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PubMed1999

The insulin-like growth factor axis and prostate cancer: lessons from the transgenic adenocarcinoma of mouse prostate (TRAMP) model.

We have characterized the temporal expression of the insulin-like growth factor (IGF) axis in the transgenic adenocarcinoma of mouse prostate (TRAMP) model as prostate cancer progression in this model closely mimics that observed in the human disease, and the model provides samples representing the earliest stages of prostate cancer that are clinically the most difficult to obtain. We report that prostate-specific IGF-I mRNA expression increased during prostate cancer progression in TRAMP mice and was elevated in the accompanying metastatic lesions, whereas prostatic IGF-I mRNA remained at nontransgenic levels in androgen-independent disease. Expression of IGF-II mRNA, however, was reduced in primary prostate cancer, metastatic lesions, and androgen-independent disease. Expression of type-1 IGF receptor (IGF1R) mRNA, encoding the cognate receptor for both IGF-I and IGF-II, as well as type-2 IGF receptor (IGF2R) mRNA was not found to be altered during primary prostate cancer progression in intact TRAMP mice but was dramatically reduced in metastatic lesions and in androgen-independent disease. Similar to reports from clinical disease, serum IGF-I levels were observed to increase precociously in TRAMP mice early in disease progression but remained at nontransgenic levels after castration. Elevated serum levels of IGF-binding protein 2 were observed to correlate with advanced prostate cancer in the TRAMP model. Together these observations implicate IGF-I as an important factor during the initiation and progression of primary prostate cancer and provide evidence that there is a strong selection against expression of IGF1R and IGF2R in metastatic and androgen-independent disease.

Adenocarcinoma↗
PubMed2003

Probasin promoter (ARR(2)PB)-driven, prostate-specific expression of the human sodium iodide symporter (h-NIS) for targeted radioiodine therapy of prostate cancer.

Prostate cancer is one of the most promising candidates for sodium iodide symporter (NIS)-mediated gene therapy. Adenovirus-mediated expression of NIS that is driven by prostate-specific promoters induces generous radioiodine accumulation in prostate cancer cells that may be used for therapy with (131)I. We have recently developed a replication-deficient adenovirus carrying the human NIS cDNA linked to a composite probasin promoter, ARR(2)PB, aiming toward specific expression of the human NIS gene (h-NIS) in prostate tissue for targeted radioactive iodide therapy of prostate cancer (Ad-ARR(2)PB/hNIS). The ability of Ad-ARR(2)PB/hNIS to cause NIS expression in tumor cells was characterized by iodide uptake assay and compared with Ad-CMV/hNIS in which the h-NIS expression is driven by the cytomegalovirus (CMV) promoter. Androgen-dependent prostate cancer cell lines (LNCaP) and non-prostate origin tumor cell lines (SNU449, MCF-7, HCT116, OVCAR-3, and Panc-1) were infected with the viral constructs, and perchlorate-sensitive (125)I uptake and NIS protein expression were measured. Ad-ARR(2)PB/hNIS-infected LNCaP cells showed androgen-dependent and perchlorate-sensitive iodide uptake. Iodide accumulation in LNCaP cells infected with Ad-ARR(2)PB/hNIS, followed by incubation with synthetic androgen, was 5.3-fold increased compared with those coincubated with perchlorate (15,184 +/- 1,173 cpm versus 2,837 +/- 187 cpm). Ad-ARR(2)PB/hNIS-infected LNCaP cells revealed a 3.2-fold increase of iodide accumulation compared with those infected with Ad-CMV/hNIS (multiplicity of infection = 30). Iodide uptake in a panel of non-prostate tumor cell lines infected with Ad-ARR(2)PB/hNIS was no more than 2,500 cpm, demonstrating the tissue specificity of this construct. These results indicate that Ad-ARR(2)PB/hNIS can be used to achieve high-magnitude and tissue-specific expression of h-NIS in prostate tissue and is a promising candidate for cancer gene therapy of prostate cancer.

