Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer of the prostate is an heterogenic, "epidemic" world-wide tumor, which represents the most common form of solid cancer in adult males, excluding nonmelanoma skin cancer. Prostate cancer now surpasses the incidence of lung cancer and becomes the second leading cause of male cancer death in the industrialized West countries. The incidence and mortality of prostate cancer are increasing to alarming rates (in the USA carcinoma prostate was projected to be responsible for 14% of all male cancer deaths in 1996). As the life expectancy of the male population increases over time, the incidence of clinical prostate cancer will also increase. There is a wide geographic variation in the incidence of clinical prostate cancer, with higher rates in the United States than in China. A difference in diagnostic practice with regard to prostate cancer can be the explanation for this wide divergence. One risk factor which could explain this fact is the high fat Western diet. It is also apparent that prostate cancer is now being detected at less advanced stages than in the past. It has become evident that there is a greater than expected incidence of this tumor in the male relatives of men who died from the disease. Hereditary prostate cancer is characterized by Mendelian autosomal dominant inheritance, and an early onset of the disease. Prostate specific antigen (PSA) represents the best serum marker for prostatic carcinoma and is considered as most perfect tumor marker available today. Nevertheless, the use of PSA to detect prostate cancer is clinically imprecise since benign and malignant prostate disease can cause elevations in PSA. The biological behaviour and the natural course of prostate cancer are poorly understood. There are far larger numbers of males who have a so-called latent, well-differentiated microscopic (clinically insignificant) prostate carcinoma that may never progress to invasive clinical disease with metastatic potential. These incidental cancers discovered histologically after the transurethral or open prostatectomy and as a result of the prostate biopsy in patients with the high level of PSA are currently not well understood. Results of the mass screening for prostate cancer are at present controversial and their benefit is still not confirmed. There is now strong evidence for the screening of first degree male relatives of men with prostate cancer, particularly male relatives of those developing the disease at a young age and those with a strong positive family history of the disease. There is no debate that the earlier diagnosis of prostate carcinoma, especially in young men give them the best chance to be cured. The "watchful waiting" seems the best treatment strategy for older men with so called insignificant carcinoma. The aggressive modalities of the therapy--radical prostatectomy, radiation therapy, interstitial brachy-therapy or interstitial cryotherapy--are the curable methods only for organ-confirmed tumors and advocated in patients with life expectancy longer than 10 years. Androgen ablation therapy is the treatment of choice for the palliation of patients with advanced prostate cancer. Maximal androgen ablation (combination of medical or surgical castration and an antiandrogen) has been shown to increase the survival of patients with metastatic prostate cancer. As the incidence and prevalence of prostate cancer have increased, so has mortality, though at a slower rate. This fact may more a reflection of earlier diagnosis rather than improvements in treatment. Five-year prostate cancer survival has improved for every stages of disease in the last decenium. Thanks to the screening programmes performed in many countries, urologists are faced with an increasing incidence of clinical less advanced prostate cancer and this trend is likely to continue. (ABSTRACT TRUNCATED)
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PMID:[Adenocarcinoma of the prostate]. 978 3

A TISSUE MARKER: Prostate specific antigen (PSA) is a tissue marker and not a tumor marker. When ordered for the right situation, i.e. when the clinical presentation is compatible with prostatic cancer, PSA assay can be a remarkable tool for early diagnosis and beneficial therapeutic care. IN PATIENTS OVER 70: A PSA assay is not necessarily indicated for men over 70 years of age unless digital exploration of the prostate or other signs suggest prostatic disease. IN PATIENTS UNDER 70: In patients whose life expectancy is greater than 10 to 15 years, serum PSA above the laboratory's upper limit for normal is an indication for ultrasonographic exploration of the prostate with systematic biopsy.
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PMID:[Prostate specific antigen: its proper diagnostic use]. 987 22

