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PubMed1991

Alterations in sphingomyelin and fatty acids in human benign prostatic hyperplasia and prostatic cancer.

The present experiments were conducted to examine and characterize the lipid composition of benign prostatic hyperplasia (BPH) and prostatic cancer tissues (CAP). Lipids were extracted from these tissues and analyzed by thin layer chromatography (TLC) and gas liquid chromatography (GLC). The protein profiles of these tissues were analyzed by SDS-polyacrylamide gel electrophoresis. The results of these studies demonstrate that the principal lipids of BPH and CAP tissues are phosphatidyl choline, phosphatidyl ethanolamine, sphingomyelin, fatty acids and cholesterol. The sphingomyelin level is significantly higher in CAP tissues compared to BPH tissues. The differences in the enzymatic activities responsible for the biosynthesis and degradation of sphingomyelin appear to explain at least partially the alteration in sphingomyelin level between BPH and CAP tissues. The major fatty acids of phosphatidyl choline and phosphatidyl ethanolamine were palmitic (16:0), stearic (18:0), oleic (18:1) and arachidonic (20:4) acid. The arachidonic acid level was significantly decreased in CAP tissues compared to BPH tissues. SDS polyacrylamide gel electrophoresis revealed several protein differences between BPH and CAP tissues. The most significant difference was the decrease in 12 kDa protein in CAP tissues compared to BPH. The present data, therefore, suggests that there are significant alterations in sphingomyelin, fatty acids and protein profiles between BPH and CAP tissues.

Electrophoresis, Polyacrylamide Gel↗
PubMed1993

[The incidences of benign prostatic hyperplasia and prostatic cancer in China].

Step-sections of 321 prostatic specimens from unselected autopsies were examined in order to understand the incidences of benign prostatic hyperplasia (BPH) and prostatic cancer (CaP) in China. The results showed that the incidence of BPH in patients of 51-60, 61-70, 71-80, and 81-90 years old was 20%, 50%, 57.1% and 33.3% respectively. The incidence of latent CaP in the above-mentioned age series, including 60 prostatic specimens from cystoprostatectomies was 9.3%, 5.7%, 26.9% and 16.7% respectively. The Incidence of CaP in BPH surgical specimens was 33/676 (4.9%). The histological incidences of BPH and CaP in China were similar to or half of that of western world. But the epidemiological incidence of CaP in China was only 1/20-1/30. Further investigation about this condition is necessary.

Adolescent↗
PubMed1993

Nuclear matrix protein patterns in human benign prostatic hyperplasia and prostate cancer.

The nuclear matrix represents the structural component of the nucleus that determines nuclear shape and higher order DNA organization. We have previously shown tissue specificity in nuclear matrix proteins (NMP), in rat sex accessory tissues, and in a rat model of prostate cancer. This study compares NMP patterns for fresh human normal prostate, benign prostatic hyperplasia (BPH), and prostate cancer for 21 men undergoing surgery for clinically localized prostate cancer or BPH. NMP patterns were compared using high resolution two-dimensional polyacrylamide gel electrophoresis. We identified by molecular weight and isoelectric point 14 different proteins that were consistently present or absent among the various tissues. One protein (PC-1), a M(r) 56,000 protein with an isoelectric point of 6.58, appeared in 14 of 14 different nuclear matrix preparations from prostate cancer and was not detected in normal prostate (0 of 13) or BPH (0 of 14). The NMP patterns are consistent with a model of disease progression in which BPH shares many of the nuclear matrix changes observed in prostate cancer.

Antigens, Nuclear↗
PubMed1996

DNA fingerprint detection of somatic mutations in benign prostatic hyperplasia and prostatic adenocarcinoma.