Adenoviruses, Human↗
PubMedDate not supplied

Salient and co-morbid features in benign prostatic hyperplasia: a histopathological study of the prostate.

OBJECTIVES: To study the salient histological features of prostatic tissues in relation to age and to analyse the co-morbid histopathological changes in benign prostatic hyperplasia. (BPH). DESIGN: Prospective study. SETTING: Histopathology unit of a busy clinical pathological laboratory in Kathmandu Metropolitan City. SUBJECTS: 106 prostatic biopsy specimens from patients diagnosed as BPH received for histopathological examination during 2001-2. MAIN OUTCOME MEASURES: Prominent histological features observed in prostatic biopsy specimens obtained from patients of various age groups and frequency of co-morbid histopathological changes in benign prostatic hyperplasia. RESULTS: Prominent histological features. All (106) specimens included in the series had BPH showing glandulostromal proliferation of which 4 cases (3.77%) (all aged below 70 years) showed predominantly stromal pattern. Corpora amylacea present in 25% (in 5th decade) increased in frequency to 100% (8th decade onwards) in the later years. Cystically dilated glands also showed age correlated increase (through 5th to 8th decade) from 50% to 100%. Other prominent features observed with an overall decreasing frequency in all age groups (taken together) were glands showing papillary infoldings (44.33%), lymphocytic collection/infiltration (31.13%), proteinaceous material (7.54%), calcification (6.60%), homogenous eosinophilic material (2.83%), and glands showing necrotic cells (1.88%). Of all these, corpora amylacea, proteinaceous material, cystically dilated glands and glands showing papillary infoldings were present in all cases beyond 7th decade. Co-morbid histopathological changes of BPH. Twenty six specimens (24.52%) showed co-morbid features in association with BPH which included inflammatory (16.98%) and neoplastic (7.54%). Acute prostatitis was observed in 2 cases (1.88%), chronic prostatitis in 16 cases (15.09%) and none showed features of both. Neoplastic changes( 8 cases) ranged from intraepithelial neoplasm (PIN) (2 cases), atypical glands (2 cases, both in 7th decade) to adenocarcinomatous changes (2 cases, one each in 6th and 7th decade) were also observed co-existent with BPH. Both PIN cases (1.88%) were grade PIN-2 and occurred one each in the 6th and 7th decade. CONCLUSION: Histological profiles of prostatic biopsy specimens were observed to correlate well with the senile changes of advancing age. A predominantly stromal proliferation was found in a relatively lower age group, while corpora amylacea and cystically dilated glands along with glandular proliferation heralded changes of senescence. Co-morbid histopathological features were associated with BPH in a quarter (24.52%) of cases. Prostatitis was twice as common as neoplastic changes. Adenocarcinomatous changes were observed (2 cases) incidentally. PIN was recorded in 1.88% of specimens examined. Peak frequency of prostatitis was noted in the 6th decade while 7 of 8 neoplastic changes occurred in those of 60-80 years.

Adult↗
PubMed2006

[A clinical study of prostat combined with an antibiotic for chronic nonbacterial prostatitis].

