyzed for angiogenic activity in a bovine capillary endothelial cell proliferation assay. In parallel the concentration of basic fibroblast growth factor and vascular endothelial growth factor was determined by enzyme immunoassay in the corresponding urine specimens. RESULTS: Urine samples from patients with BPH and prostate cancer increased bovine capillary endothelial cell proliferation by 13.1% and 15.1%, respectively, whereas urine from the control group showed a significantly lower angiogenic activity, increasing endothelial cell proliferation by only 0.7% (p = 0.001). Urinary basic fibroblast growth factor and vascular endothelial growth factor were highest in patients with BPH and lowest in the group with prostate cancer (p = 0.0001). CONCLUSIONS: Urine from patients with BPH and prostate cancer stimulates endothelial cell proliferative activity. The degree of endothelial cell stimulation does not correlate with the concentration of basic fibroblast growth factor or vascular endothelial growth factor. Whether the observed pro-angiogenic activity is due to an increased production or release of (an) other angiogenic factor(s) and/or loss of (an) angiogenesis inhibitor(s), deserves further investigation.

Adult↗