Genetic alterations within diseased prostate tissue were analysed by genomic DNA fingerprinting using a minisatellite probe (lambda 33.6), a simple repetitive oligonucleotide probe (GTG)5, and an additional human multilocus probe (pV47-2). In prostatic adenocarcinoma, somatic mutations were detected in 77% of the samples compared with 38% of the benign prostatic hyperplasia samples. No correlation was evident with either the tissue histopathology or the grading or staging classification of the malignant tissue. Because one of the probes (pV47-2) did not demonstrate any changes in the tumour tissue, and because the probes exhibited specificity for different regions of the genome, it is possible to conclude that mutations occur widely throughout the genome, perhaps with the exception of certain domains. The results suggest that somatic mutations accompany the development of both benign and malignant pathologies of the prostate. Furthermore, benign prostatic hyperplasia should be considered as a risk indicator for processes leading to prostatic adenocarcinoma.

Adenocarcinoma↗
PubMed1998

Free and complexed prostate specific antigen in the differentiation of benign prostatic hyperplasia and prostate cancer: studies in serum and plasma samples.

PURPOSE: We prospectively evaluated serum and plasma concentrations of total and free prostate specific antigen (PSA), and PSA complexed to alpha1-antichymotrypsin in 170 patients who underwent biopsy, including 59 with prostate cancer and 111 with benign prostatic hyperplasia. We compared the usefulness of the ratios of free-to-total and complexed-to-total PSA for distinguishing between prostate cancer and benign prostatic hyperplasia, and studied the influence of blood clotting on the ratios. MATERIALS AND METHODS: Blood samples were processed to generate serum and citrated plasma. To calculate complexed-to-total and free-to-total PSA we assayed plasma and serum samples for total and complexed PSA using homemade immunoassays, and total and free PSA using the Immulite assay. The 2 total PSA assays were compared using the Tandem-E PSA assay. Receiver operating characteristics curves were constructed for the total population, and for 2 to 20, 4 to 20, 2 to 10 and 4 to 10 ng./ml. total PSA. RESULTS: In all groups complexed-to-total PSA had higher specificity than free-to-total and total PSA, especially at 90 to 100% sensitivity. Generally citrated plasma samples provided higher specificity than serum samples for all sensitivity values. The best performance for complexed-to-total and free-to-total PSA was obtained in the subset of patients in whom total PSA was 2 to 10 ng./ml. CONCLUSIONS: Our results indicate that the complexed-to-total PSA ratio performed better for classifying disease status than the free-to-total PSA ratio in the whole patient population and in the diagnostic gray zone of 2 to 10 ng./ml. In addition, plasma samples should be used to calculate the complexed-to-total and free-to-total PSA ratio.

Aged↗
PubMedDate not supplied

Expression of vascular endothelial growth factor (VEGF) and association with microvessel density in benign prostatic hyperplasia and prostate cancer.

BACKGROUND: Tumor angiogenesis is an absolute requirement for tumor growth and a prognostic factor for various malignant neoplasms. Recent reports in the literature have addressed the importance of the VEGF system in benign prostatic hyperplasia (BPH) and adenocarcinoma, however the results are controversial. The aim of the present study was to determine and compare the levels of VEGF expression and vascularity in BPH and prostate carcinoma. MATERIALS AND METHODS: We examined 60 prostate adenocarcinomas and 64 benign prostatic hyperplasias. Angiogenesis was estimated by determining microvessel counts (MVC), with the use of anti-CD31 and anti-CD34 antibodies. Expression of VEGF was also evaluated immunohistochemically. RESULTS AND CONCLUSION: Our data showed that angiogenesis was more prominent in carcinomas than in BPH. Furthermore, increased MVC was significantly associated with high-grade carcinomas. Angiogenesis was correlated with VEGF expression and it was, at least in part, mediated by the latter. Thus, prostate adenocarcinoma may represent a suitable neoplasm for antiangiogenic treatment in combination with conventional therapies.

Adenocarcinoma↗
PubMed2006

mRNA expression analysis of human kallikrein 11 (KLK11) may be useful in the discrimination of benign prostatic hyperplasia from prostate cancer after needle prostate biopsy.