OBJECTIVE: To evaluate the efficacy and safety of Prostate in combination with an antibiotic for the treatment of chronic nonbacterial prostatitis. METHODS: A double-blind, parallel contrasted, multi-central method was applied in the study. After the Stamey test and expressed prostate secretion (EPS) examination, 160 patients with prostatitis were recruited and randomized into a trial group (80 cases with 1 case missing) and a control group (80 cases). In the trial group, the patients used the levofloxacin and Prostate during the first 4 weeks and Prostate only during the following 4 weeks. In the control group, the patients used the levofloxacin and placebo during the first 4 weeks, and placebo only during the following 4 weeks. Before and 4 and 8 weeks after the treatment, the patients were visited and evaluated by the national institute health-chronic prostatitis symptom index (NIH-CPSI), EPS, and asked about the side. RESULTS: After 4-week and 8-week treatment, the pain index dropped by 3.34 +/- 2.45 and 4.06 +/- 3.03 in the trial group, and effects. 2.28 +/- 2.42 and 3.30 +/- 3.29 in the control; the voiding index dropped by 2.22 +/- 1.79 and 2.77 +/- 2.04 in the trial group, and 1.24 +/- 1.67 and 1.83 +/- 2.25 in the control respectively. There was significant difference between pre-treatment and post-treatment in both the two groups (P < 0.01), while the difference was not significant between 4-week and 8-week post-treatment (P > 0.05). And there was significant difference between the two groups in the pain index and voiding index (P < 0.01), but not in the white blood cell count and lipid in the EPS (P > 0.05). No serious side effects were recorded, and the tolerance to Prostate and placebo showed no significant difference. CONCLUSION: Prostate in combination with an antibiotic can effectively relieve the pain and voiding symptoms and improve the life quality of the patients with nonbacterial prostatitis and well deserves to be recommended in clinical practice.

Adult↗
PubMed1997

Human prostatic carcinoma oncogene PTI-1 is expressed in human tumor cell lines and prostate carcinoma patient blood samples.

Rapid expression cloning and differential RNA display identifies a gene, named prostate tumor inducing gene-1 (PTI-1), that is differentially expressed in prostate cancer versus normal prostate and benign prostatic hypertrophy. PTI-1 encodes a truncated and mutated human elongation factor 1 alpha, and its 5' untranslated region (UTR) shares significant homology with the 23S rRNA gene of Mycoplasma hyopneumoniae. PCR with human genomic DNAs, using PTI-1 5' UTR-specific primers, suggests that this sequence is part of the human genome. Furthermore, reverse transcription (RT)-PCR, with one primer specific to the 5' UTR region and the other to the elongation factor 1 alpha coding region, amplifies PTI-1 transcripts from total RNA of various human tumor cell lines and blood samples from prostate carcinoma patients. RT-PCR products with the predicted size and sequence of PTI-1 are detected in RNAs from cell lines of human prostate, breast, and colon carcinomas. This RT-PCR product is shown by Southern blotting and sequence analyses to contain the junction sequence between the 5' UTR and the coding region of the PTI-1 gene. Furthermore, RT-PCR analysis indicates that the PTI-1 gene is also expressed in prostate carcinoma patient-derived blood samples. On the basis of serial dilution experiments, PTI-1 can detect 1 prostate carcinoma cell in 10(8) cells not expressing PTI-1. In this context, PTI-1 represents a sensitive marker for detecting human prostate cancer in the bloodstream. This study confirms the authenticity of the PTI-1 gene and documents its potential clinical utility as a sensitive and specific indicator of prostate cancer progression.

Base Sequence↗
PubMed1997

Cryosurgical ablation of the normal ventral prostate plus adjuvant does not protect Copenhagen rats from Dunning prostatic adenocarcinoma challenge.

PURPOSE: We wished to determine if cryosurgical ablation of the normal ventral prostate of Copenhagen rats confers protective immunity against a subsequent challenge with Dunning R3327 MatLyLu prostatic adenocarcinoma. In human melanoma, tumor antigens have been characterized as normal cellular proteins. We reasoned that cryosurgical ablation of the normal prostate along with immunostimulatory adjuvants might release prostatic antigens to the immune system engendering an immune response and rendering rats immune to prostatic cancer cells. MATERIALS AND METHODS: On day 0, Copenhagen rats underwent cryosurgical ablation of the normal ventral prostate, cryosurgery and intraprostatic injection of Complete Freund's Adjuvant (CFA), CFA injection alone, or laparotomy alone. On day 21, animals received a subcutaneous challenge of MatLyLu tumor cells. Tumor dimensions were recorded at regular intervals by a single blinded investigator. RESULTS: Animals receiving cryosurgical ablation of the normal ventral prostate or intraprostatic CFA developed tumors more frequently than animals receiving laparotomy alone and the effect was statistically significant if animals received both cryosurgical ablation of the prostate and intraprostatic CFA (3 experiments, 1 x 10(4) MatLyLu cells), total number with tumors/total number challenged: laparotomy alone 3/17, cryosurgical ablation 7/17, cryosurgery plus CFA 10/16 (p = 0.013 versus laparotomy, Fisher's exact test), CFA alone 9/17. CONCLUSIONS: Cryosurgical ablation of the normal rat ventral prostate and intraprostatic CFA does not protect against and can enhance the tumorigenicity of MatLyLu prostatic cancer cells at distant sites. This could be occurring through specific immunologic effects or non-specific mechanisms induced by cryosurgery and CFA.

