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PubMed2006

Catechol-O-methyltransferase gene polymorphisms in benign prostatic hyperplasia and sporadic prostate cancer.

Various carcinogenic metabolites, including catechol estrogens, play a role in malignant transformation. An enzyme that is capable of neutralizing the genotoxic effects of these compounds is catechol-O-methyltransferase (COMT). A variant form of this enzyme has been shown to reduce its activity by up to 4-fold; thus, we hypothesize that single nucleotide polymorphisms of the COMT gene can be a risk factor for benign prostatic hyperplasia (BPH) and prostate cancer. To test this hypothesis, the genetic distribution of three different COMT polymorphisms at codon 62 (C-->T), codon 72 (G-->T), and codon 158 (G-->A) were analyzed in 131 normal healthy subjects, 134 BPH, and 178 sporadic prostate cancer samples from a Japanese population. Results of these experiments show that the variant genotype at codon 62 (P = 0.060) and codon 158 (P = 0.047) are risk factors for prostate cancer but not BPH when compared with normal controls. Odds ratio (OR) and 95% confidence interval (95% CI) for cancer were 3.24 and 1.38 to 7.61, respectively, for codon 62 T/T genotype when compared with wild type. At codon 158, the A/A variant for cancer had an OR of 3.00 with a 95% CI of 1.38 to 6.54 compared with wild type. Codons 62 and 158 were in linkage disequilibrium (LD), and when compared with the C-G haplotype, other types (C-A, T-G, T-A) were observed to be associated with prostate cancer (P = 0.040) but not BPH. Codon 72 on the other hand, was not in LD with either codon 62 or 158. The homozygous variant on codon 72 was rare in this Japanese population, and the heterozygous G/T at this codon was not associated with either prostate cancer or BPH. When evaluating the risk of COMT polymorphisms with stage or grade of cancer, no associations were observed for any of the genotypes with the exception of a tendency (P = 0.096) for the variant A allele on codon 158 to be correlated with higher stages (> or = T3) of cancer. This is the first report that shows the polymorphisms of COMT to be associated with sporadic prostatic carcinogenesis. These results are important in understanding the role of COMT polymorphisms in the pathogenesis of prostate cancer.

Alleles↗
PubMed2006

Variants in the prostate-specific antigen (PSA) gene and prostate cancer risk, survival, and circulating PSA.

An A to G substitution, rs925013, in the promoter of the prostate-specific antigen gene (PSA) was recently found to be associated with promoter activity and circulating PSA levels. The objective of this study was to test the associations between rs925013 and another A to G substitution, rs266882, in the PSA gene with prostate cancer risk using a population-based case-control study of 821 prostate cancer cases and 734 controls carried out in Perth and Melbourne, Australia. The study focused on young (i.e., < 70 years) and aggressive cases (i.e., well-differentiated tumors were excluded). Cases in the Melbourne arm of the study (N = 638) were followed up prospectively for an average period of 8.2 years and deaths from prostate cancer ascertained through record linkage to study the possible association between genetic variants and disease-specific survival. PSA-circulating levels were measured in controls to test the association with the genetic variants using a cross-sectional design. Linear regression of log PSA levels, unconditional logistic regression, Cox regression, and haplotype analyses were undertaken. For rs925013, the G allele was associated with an increased risk of prostate cancer [odds ratio, 1.4; 95% confidence interval (95% CI), 1.1-1.7; P = 0.001], and the hazard ratio for survival for cases homozygous for the G allele compared with cases homozygous for the A allele was increased but not statistically significant (hazard ratio, 2.3; 95% CI, 1-5.6; P = 0.06). For rs266882, there was no association with overall prostate cancer risk and survival (all P > 0.1). Men homozygous or heterozygous for the G/G (rs925013/rs266882) haplotype were at higher risk of prostate cancer than men homozygous for the A/A haplotype (odds ratio, 1.3; 95% CI, 1.1-1.7; P = 0.009). Adjusted geometric means of circulating PSA levels in controls were similar in men with zero, one, and two copies of the G allele in rs266882 (1.2, 1.1, and 1.3 ng/mL, respectively; all P > or = 0.2) and rs925013 (1.1, 1.2, and 1.5 ng/mL, respectively; all P > 0.1). For rs925013, our study provides good evidence of association with prostate cancer risk, marginal evidence of association with survival, and little evidence of detectable association with circulating PSA levels in controls. We found no evidence of an independent association between rs266882 and any of the outcomes. The genotypes and haplotypes studied might be associated with the PSA gene function or be in linkage disequilibrium with other unmeasured and functional variants in the PSA or other genes.