Kallikrein 11 (KLK11, TLSP, hippostatin) is a member of the human kallikrein gene family, which includes PSA, KLK2 and 12 other members, all localized on chromosome 19q13.4. The aim of this study was to investigate whether KLK11 expression could be used to discriminate prostate cancer (CaP) from benign prostatic hyperplasia (BPH) in needle prostate biopsies. We analyzed the expression of the prostate-type variant of the KLK11 gene in 64 CaP and BPH tissues obtained by transrectal ultrasound-guided needle biopsy. Reverse transcription (RT), PCR and image analysis methodologies were developed and used. Of the 42 BPH tissues examined, only 10 (23.8%) were positive for prostate-type KLK11 expression, while of the 22 CaP patients, 12 (54.5%) were KLK11-positive (p=0.025). Logistic regression and receiver operating characteristic curve analyses demonstrated that KLK11 expression has a significant discriminatory value (crude odds ratio=3.84, p=0.016; area under the curve, 0.65, 95% CI 0.51-0.80) between CaP and BPH in needle prostate biopsies.

Age Distribution↗
PubMed1988

Metachromasia in the human prostate: a histochemical difference between benign prostatic hyperplasia and prostatic carcinoma.

Metachromasia is a histological staining reaction in which a dye is changed by the tissue from its original to a contrasting color. With toluidine blue at a pH of 8.3 or 3.8 metachromatic staining is seen in the tissue of benign prostatic hyperplasia. When adenocarcinoma is adjacent to or even within the prostate containing benign hyperplasia, no metachromasia is seen around the benign acini. No such staining was seen in glands examined that contained either well differentiated or moderately well differentiated adenocarcinoma. No metachromatic periacinar staining was noted in the normal prostate. This observation may provide information as to the morphogenesis of prostatic hyperplasia.

Adenocarcinoma↗
PubMed2002

Serum pro-gastrin-releasing peptide (31-98) in benign prostatic hyperplasia and prostatic carcinoma.

OBJECTIVES: To clarify whether serum levels of pro-gastrin-releasing peptide (ProGRP) (31-98) could be a useful marker in patients with prostatic carcinoma. GRP is produced and secreted by prostatic neuroendocrine cells. METHODS: Serum levels of ProGRP(31-98) were measured by enzyme-linked immunosorbent assay in 20 patients with benign prostatic hyperplasia and 107 patients with prostatic carcinoma. RESULTS: The mean serum levels of ProGRP(31-98) in patients with distant metastasis and hormone-resistant prostate cancer were significantly elevated compared with those in patients with organ-confined disease. Significantly elevated levels of ProGRP(31-98) were detected in 9 patients with prostatic carcinoma before any treatment. During hormone-resistant prostate cancer progression, ProGRP(31-98) levels were elevated in 9 patients (23%). Of the 9 patients with Stage D3 and elevated serum ProGRP, 4 had a normal serum prostate-specific antigen level. CONCLUSIONS: ProGRP may be a potential tumor marker for prostate cancer. Additional studies in large groups of patients are needed to define the clinical value of ProGRP.

Adenocarcinoma↗
PubMed1998

Distinct altered patterns of p27KIP1 gene expression in benign prostatic hyperplasia and prostatic carcinoma.

BACKGROUND: The p27KIP1 gene, whose protein product is a negative regulator of the cell cycle, is a potential tumor suppressor gene; however, no tumor-specific mutations of this gene have been found in humans. This study was undertaken to identify and to assess potential alterations of p27KIP1 gene expression in patients with benign prostatic hyperplasia (BPH) and patients with prostate cancer. METHODS: We analyzed 130 prostate carcinomas from primary and metastatic sites, as well as prostate samples from normal subjects and from patients with BPH. Immunohistochemistry and in situ hybridization were used to determine the levels of expression and the microanatomical localization of p27 protein and messenger RNA (mRNA), respectively. Immunoblotting and immunodepletion assays were performed on a subset of the prostate tumors. Associations between alterations in p27KIP1 expression and clinicopathologic variables were evaluated with a nonparametric test. The Kaplan-Meier method and the logrank test were used to compare disease-relapse-free survival. Prostate tissues of p27Kip1 null (i.e., knock-out) and wild-type mice were also evaluated. RESULTS: Normal human prostate tissue exhibited abundant amounts of p27 protein and high levels of p27KIP1 mRNA in both epithelial cells and stromal cells. However, p27 protein and p27KIP1 mRNA were almost undetectable in epithelial cells and stromal cells of BPH lesions. Furthermore, p27Kip1 null mice developed enlarged (hyperplastic) prostate glands. In contrast to BPH, prostate carcinomas were found to contain abundant p27KIP1 mRNA but either high or low to undetectable levels of p27 protein. Primary prostate carcinomas expressing lower levels of p27 protein appeared to be biologically more aggressive (two-sided P = .019 [Cox regression analysis]). CONCLUSIONS/IMPLICATIONS: On the basis of these results, we infer that loss of p27Kip1 expression in the human prostate may be causally linked to BPH and that BPH is not a precursor to prostate cancer.