Adenocarcinoma↗
PubMed1997

Human prostatic tumor cells in culture produce growth and differentiation factors active on osteoblasts: a new biological and clinical parameter for prostatic carcinoma.

Prostate cancer (PRCA) cells metastasize to bone with high frequency, inducing typical osteosclerotic lesions. To establish if local stimuli on the bone tissue may derive from metastatic colonies of prostatic origin, we evaluated the biologic activities secreted by human prostatic epithelium and effective on osteoblast-like cells in vitro. Supernatant from short-term tissue cultures of human prostatic tissue samples obtained from PRCA (35 cases) and benign prostatic hyperplasia (BPH, 12 cases) patients were applied to three models of cells with osteoblastic phenotype: two normal [rabbit osteoblasts (OB) and rat periosteal cells (PO)] and one transformed (human osteosarcoma cell line, MG63). Proliferative activity was monitored through enzymatic reduction of tetrazolium salts and expressed as relative mitogenic activities (RMA). Analysis of proliferation and alkaline phosphatase (ALP) activity, a marker of osteoblast function, demonstrates that conditioned media (CM) from PRCA cultures stimulate both growth and activity of osteoblast-like cells to a greater extent compared to CM from BPH. Furthermore, cell growth and activity of osteoblast-like cells are progressively increased by CM derived from patients with stage B (tumor confined within the prostate capsule), stage C (locally invasive tumor), and stage D (invasive tumor with distant metastasis) disease. One of the mechanisms potentially underlying the CM-stimulated effects on bone cells is associated with the urokinase (uPA) enzyme route, whose release progressively increases with the stage of disease. However, antibodies against uPA and p-aminobenzamidine (a low molecular weight urokinase inhibitor) treatment, which both inhibit the proliferative and differentiative effects induced by exogenous urokinase, partially slow down the effects of CM from PRCA tissue cultures, suggesting that additional factors are secreted by prostatic tumor cells in vitro. In conclusion, we show that the mitogenic and differentiative activities for osteoblasts produced by prostatic tumor cells in short-term tissue cultures are related to PRCA stage and may predict the behavior of skeletal metastases in single cases of tumor. In addition, the culture methods used may represent a valid model to study prostatic and bone cellular interactions, which may indicate new therapeutic approaches in metastatic prostate tumors.

Alkaline Phosphatase↗
PubMed1998

Novel role of zinc in the regulation of prostate citrate metabolism and its implications in prostate cancer.

The prostate gland of humans and many other animals has the major function of accumulating and secreting extraordinarily high levels of citrate. This specialized metabolic process of "net citrate production" is the result of unique metabolic capabilities of the secretory epithelial cells. Most importantly, in prostate cancer (Pca) the capability for net citrate production is lost. In addition to citrate, the normal and BPH (benign prostatic hyperplasia) prostate also accumulates the highest levels of zinc in the body. As with citrate, in Pca the ability for high zinc accumulation is diminished. These and other correlations between zinc and citrate in the prostate have been indicative of an important role of zinc in the regulation of citrate metabolism in normal and malignant prostate epithelial cells. The link between zinc and citrate metabolism has now been established. The intramitochondrial accumulation of high zinc levels inhibits mitochondrial (m-) aconitase activity, which inhibits citrate oxidation. This essentially truncates the Krebs cycle and markedly decreases the cellular energy (ATP) production normally coupled to citrate oxidation. It is also clear that zinc accumulation in citrate-producing prostate epithelial cells is regulated by testosterone and by prolactin. These relationships form the basis for a new concept of the role of zinc and citrate-related energy metabolism in prostate malignancy. The inability of malignant prostate cells to accumulate high zinc levels results in increased citrate oxidation and the coupled ATP production essential for the progression of malignancy. The concept offers new approaches to the treatment of Pca.