Aged↗
PubMed2004

Regression of mouse prostatic intraepithelial neoplasia by nonsteroidal anti-inflammatory drugs in the transgenic adenocarcinoma mouse prostate model.

PURPOSE: Epidemiologic studies have revealed a decreased risk of colon cancer among people who have regularly taken cyclooxygenase (COX)-2 inhibitors such as aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Whereas the selective COX-2 inhibitor celecoxib and exisulind, a metabolic product of sulindac, have gained increasing attention as efficacious chemopreventive agents against colon and prostate cancer, not much is known about the underlying molecular targets and mechanisms. Moreover, the side effects of NSAIDs are a major obstacle for large-scale application to the prevention of cancer in humans; for example, in the United States in 1998, there were 16,550 deaths from NSAID-induced gastrointestinal complications. The toxicity associated with these compounds is raising concerns, and more needs to be known about their mode of action and molecular targets. EXPERIMENTAL DESIGN: We used the transgenic mouse prostate (TRAMP) model, which exhibits similarities with human prostate cancer, including epithelial origin, progression from the PIN stage to adenocarcinoma, and metastasis by a transgene that is hormonally regulated by androgens. In addition to histologically analyzing the PIN lesions of the dorsolateral prostate from TRAMP mice, we delineated the molecular targets and mechanisms of celecoxib and exisulind against mouse PIN lesions. We performed Western blot analysis of the total protein lysate from the tissues of mouse PIN lesions to measure the level of expression of androgen receptor, vascular endothelial growth factor, nuclear factor-kappaB p65, BclII, AKT (total and phosphorylated Ser473), p53, cyclin-dependent kinase inhibitor p21WAF1/CIP1, p27, BAX, and caspase-3 to demonstrate the COX-2-independent mechanism involved in the inhibition of PIN lesions of the dorsolateral prostate by both celecoxib and exisulind. RESULTS: We found for the first time that (a) both celecoxib and exisulind as dietary supplements induce strong inhibitory effects against prostate cancer at doses of 800 and 500 ppm, respectively, after 16 weeks; (b) the histologic analysis of the dorsolateral prostate after 2 weeks of treatment indicated a reduction of PIN lesions from 75% to 19% with celecoxib and to 16% with exisulind; (c) more importantly, those few PINs and adenocarcinomas in the groups treated with celecoxib or exisulind showed more apoptotic cells, lower levels of proliferating cell nuclear antigen, and a lower number of mitotic cells. To understand the molecular mechanisms involved in the inhibition of PIN lesions, first, we examined the expression of molecular targets involved in angiogenesis and inflammatory processes. It was clearly evident from Western blot analysis of the total protein lysate derived from the dorsolateral prostate tissues with PIN lesions that expression of androgen receptor, vascular endothelial growth factor, nuclear factor-kappaB p65, and BclII is down-regulated more effectively by celecoxib. Down-regulation of AKT protein (total and phosphorylated at Ser473) signaling by celecoxib clearly indicates an inhibition of the survival gene and the pathological process that could otherwise lead to adenocarcinoma. CONCLUSIONS: Overall, the findings from this study clearly show the effectiveness of celecoxib and exisulind in reducing the PIN lesions by modulating a cascade of molecular targets involved in COX-2-dependent and -independent mechanisms. Whereas these agents are already in clinical trial or in use as chemopreventive agents, findings from this study demonstrate the difference in their mode of action, thus helping us to understand the side effects.

Adenocarcinoma↗
PubMed1999

Subtle morphological and molecular changes in normal-looking epithelium in prostates with prostatic intraepithelial neoplasia or cancer.