Animals↗
PubMed1989

Urinary oestrogen excretion in benign prostatic hyperplasia and prostatic cancer.

Urinary oestrogen excretion was measured in 20 healthy middle-aged men (controls), in 30 patients with benign prostatic hyperplasia (BPH) and in 32 prostatic cancer (PC) patients. The mean oestradiol (E2) excretion was significantly lower in the PC patients than in the controls and BPH patients. No other significant differences were found in oestrone (E1), oestriol (E3) and total oestrogen (E1 + E2 + E3) excretion between the 3 groups. The decreased E2 excretion in the PC patients is in accordance with our previous finding concerning significantly lower E2 plasma levels in PC patients. It seems possible that elderly men with lower endogenous oestrogen levels are at higher risk of developing cancer. On the other hand, the age-dependent increased oestrogen levels may play an aetiological role in BPH.

Aged↗
PubMed2001

Insulin-like growth factor I (IGF-I) and IGF-binding protein-3 in benign prostatic hyperplasia and prostate cancer.

In view of evidence indicating significant involvement of the insulin-like growth factor (IGF) system in the pathogenesis of prostate cancer, we measured serum IGF-I and IGF-binding protein-3 (IGFBP-3) in men with benign prostatic hyperplasia (BPH; n = 75) or prostatic carcinoma (CaP; n = 84). The age-matched patient populations were selected to have circulating prostate-specific antigen (PSA), the most reliable predictor of CaP, in the overlapping diagnostic gray zone range of approximately 4--10 microg/L. Of particular interest was investigation of intact, fragment, and total IGFBP-3 levels in relation to PSA, which is also a well established IGFBP-3 protease. Among the key findings were significantly higher IGF-I and intact IGFBP-3 levels in CaP vs. BPH (P < 0.001), whereas changes in fragment and total IGFBP-3 were statistically insignificant. As expected, total PSA levels were similar in the two groups of patients (P = 0.173), whereas free PSA levels were significantly lower in those with CaP (P < 0.001). IGF-I and IGFBP-3 (intact and total) correlated significantly (P = 0.024 to <0.001) and inversely (r = -0.26 to -0.35) with free PSA in BPH, but not in CaP, and no correlations were found in comparisons involving total PSA. Statistical analysis of the various markers and their combinations indicated enhanced performance of IGF-I/free PSA [receiver operating characteristics area under the curve (AUC) = 0.728] and intact IGFBP-3/free PSA (AUC = 0.737) ratios in discriminating between BPH and CaP compared with the currently used free/total PSA ratio (AUC = 0.689). Multivariate logistic regression models confirmed the observed relationships and identified IGF-I/free PSA and intact IGFBP-3/free PSA as independent factors in predicting the presence of CaP. We conclude that increases in IGF-I and intact IGFBP-3 levels are positively associated with the presence of CaP in this group of patients with low to moderately elevated PSA, and that their measurements in relation to PSA may help improve diagnostic discrimination between BPH and prostate cancer.

Analysis of Variance↗
PubMed1998

Transforming growth factor beta 1 and its receptor types I and II. Comparison in human normal prostate, benign prostatic hyperplasia, and prostatic carcinoma.