Aconitate Hydratase↗
PubMed2000

Prostate-specific membrane antigen (PSMA) enzyme activity is elevated in prostate cancer cells.

BACKGROUND: Prostate-specific membrane antigen (PSMA) is a glutamate carboxypeptidase that cleaves terminal carboxy glutamates from both the neuronal dipeptide N-acetylaspartylglutamate (NAAG) and gamma-linked folate polyglutamate. The prostate enzyme has activity in both the membrane and cytosolic fractions termed PSMA and PSMA', respectively. METHODS: Using a NAAG hydrolytic radioenzymatic assay, we quantitated the enzymatic activity of PSMA and PSMA' in normal, benign prostatic hyperplasia (BPH), and prostate cancer (PC) tissues from radical prostatectomies. PSMA enzyme activity was evaluated in each tissue type and expressed per milligram protein and epithelial cell content. RESULTS: PSMA and PSMA' enzyme activities were significantly elevated in prostate cancer when compared to normal prostate tissue and BPH. Ratios of PSMA to PSMA' were also decreased in BPH as compared to cancerous and normal tissue. CONCLUSIONS: Prostate carcinogenesis is associated with an elevation in PSMA and PSMA' enzyme activity. In contrast, no such enhancement in PSMA activity is observed with benign neoplastic changes in BPH. Thus, the enhancement observed in prostate cancer is not simply related to a generalized prostatic hyperplasia, but is specific to its malignancy.

Antigens, Surface↗
PubMed1985

Approaches to prostatic cancer chemotherapy using the Dunning R3327H prostatic adenocarcinoma.

Androgen-responsive cells: To determine if testosterone or dihydrotestosterone is the main trophic hormone of prostatic adenocarcinoma, we have treated Dunning R3327H prostatic adenocarcinoma-bearing rats with 6-methylene progesterone, which blocks conversion of testosterone to dihydrotestosterone. Copenhagen-Fisher rats were treated with steroid (20 mg/Kg daily) immediately following implantation of tumor and thereafter for 117 days. There was a 92% inhibition of growth of tumors and a lesser effect upon prostate and seminal vesicles. Tumor-free body weights remained unchanged. Both treated and untreated tumors had equivalent DNA content on a per weight basis. This result supports the thesis that prostatic adenocarcinoma requires dihydrotestosterone for growth. Androgen-insensitive cells: Advanced prostate cancer does not respond to endocrine therapy but is temporarily controlled by the cytotoxic steroid estramustine. The latter shows significant selective binding to prostatic protein. To develop chemotherapeutic agents that will control androgen-insensitive cells and possess improved selectivity for prostatic protein, we have studied a number of steroids for their ability to displace 3H-labeled estramustine from prostatic cytosolic proteins. Surprisingly, a carbamido substituent at the C17 position was found to confer significant binding affinity for prostatic estramustine-binding protein. Extension of this structural characteristic to the estramustine type of molecule is being studied.

5-alpha Reductase Inhibitors↗
PubMed1995

Transforming growth factor-beta localization during mouse prostate morphogenesis and in prostatic growth abnormalities.