BACKGROUND: Prostate cancer develops over an extended period of time. Until recently, the events initiating the process and the developments concomitant with the evolution towards invasive disease were largely unknown. METHODS: Analytical and quantitative methods are applied to provide insights into certain individual molecular events and their effects on the complex multiple feedback system of cellular metabolism and regulation in prostate neoplasia. RESULTS: Prostatic intraepithelial neoplasia (PIN) and prostate cancer (PCa) are associated with or possibly preceded by changes in the chromatin of secretory cell nuclei. The changes are detectable with a Bayesian belief network and quantifiable by computer image analysis in prostatic tissue that still appears histologically normal. In addition, normal-looking prostate epithelium shows some molecular changes similar to those present in the associated preneoplastic and neoplastic lesions. Such changes are also occasionally present in normal prostate glands without PIN and cancer. CONCLUSIONS: The subtle morphological and molecular changes of normal-looking epithelium might be seen as the onset of the development of prostatic neoplasia.

Adenocarcinoma↗
PubMed2004

Giant multilocular cystadenoma of the prostate: a rare differential diagnosis of benign prostatic hyperplasia.

We report a case of giant multilocular cystadenoma of the prostate in a 43-year-old man. This is a rare benign entity of the prostate imitating symptoms of benign prostatic hyperplasia and originates from the prostate with extensive spread into the pelvis. Histologically, prostatic glands and cysts lined by cuboid to columnar epithelial cells with basally located nuclei are characteristic. Immunohistochemical staining is positive for prostate-specific antigen in the epithelial cells. Giant multilocular prostatic cystadenoma should be taken into account in the differential diagnosis in any case of a large cystic mass originating from the prostate.

Adult↗
PubMed1997

Prostate-specific antigen and early detection of prostate cancer.

Prostate-specific antigen (PSA) is biochemically a 33-kDa serine protease and is the prototype of tumor marker most useful in investigating basic science and clinical application of prostate cancer. As an immunohistopathological marker, PSA is especially effective in the identification of distant metastatic prostate carcinoma and in the differential diagnosis of poorly differentiated transitional cell carcinomas of the bladder from prostate carcinoma. As a serologic marker, PSA is most useful in staging, monitoring and in early detection of recurrent disease. The greatest value of PSA is as a screening aid along with digital rectal examination for early detection of prostate cancer. PSA-based screening tests have been performed in various regions of the world and have yielded prostate cancer detection rates proportional to that of incidence rates in the countries. Most significantly, PSA detects early nonpalpable prostate cancer. Approximately 85% of the prostate tumors detected through PSA have the clinical features associated with medically important cancer. Further, a majority of the tumors, 70%, are confined to the organ. Although the issues of cost-benefit and increase in ultimate survival rate are still being evaluated in two large-scale randomized national trials, timely and definitive therapies of these potentially lethal tumors can result in high cure rate and improve the quality of patients' life.

Biomarkers, Tumor↗
PubMed1996

Role of the basal cells in premalignant changes of the human prostate: a stem cell concept for the development of prostate cancer.

OBJECTIVES: Prostatic intraepithelial neoplasias (PIN) result from abnormal differentiation and proliferation processes within the prostatic epithelial cell system. Recent data indicate that basal cells are essentially involved in normal and abnormal growth patterns of the human prostate. RESULTS: The basal cell layer represents the proliferative compartment and most probably houses the prostatic stem cell population. Basal cells are targets of several regulatory factors including estrogens, androgens, epidermal growth factor and other nonsteroidal growth factors. During the malignant transformation of the prostatic epithelium (PIN), the basal cell layer loses its proliferative function which is transferred to secretory luminal cell types. These proliferative abnormalities are attended by severe regulatory disorders of the programmed cell death within the prostatic epithelial cell system. The Bcl-2 oncoprotein which blocks the programmed cell death in the proliferative compartment (basal cell layer) in normal conditions, extends to the secretory luminal cell types in high-grade PIN lesions. This, in turn, may increase the genetic instability of the dysplastic epithelium. During the process of tumor invasion, the transformed cells lose their basal cell-specific phenotype and acquire features of exocrine cell types which represent the major phenotype in common prostate cancer. At the point of stromal invasion, the transformed cells produce neoplastic basement membrane material which allows them to penetrate the extracellular matrix. CONCLUSION: These data provide theoretical bases for a stem cell concept in the development of prostate cancer and highlights the importance of basal cells in this multifactorial process.