An immunohistochemical and semiquantitative comparative study of transforming growth factor beta 1 (TGF-beta 1) and its receptor types I (TGF-beta RI) and II (TGF-beta RII) was carried out in normal prostates and in the prostates from men with benign prostatic hyperplasia (BPH), and men with prostatic adenocarcinoma. Immunoreaction to TGF-beta 1 was limited to the basal epithelial cells in the normal prostates. Some cells in the connective tissue stroma were also stained. In BPH immunolabelling was also observed in columnar (secretory) cells of the epithelium. In prostatic adenocarcinoma, all epithelial cell types were intensely immunostained. Some stromal cells were also stained. Immunostaining to TGF-beta RI was only present in the basal cells in normal prostates. In BPH, this immunoreaction was found in the whole epithelium and in some stromal cells. In prostatic cancer, the immunostaining pattern for this receptor was similar to that of BPH but more intense in the epithelial cells. Immunoreactivity to TGF-beta RII appeared in some basal cells and some scattered columnar cells of the normal prostate epithelium. In the BPH sections, this pattern was maintained, and a weak immunolabelling was also observed in the stroma. In prostate cancer, all epithelial cells appeared intensely labelled. In the stroma, immunolabelling was similar to that of the BPH specimens. The results of the present study suggest that, in normal prostates, only the basal cells of the epithelium possess both receptor types, and hence can transduce TGF-beta 1 signal intracellularly. The basal cells can also secrete this growth factor which would act as an autocrine inhibitory growth factor for them. In addition, TGF-beta 1 is secreted in some zones by stromal cells, acting then as a paracrine growth factor for basal cells in those areas. In BPH, in addition to the basal cells, some secretory columnar cells also secrete TGF-beta 1 and possess both types of TGF-beta 1 receptors, and thus, both epithelial cell types are susceptible to TGF-beta 1 action. Since both receptor types are also present in some stromal cells, these cells also perform an autocrine secretion, in addition to their paracrine secretion to the epithelial cells. TGF-beta RIIs seem to be more numerous than TGF-beta RIs and this lead us to hypothesize that these incomplete receptors might be a protection against the inhibition caused by TGF-beta 1 action. In prostatic carcinoma all cell types display the same characteristics as in BPH, although both receptor types are found in similar numbers, and thus, the above mentioned protection would not occur.

Adenocarcinoma↗
PubMedDate not supplied

[Effects of chronic bacterial prostatitis on changes in concentration and free and total prostatic specific antigen in the serum and urine from patients with benign prostatic hyperplasia and prostatic cancer].

A comprehensive urological examination was performed in 145 men with benign prostatic hyperplasia (BPH). Concentrations of total prostatic specific antigen (TPSA) suggested prostatic cancer (PC) in 38 patients while finger rectal examination and transrectal ultrasonic investigation gave no evidence for this diagnosis. All the patients have symptoms of chronic prostatitis (CP). All the patients with chronic bacterial prostatitis have undergone a course of antibacterial treatment after which the levels of TPSA and free prostatic specific antigen (FPSA) were evaluated. A polyposition biopsy of the prostate was also made. By its results two groups of patients were formed: 20 patients with BPH and CP (group 1) and 12 patients with CP and PC or prostatic ultraepithelial neoplasia. Low blood concentrations of TPSA high FPSA/TPSA, low urinary concentrations of TPSA and FPSA were registered after antibacterial and antiinflammatory treatment of CP combined with BPH. It is inferred that chronic bacterial prostatitis has a significant effect on PSA expression in BPH. This fact should be considered in interpretation of PSA values.

Adult↗
PubMed1982

Prostatic hexosaminidase activity in patients with benign prostatic hyperplasia and prostatic carcinoma.

Hexosaminidase activity in prostatic tissue has been compared in 15 patients with benign prostatic hyperplasia and 15 patients with prostatic carcinoma. The ratio of enzymatic activity for the two substrates tested (p-nitrophenyl-2-acetamido-2-deoxy-beta-D-glucopyranoside and p-nitrophenyl-2-acetamido-2-deoxy-beta-D-galactopyranoside) was not significantly different in the two groups of patients. The proportion of hexosaminidase represented by the B isozyme was not significantly different for the two groups of patients. Prostatic tissue hexosaminidase was greater (p = 0.0141) in carcinomatous prostates than in hyperplastic prostates.

Acetylglucosaminidase↗
PubMed1997

Practice patterns among primary care physicians in benign prostatic hyperplasia and prostate cancer.