Growth and morphogenesis of the prostate involves mesenchymal-epithelial interactions. Transforming growth factor-beta 1 (TGF-beta1) is one growth factor that may play a role in these paracrine interactions. We have localized TGF-beta1 by molecular and immunohistochemical analysis in the developing mouse prostate. Accumulations of TGF-beta1 protein were localized in the mesenchyme surrounding ductules in fetal and neonatal prostate. Previous studies in the mouse prostate reconstitution (MPR) model system have localized accumulations of TGF-beta1 to regions of oncogene-induced abnormalities. In surgically excised adult human prostate tissues, localized accumulations of TGF-beta1 are associated with prostate cancer and benign prostatic hyperplasia (BPH). Intracellular TGF-beta1 was more often associated with stromal cells in BPH and with neoplastic epithelial cells in prostate cancer. The production and accumulation of TGF-beta1 appears to involve interactions between mesenchymal and epithelial cells. Further experimental studies may clarify the relationships between TGF-beta1 and abnormal prostatic growth.

Animals↗
PubMed2006

The correlation between serum prostate specific antigen levels and asymptomatic inflammatory prostatitis.

INTRODUCTION: Asymptomatic inflammatory prostatitis is a common pathological finding in patients with benign prostatic hyperplasia (BPH). In the present study, we evaluated the correlation between serum prostate specific antigen (PSA) level and extent and aggressiveness of inflammation in surgical specimens of patients who underwent to surgery for BPH without any evidence of clinical prostatitis. METHODS: Histological sections of the prostatic tissues of 52 patients were scored for the extent of inflammation and aggressiveness of inflammation, using the four point scale designed by Irani et al. Extent of inflammation is graded from 0 to 3 according to the degree of invasion of inflammatory cells in prostate tissue. Aggressiveness of inflammation is graded from 0 to 3 according to the degree of contact or disruption of prostatic glandular epithelium by inflammatory cells. The serum PSA levels in different inflammation grades were compared. RESULTS: There was a significant correlation between inflammation and aggressiveness scores (r = 0.39, P < 0.01). Median PSA levels in grades 1, 2 and 3 extent of inflammation were 2.4, 5.2 and 5.7 ng/ml, respectively. There was not any significant difference between these grades for PSA. Furthermore, median PSA levels in grades 1, 2 and 3 aggressiveness of inflammation were 4.4, 4.8 and 8.7 ng/ml, respectively. There was a significant difference between grades of aggressiveness of inflammation and PSA levels. CONCLUSION: High serum PSA levels may correlate with asymptomatic inflammatory prostatitis with high aggressiveness score in BPH patients without clinical prostatitis.

Aged↗
PubMed2005

Prostatitis and serum prostate-specific antigen.

Prostatitis is an inflammatory condition of the prostate and has been divided into four categories according to the National Institutes of Health classification. This article reviews the various types of prostatitis and their effect on serum prostate-specific antigen levels. Various proposed mechanisms of this elevation include leakage of prostate-specific antigen (PSA) into the blood stream, hypervascularity, and altered vascular permeability secondary to inflammation. Acute prostatitis can lead to an increase in PSA, which usually returns to normal levels with appropriate antibiotics within 1 to 3 months. Patients with chronic prostatitis have a less well-defined decrease in PSA after an antibiotic course. Whether a course of antibiotics prior to biopsy increases the yield has not been well established. Asymptomatic inflammation of the prostate has been recognized to be an important confounding factor in patients with an elevated PSA. Inflammation has been proposed to be a precursor of prostate adenocarcinoma.

Anti-Bacterial Agents↗
PubMed1995

Endocrine-paracrine cell types in the prostate and prostatic adenocarcinoma are postmitotic cells.

Neuroendocrine (NE) differentiation frequently occurs in common prostatic malignancies and has potential prognostic and therapeutic implications. In a recent study we were able to provide immunohistochemical evidence that endocrine-paracrine cell types represent an androgen-insensitive cell population in prostate cancer, documented by the consistent lack of the pertinent receptor. In this study we investigated the proliferative activity of endocrine-paracrine cell types in normal, hyperplastic, and neoplastic prostate tissue. Using double-label techniques for the endocrine marker chromogranin A (chr A) and the proliferation-associated MIB-1 antigen, we evaluated the proliferative status of endocrine-paracrine cell types in the prostate and prostatic adenocarcinoma showing marked NE differentiation. In this series of carcinomas and in nonneoplastic tissue the proliferative activities were exclusively restricted to nonendocrine cell populations, whereas endocrine-paracrine cell types characterized by Chr A consistently lack MIB-1 immunoreactivity. This may indicate that prostatic endocrine-paracrine cell types do not participate in the cell cycle during normal, hyperplastic, and neoplastic prostatic growth. Based on the present information, the endocrine phenotype can be considered to be an androgen-insensitive, postmitotic subpopulation in the prostate and prostate cancer.