Basement Membrane↗
PubMed1993

Connection between the length of the heating antenna and volume of the prostate in transurethral thermotherapy for benign prostatic hyperplasia.

From June 1990 to June 1991, 79 poor surgical risk patients with benign prostatic hyperplasia (BPH) were treated with transurethral hyperthermia. The patients were divided into 2 treatment groups. In group I, 40 patients were treated by two 2-hour sessions at 44.5 degrees C and a heating antenna of 1 cm long. In group II, 39 patients received one 3-hour treatment session at a temperature of 46 degrees C and a 2-cm-long heating antenna. The mean follow-up period was 7.9 months for group I and 8.4 months for group II patients. In group I, 22 of 40 patients (55%) showed subjective and objective improvement. In group-II patients a major improvement was noted in 25 of 39 patients (64%). The patients in both groups were subdivided into those with prostates smaller or larger than 50 ml. Significantly better treatment results were obtained in patients with prostates smaller than 50 ml in group-I and group-II patients. The mean Madsen-Iversen score, residual urine and maximum flow rate improved significantly in 47% of groups-I patients with larger prostates and 62% of those with prostates < 50 ml (p < 0.05), and in 50% of group-II patients with prostates > 50 ml and 82% of those with prostates < 50 ml (p < 0.01). A temperature of 46 degrees C with a 2-cm-long heating antenna in patients with prostates < 50 ml gave the best treatment results (82%).

Aged↗
PubMed2000

Clinical utility of the percentage of positive prostate biopsies in defining biochemical outcome after radical prostatectomy for patients with clinically localized prostate cancer.

PURPOSE: To determine the clinical utility of the percentage of positive prostate biopsies in predicting prostate-specific antigen (PSA) outcome after radical prostatectomy (RP) for men with PSA-detected or clinically palpable prostate cancer. METHODS: A Cox regression multivariable analysis was used to determine whether the percentage of positive prostate biopsies provided clinically relevant information about PSA outcome after RP in 960 men while accounting for the previously established risk groups that are defined according to pretreatment PSA level, biopsy Gleason score, and the 1992 American Joint Committee on Cancer (AJCC) clinical T stage. The findings were then tested using an independent surgical database that included data for 823 men. RESULTS: Controlling for the known prognostic factors, the percentage of positive prostate biopsies added clinically significant information (P <.0001) regarding time to PSA failure after RP. Specifically, 80% of the patients in the intermediate-risk group (1992 AJCC T2b, or biopsy Gleason 7 or PSA > 10 ng/mL and </= 20 ng/mL) could be classified into either an 11% or 86% 4-year PSA control cohort using the preoperative prostate biopsy data. These findings were validated in the intermediate-risk patients using an independent surgical data set. CONCLUSION: The validated stratification of PSA outcome after RP using the percentage of positive prostate biopsies in intermediate-risk patients is clinically significant. This information can be used to identify men with newly diagnosed and clinically localized prostate cancer who are at high risk for early (</= 2 years) PSA failure and, therefore, may benefit from the use of adjuvant therapy.

Biopsy↗
PubMed1998

Regulation of rat DOC-2 gene during castration-induced rat ventral prostate degeneration and its growth inhibitory function in human prostatic carcinoma cells.

Androgen is a mitogen as well as a morphogen for prostatic epithelium. However, the detailed mechanisms of these distinct androgenic actions have not yet been delineated. Therefore, we employed differential display PCR to unveil any potential genes that may be involved in these processes. In this study, we report the isolation and characterization of two alternative splicing forms (p82 and p59) of C9 complementary DNA, the rat homolog of the human deletion of ovarian carcinoma 2 (DOC-2) gene and mouse p96 phosphoprotein, from rat ventral prostate (VP). We found that C9 was up-regulated in rat VP after castration, suggesting that C9 may be regulated by androgen receptor directly or indirectly during prostate degeneration. A similar regulatory pattern was also observed in both the seminal vesicle and dorsolateral prostate, but not in the coagulating gland or other androgen-independent organs. Immunohistochemical analysis of rat VP demonstrated that C9 is detected in the basal epithelia and surrounding stromal cells after prolonged castration. Ribonuclease protection assay and Western blot analysis revealed that p59 is the predominant C9 isoform in rat VP. To unveil the function of C9 in cell growth, we transfected p59 complementary DNA into the C4-2 cells, a derivative of the LNCaP prostatic carcinoma cell line. The p59 stable transfectants exhibited a slower growth rate and an increase in the cell fraction in the G1 phase under our experimental conditions. These data indicate that C9-p59 has growth inhibitory activity for prostatic epithelial cells. Taken together, our results suggest that C9 is up-regulated during prostate degeneration process and may play an active role in the proliferation and differentiation of prostatic epithelium.