BACKGROUND AND OBJECTIVES: Although patients with prostate disorders are frequently referred to urologists for diagnosis and management, primary care physicians (PCPs) are beginning to take a more active role. However, there is concern that PCPs are not optimally educated in the diagnosis and management of these disorders. This survey determined PCP practice patterns in evaluating and treating benign prostatic hyperplasia (BPH) and screening for prostate cancer. METHODS: A 10-question survey was completed by 344 physicians attending various scientific meetings in 1995. RESULTS: Most PCPs (89%) indicated that up to 30% of their patients have symptomatic BPH, and a significant proportion of these are treated initially by the PCP. Although 61% of PCPs are aware of the American Urological Association (AUA) symptom score and its recommended role in clinical practice guidelines, only 38% currently use it. Indications for using the AUA score include men with BPH symptoms (80%), men > 50 years (55%), and men with an abnormal digital rectal examination (DRE) (42%). The most popular BPH therapies are long-acting alpha blockers and watchful waiting. DRE is performed routinely by 84% of PCPs in men > 50 years, and annual serum prostate-specific antigen is routinely requested by 69% of PCPs. CONCLUSIONS: Although PCPs play an increasing role in the diagnosis and management of prostate disorders, they are not taking full advantage of published clinical practice guidelines.

Adult↗
PubMed2005

Serum hepatocyte growth factor activator (HGFA) in benign prostatic hyperplasia and prostate cancer.

OBJECTIVES: Hepatocyte growth factor activator (HGFA) is responsible for proteolytic activation of the precursor form of hepatocyte growth factor (HGF). We attempted to clarify whether serum levels of HGFA could be used as a marker for prostate cancer. MATERIAL AND METHODS: Serum levels of total HGF and HGFA were measured by enzyme-linked immunosorbent assay in 99 healthy controls, 27 patients with benign prostatic hyperplasia (BPH) and 119 patients with prostate cancer. RESULTS: : The mean+/-S.D. serum levels of HGFA in untreated prostate cancer and BPH cases were 0.42+/-0.24 and 0.50+/-0.26 ng/ml, respectively (no significant difference). Serum HGFA was significantly elevated in hormone-refractory prostate cancer (stage D3) compared to other stages, while HGF did not significantly differ with regard to clinical stage. CONCLUSIONS: Serum HGFA tends was elevated in patients with advanced stage prostate cancer. Further studies in large groups of patients are needed to clarify the clinical value of HGFA.

Aged↗
PubMed1994

Preliminary study of the frequency of benign prostatic hyperplasia and prostatic cancer in China.

OBJECTIVES: This study determined the frequency of benign prostatic hyperplasia (BPH) and cancer of the prostate (CaP) in China. METHODS: Prostate specimens from 321 unselected autopsies were collected from 1989 to 1992. Slices were cut vertically every 0.5 cm from apex to base. Five to 12 slices were obtained from each prostate. Specimens were stained with hematoxylin-eosin and Masson trichrome. Sixty surgical specimens obtained from cystoprostatectomies with intact prostate were included to determine the frequency of latent CaP. RESULTS: The frequency of BPH, by age, was as follows: 41 to 50 years, 13.2%; 51 to 60 years, 20%; 61 to 70 years, 50%; 71 to 80 years, 57.1%; 81 to 90 years, 83.3%. The frequency of latent CaP, by age, was as follows: 41 to 50 years, 2.2%; 51 to 60 years, 9.3%; 61 to 70 years, 5.9%; 70 years or older, 25%. Incidental CaP was found in 4.9% (33 of 676) of BPH surgical specimens. The incidence of and mortality from CaP in Beijing were 2.41 per 100,000 men and 1.19 per 100,000 men, respectively, between 1985 and 1987. CONCLUSIONS: BPH was rare in China in the early years of this century, but it has become a common disease in recent decades. The histologic frequency of BPH in China was similar to that in Western countries, but the histologic frequency of latent CaP was less than half that in Western countries. The incidence of and mortality from CaP in China are about 20 times less than those in Western countries. Histologic CaP in a Chinese man is not as likely to evolve into clinical CaP as in a Western man.

Adolescent↗