Adenocarcinoma↗
PubMed1994

Alpha 1-antichymotrypsin production in PSA-producing cells is common in prostate cancer but rare in benign prostatic hyperplasia.

OBJECTIVE: To investigate the distribution and production of alpha 1-antichymotrypsin (ACT) and prostate-specific antigen (PSA) in benign hyperplastic and malignant prostatic tissue, respectively. METHODS: Using monoclonal anti-ACT and anti-PSA IgGs for immunocytochemistry and alkaline phosphatase conjugated 30-mer oligodeoxynucleotide probes for nonradioactive in situ hybridization, tissue specimens were studied from 15 patients with benign prostatic hyperplasia after transurethral resection of the prostate (TURP) and from 9 patients with bladder cancer who underwent cystoprostatectomy. Cancer specimens were from 23 TURP patients and from ultrasound guided core biopsies in 14 patients. Prostate tumors were graded according to the Gleason system. RESULTS: We found no or only occasional small foci of immunostaining for ACT, and no ACT transcripts in the PSA-producing epithelium in areas with benign nodular hyperplasia. By contrast, a high proportion of cells expressed both ACT and PSA in prostate cancers with low Gleason score, as detected by immunocytochemistry and in situ hybridization. Poorly differentiated tumor cells manifested greater variation in immunostaining for both ACT and PSA. As compared to tumors of low Gleason score, high-score tumors less frequently manifested immunostaining for ACT than for PSA, and less frequently generated hybridization signals for both PSA and ACT transcripts. CONCLUSIONS: A significantly higher proportion of serum PSA has been reported to be complexed to ACT in patients with prostate cancer than in patients with benign prostatic hyperplasia. The presently reported lack of ACT production in PSA-containing BPH nodules may contribute to this by making conditions less optimal for complex formation between PSA and ACT. As opposed to this, production of both ACT and PSA in prostate cancers may enhance the complex formation between PSA and ACT.

Aged↗
PubMed1997

Inflammation in benign prostatic hyperplasia: correlation with prostate specific antigen value.

PURPOSE: We attempted to identify morphological parameters of benign prostatic hyperplastic inflammation that correlate with pre-biopsy prostate specific antigen (PSA) concentrations. MATERIALS AND METHODS: Patients undergoing prostate biopsy at our department were prospectively studied between January 1995 and January 1996. preoperative blood and 24-hour urine samples were measured for PSA. Biopsy samples harboring exclusively benign prostatic tissue were graded on a 4-point scale for inflammation (0-no inflammatory cells, 1-scattered inflammatory cell infiltrate, 2-nonconfluent lymphoid nodules and 3-large inflammatory areas with confluence of infiltrate) and aggressiveness (0-no contact between inflammatory cells and glandular epithelium; 1-contact between inflammatory cell infiltrate and glandular epithelium; 2-clear but limited, that is less than 25% of the examined material, glandular epithelium disruption, and 3-glandular epithelium disruption on more than 25% of the examined material). RESULTS: A total of 66 patients with exclusively benign prostatic tissue on prostate biopsies was analyzed. Difference between inflammation graded groups was not significant when considering serum or urinary PSA. There was a significant correlation between aggressiveness grading and serum PSA (rho = 0.51, p < 0.0001), whereas aggressiveness grading and urinary PSA did not correlate (rho = -0.06, p = 0.6). CONCLUSIONS: Prostatic subclinical inflammation is not associated with high urinary PSA. Unless associated with glandular epithelial disruption, density of prostatic interstitial inflammatory cell infiltrate is not significantly correlated with serum PSA concentration. We believe that this issue should be considered when interpreting a prostate biopsy.