Adaptor Proteins, Signal Transducing↗
PubMed1993

Serum insulin-like growth factor-binding protein-2 (IGFBP-2) is increased and IGFBP-3 is decreased in patients with prostate cancer: correlation with serum prostate-specific antigen.

Insulin-like growth factors (IGFs) are potent mitogens that stimulate the growth of prostate cells. In serum, IGFs circulate bound to IGF-binding proteins (IGFBPs), which modulate their proliferative action. We studied the electrophoretic pattern of IGFBPs in the serum of patients with prostate cancer and in individuals with increased serum levels of prostate-specific antigen (PSA) in the absence of prostate malignancy. Serum IGFBP-2 was dramatically increased in patients with metastatic prostate cancer compared with healthy controls (23.83 +/- 6.93% vs. 2.95 +/- 0.52% of total serum IGFBPs; P < 0.02). A moderate rise in IGFBP-2 was also observed among patients with increased PSA without malignancy. In contrast, a decrease in serum IGFBP-3 was detected in most patients with metastatic prostate cancer (68.2 +/- 9.1% vs. 95.4 +/- 0.9% of total serum IGFBPs; P < 0.02) and was more pronounced in advanced cases. A highly significant correlation between serum IGFBP-2 and PSA levels was found (r = 0.62; P < 0.002), with a significant negative correlation between serum PSA and IGFBP-3 (r = -0.63; P < 0.002). We suggest that IGFBPs may be involved in growth modulation of prostate malignancy and that alterations in their serum levels may serve as a marker for prostate cancer.

Aged↗
PubMed1995

Somatostatin receptors in human prostate and prostate cancer.

Benign as well as malignant human prostatic tissues were evaluated for their content of somatostatin (SRIH) receptors (SRIH-R). In vitro receptor autoradiography techniques on cryostat sections were performed using 125I-labeled [Tyr3]octreotide as well as 125I-labeled [Leu8,D-Trp22,Tyr25]SRIH-28 as radioligands. SRIH-R were identified in all normal and hyperplastic prostates in the smooth muscles of the stroma, whereas the glands did not express the receptors. Muscular nodules were strongly receptor positive as well. The receptors were of high affinity (Kd = 0.4 nmol/L) and high specificity for biologically active SRIH analogs; high affinity for SRIH-14, SRIH-28, and octreotide was detected, suggesting the presence of the SSTR2 receptor subtype. In situ hybridization studies confirmed the presence of SSTR2 messenger ribonucleic acid in these tissues. Primary prostate cancers did not have SRIH-R identified with 125I-labeled [Tyr3]octreotide. However, they were expressing SRIH-R identified with 125I-labeled [Leu8,D-Trp22,Tyr25]SRIH-28, with a high affinity for SRIH-14 and SRIH-28, but low affinity for octreotide. The receptors were located on tumoral cells. In situ hybridization studies revealed a preferential expression of SSTR1. Primary human prostate cancers, therefore, express a different SRIH-R subtype than benign prostate tissue. Several veins and the ganglion cells from the prostatic plexus in the surroundings of the tumors were expressing SRIH-R with high affinity for octreotide as well. These data suggest that the human prostate as well as prostate cancers may be targets for SRIH therapy; however, SRIH analogs with different selectivities for SRIH-R subtypes are required in each case.

Aged↗
PubMed1998

Is prostate specific antigen density an important prognostic indicator for patients with prostate cancer treated with external beam therapy?

The purpose of this study was to determine if prostate specific antigen density (PSAD) is a predictor of outcome following external beam radiotherapy for prostate cancer, and to compare it with other prognostic factors. Between January 1990 and December 1993, 205 patients with T1-T3 adenocarcinoma of the prostate received a radical course of external beam irradiation, with no prior or adjuvant hormonal therapy. All patients had pre- and post-treatment serum prostate specific antigen (PSA) evaluation. They were followed up for at least 24 months. PSAD was defined as the ratio of pre-treatment serum PSA to the prostate volume, as determined from CT treatment planning scans. Prostate volumes were calculated using the prostate ellipse formula. Median PSA density was 0.37, with a range 0.01-6.7. Biochemical failure was defined as three consecutive rises in serum PSA, regardless of the magnitude of elevation. 4-year biochemical disease-free survival (BDFS) for patients with PSAD < or = 0.3 was 60%, compared with 22% for patients with PSAD > 0.3 (p = < 0.001). In a multivariate analysis, pre-treatment PSA (p = < 0.001), Gleason score (p = 0.002), and stage (p = 0.03) were independent predictors of BDFS, while PSAD was not an important prognosticator (p = 0.62). Pre-treatment serum PSA is the most important prognosticator of BDFS, following external beam radiotherapy, for patients with prostate cancer. PSA density did not predict treatment outcome.

Adenocarcinoma↗
PubMed2002

Prostate-specific antigen and the early diagnosis of prostate cancer.

With digital rectal examination (DRE), prostate-specific antigen (PSA) is a major screening tool for prostate cancer. PSA is specific for the prostate, but not for prostate cancer. Multiple factors influence PSA value. Determination of PSA levels is not 100% sensitive for prostate cancer, as PSA levels may be normal despite presence of prostate cancer. The cutoff value for PSA of 4.0 ng/mL gives the highest sensitivity and highest specificity. Several modifications of PSA testing have been developed and may be beneficial for select populations. Uncertainty about the natural progression of prostate cancer and inherent limitations of PSA testing make it unclear whether universal screening is beneficial, and the recommendations of various organizations conflict. Randomized studies are in progress to address the role of PSA testing and of modifications of this test in the early detection of prostate cancer.

Humans↗
PubMed2007

Histopathological changes induced by therapies in the benign prostate and prostate adenocarcinoma.

The effect of androgen deprivation and other hormonal therapies, radiation therapy, thermal ablation therapies, chemotherapy, and other systemic treatments is evident in the histology of non-neoplastic and neoplastic human prostate gland. Androgen deprivation may be achieved with: a. orchidectomy, b. exogenous oestrogen administration, c. drugs with the capacity to deplete the hypothalamus of luteinizing hormone-releasing hormone, d. antiandrogens administration: drugs, which block the conversion of testosterone to its active form of 5-alpha dihydrotestosterone (i.e. finasteride, dutasteride), and drugs which block the androgen receptor on individual cells (i.e. flutamide). Androgen deprivation therapies cause atrophy of non-neoplastic and neoplastic prostatic epithelium, as the result of apoptosis, and are mainly used as a palliative measure in metastatic prostate cancer or as neoadjuvant or adjuvant treatment, in clinically localized prostate cancer. Morphological tumour regression may complicate the recognition and grading of treated carcinomas in radical prostatectomy specimens. Radiation therapy may be applied in the form of external beam, interstitial implantation (brachytherapy), or a combination, as a mainstay or adjuvant (external beam) treatment in localized prostate cancer. The primary effect is the damage of endothelial cells, which cause ischemia that leads to atrophy. The difficulty of post-radiation prostate needle biopsy interpretation includes the distinction of treatment effect in normal prostatic tissue from recurrent or residual tumour. Histological changes after thermal ablation mainly include lesions observed in prostatic infarcts due to periurethral coagulative type necrosis of variable volume. The correlation between the histopathological effects of the above therapies and their clinical significance is not absolutely clear.

Adenocarcinoma↗
PubMed1997

Effects of gonadotropin and testosterone treatments on prostate volume and serum prostate specific antigen levels in male hypogonadism.