Aged↗
PubMed1993

Does high grade prostatic intraepithelial neoplasia result in elevated serum prostate specific antigen levels?

Prior studies have evaluated high grade prostatic intraepithelial neoplasia on biopsy material when undiagnosed carcinoma or benign prostatic hyperplasia (BPH) may have been associated with elevated serum prostate specific antigen (PSA) levels. We studied 65 totally embedded radical prostatectomy specimens with minimal carcinoma (tumor volume 0.5 cc or less) and relatively minimal BPH (gland weight less than 65 gm.). Even for these relatively small glands, PSA showed a significant correlation with gland volume (r = 0.64). To account for BPH, PSA density (PSA divided by gland volume) was also calculated. In these specimens with trivial tumor the tumor volume did not correlate with PSA (r = 0.12) or PSA density (r = 0.23). The volume of high grade prostatic intraepithelial neoplasia also showed no correlation with PSA (r = 0.16) or PSA density (r = 0.14). The 11 cases with extensive high grade prostatic intraepithelial neoplasia (0.50 cc or more) had PSA density values of 0.03 to 0.14, with 10 less than 0.1. Of the 6 cases with PSA density values of 0.1 or more only 1 had a high grade prostatic intraepithelial neoplasia volume of 0.5 cc or more. These results indicate that high grade prostatic intraepithelial neoplasia in and of itself does not account for elevated serum PSA levels. In a patient with high grade prostatic intraepithelial neoplasia on biopsy material and elevated serum PSA values, BPH may account for the elevated serum PSA levels. More likely, because of the association between high grade prostatic intraepithelial neoplasia and carcinoma these patients have undiagnosed carcinoma as the source of the elevated serum PSA values.

Humans↗
PubMed1988

Prostate specific antigen in the preoperative and postoperative evaluation of localized prostatic cancer treated with radical prostatectomy.

The usefulness of prostate specific antigen to predict final pathological stage was studied in 178 consecutive patients. Prostate specific antigen was determined preoperatively in all patients by a monoclonal immunoradiometric assay. All pathological specimens were examined for capsular penetration, seminal vesicle involvement and lymph node involvement. Prostate specific antigen correlated directly with capsular penetration (p less than 0.002), seminal vesicle involvement (p less than 0.02) and lymph node involvement (p less than 0.05). However the diagnostic accuracy of an elevated serum antigen level on an individual basis was only 55 per cent for capsular penetration and 50 per cent for seminal vesicle involvement and lymph node involvement. With a log-linear regression model, the half-life of prostate specific antigen was calculated to be 3.15 +/- 0.09 days. From the equation PSA (t) equals PSA (2) e[-0.2197(t-2)], prostate specific antigen can be used to detect residual cancer on day t in the immediate postoperative period. With respect to long-term followup, 127 patients have been monitored for longer than 2 months postoperatively with prostate specific antigen (mean followup 2 years, range 2 months to 8.6 years). Of the 101 patients who had favorable pathological findings at operation (organ-confined cancer or capsular penetration only) 92 (91 per cent) had a followup antigen concentration in the female range (0.0 to 0.2 ng. per ml.), whereas only 5 of 26 men (19 per cent) with either seminal vesicle involvement or lymph node involvement had an antigen value that was less than 0.2 ng. per ml. All patients with a documented clinical recurrence (8 of 127, 6 per cent) had an elevated followup serum prostate specific antigen concentration. These findings suggest that preoperative levels of prostate specific antigen are not sufficiently reliable to predict final pathological stage on an individual basis in patients with early prostatic cancer, and that the antigen is a sensitive tumor marker for the detection of residual disease after radical prostatectomy and subsequent recurrence of tumor on long-term followup.

Adenocarcinoma↗