It is known that prostate specific antigen (PSA) is strongly androgen dependent, but little is known about the effects of gonadotropin and testosterone treatments on the prostate and serum PSA levels in male hypogonadism. We have therefore determined serum PSA levels before and 3 months after treatment in 13 patients with idiopathic hypogonadotropic hypogonadism (IHH) and 14 patients with Klinefelter's syndrome. Plasma FSH, LH, testosterone, PRL, testis and prostate volumes were also determined before and 3 months after treatments. Patients with IHH were treated with hCG/hMG and patients with Klinefelter's syndrome received testosterone treatment. PSA levels were determined by a kinetic enzyme immunoassay method. In patients with Klinefelter's syndrome FSH and LH levels were significantly decreased but total and free testosterone and PSA levels were significantly increased after 3 months of treatment. Right and left testicular volumes were not significantly changed whereas prostate volumes were significantly increased after treatment. In this group PSA levels were significantly and positively correlated with the prostate volume both before (r=0.54, P=0.048) and after treatment (r=0.61, P=0.012). In the IHH group total and free testosterone and PSA levels were significantly increased after gonadotropin treatment but FSH and LH levels did not change significantly. Right and left testicular volumes and the prostate volumes were also significantly increased after 3 months of gonadotropin treatment. In this group PSA levels were correlated with prostate volume before (r=0.74, P=0.004) treatment but not after therapy (r=0.35, P=NS). Our results show that serum PSA levels increase after gonadotropin and testosterone treatment in male hypogonadism, but this could not be used as an index for the evaluation of the androgen action in the treatment of male hypogonadism, since PSA levels following treatments were correlated with the prostate volume or T levels only in patients with Klinefelter's syndrome but not in the IHH group.

Adult↗
PubMed1998

Prostate-specific antigen and new related markers for prostate cancer.

Although prostate-specific antigen (PSA), or human kallikrein 3, is the most valuable tool available for the diagnosis and management of prostate cancer, as currently used it is insufficiently sensitive and specific for early detection or staging of the malignancy. Many new concepts have been introduced in order to optimize the clinical use of PSA measurements, but each one has its own drawbacks. The molecular forms of PSA, especially the free PSA, seem to be useful for the detection of prostate cancer in men with PSA concentrations falling in the 4-10 microg/l range. New molecular techniques, such as reverse transcriptase polymerase chain reaction for the detection of minimal amounts of PSA messenger RNA and prostate-specific membrane antigen, offer new promise for the prognosis and possibly staging of prostate cancer. On the other hand, human kallikrein 2, a serine protease closely related to PSA that is also expressed predominantly in the prostate, may be a new adjuvant marker for prostate cancer. As for its biological functions, PSA can no longer be regarded as a specific prostate molecule associated mainly with semen liquefaction when it has a possible role as a prognostic indicator in female breast cancer. The biological role of PSA in normal tissues and tumors may be much more complex than previously thought and requires further investigation.

Female↗
PubMed2006

Effect of the consumption of tomato paste on plasma prostate-specific antigen levels in patients with benign prostate hyperplasia.

The consumption of tomatoes and tomato products has been associated with a reduced risk of prostate cancer. We observed a decrease of 10.77% in prostate-specific antigen (PSA) levels in patients with benign prostate hyperplasia who were submitted to daily ingestion of tomato paste. This was an experimental rather than a controlled study with a sample of 43 men ranging in age from 45 to 75 years, all with histological diagnoses of benign prostate hyperplasia and plasma PSA levels of 4-10 ng/mL. All patients received 50 g of tomato paste once a day for 10 consecutive weeks and PSA levels were analyzed before, during and after the consumption of tomato paste. ANOVA for repeated measures was used to compare PSA levels before, during and after the consumption of tomato paste. The mean +/- SD PSA level was 6.51 +/- 1.48 ng/mL at baseline and 5.81 +/- 1.58 ng/mL (P = 0.005) after 10 weeks. Acceptance was good in 88.3, regular in 9.3, and poor in 2.3% of the patients. Dietary ingestion of 50 g of tomato paste per day for 10 weeks significantly reduced mean plasma PSA levels in patients with benign prostate hyperplasia, probably as a result of the high amount of lycopene in tomato paste. This was not a prostate cancer prevention study, but showed some action of tomato paste in prostate biology. The development of prostate cancer is typically accompanied by an increase in plasma PSA levels, thus any intervention that affects plasma PSA levels can suggest an impact in the progression of disease.

Aged↗