Galectin-1 has been implicated in the process of vertebrate developmental regulation. Sodium butyrate is an established differentiation-inducing agent and has been shown to increase galectin-1 expression in colon carcinoma cells. We studied the roles of butyrate and galectin-1 in the induction of differentiation and apoptosis in the prostate cancer cell line LNCaP. Treatment of LNCaP cells with butyrate resulted in induction of galectin-1 expression in a time- and dose-dependent manner. Treatment with butyrate also resulted in inhibition of proliferation, morphologic changes consistent with a differentiated phenotype, and induction of apoptosis. Prostate specific antigen expression was transiently reduced. To determine which of these effects might be secondary to the induction of galectin-1, LNCaP cells were transfected with a galectin-1 expression vector. The transfected cells displayed growth inhibition and an increased rate of apoptosis. PSA expression was not affected. We conclude that galectin-1 may be responsible for many of the phenotypic changes resulting from butyrate treatment and may function downstream in the pathway of butyrate-induced differentiation. We also found PSA to be somewhat inconsistent as an indicator of differentiation of LNCaP cells, likely due to other factors influencing its expression.
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PMID:Induction of differentiation and apoptosis in the prostate cancer cell line LNCaP by sodium butyrate and galectin-1. 991 96

Prostate specific antigen (PSA) is serine protease produced at high concentrations by normal and malignant prostatic epithelium. It is mainly secreted into seminal fluid, where it digests the gel forming after ejaculation. Only minor amounts of PSA leak out into circulation from the normal prostate, but the release of PSA is increased in prostatic disease. Thus PSA is a sensitive serum marker for prostate cancer but its specificity is limited by a high frequency of falsely elevated values in men with benign prostatic hyperplasia (BPH). Approximately two-thirds of all elevated values (>4 microg/l) in men over 50 years of age are due to BPH. In serum, most of the PSA immunoreactivity consists of a complex between PSA and alpha1-antichymotrypsin (PSA-ACT) whereas approximately 5-40% are free. The proportion of PSA-ACT is larger and the free fraction is smaller in prostate cancer than in benign prostatic hyperplasia (BPH). Determination of the proportion of free PSA has become widely used to improve the cancer specificity of PSA especially in men with PSA values in the 'grey zone' (4-10 microg/l). PSA also occurs in complexes with other protease inhibitors and determination of these and other markers may further improve the diagnostic accuracy for prostate cancer. Interpretation of the results for many different markers is complicated, but this can be simplified by using statistical methods. The diagnostic accuracy can be further improved by using logistic regression or neural networks to estimate the combined impact of marker results and other findings like digital rectal examination (DRE), transrectal ultrasound (TRUS) and heredity.
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PMID:Prostate-specific antigen. 1020 30

Following hormonal therapy, few treatment regimens have activity in metastatic prostate cancer. Cytotoxic agents have minimal activity in this disease. However, combinations of cytotoxic agents may be beneficial. The activity of estramustine, vinblastine, etoposide, and suramin on cell growth was evaluated. Prostate specific antigen (PSA) is routinely used as a surrogate marker for disease progression. Many pharmacological agents alter PSA levels independently of their effect on tumor growth, the effect of these agents on PSA secretion was determined. Each agent was evaluated alone and in combination with the other drugs in two prostate cancer cell lines. In LNCaP cells, estramustine and suramin were cytostatic, while vinblastine and etoposide were cytotoxic. Estramustine down-regulated etoposide PSA secretion, while suramin had no effect. The effects of etoposide and vinblastine on PSA secretion were not evaluable. In PC-3 cells, only etoposide was cytotoxic. Tandem combinations were more cytotoxic than single agents in both cell lines. The addition of a third agent to the tandem combination produced less cytotoxicity. In our hands, the best combinations were estramustine/vinblastine, suramin/vinblastine, and suramin/etoposide. These combinations yielded 20-60% higher cytotoxicity than any of the drugs alone.
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PMID:Enhanced activity of estramustine, vinblastine, etoposide, and suramin in prostate carcinoma. 1046 36

Prostate specific antigen (PSA) is currently the tumour marker of choice for prostatic carcinoma. Various indices of PSA have been developed in an attempt to refine its sensitivity and improve its clinical value. These include the ratio of serum PSA level and prostate volume, the rate of change of the PSA level with time, age-referenced PSA, and the proportion of free PSA in serum relative to total PSA (free to total PSA ratio). The free to total PSA ratio is lower in patients with prostate cancer than in those with elevated PSA levels due to benign prostatic hyperplasia.
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PMID:[Prostate-specific antigen as a tumor marker of prostate carcinoma]. 1049 19

Benign prostatic hyperplasia is a common condition in males over 50 years, but prostate cancer can develop in the same population. Prostate specific antigen, the best marker for prostate cancer, is also produced by benign epithelial cells, and there is an overlapping phenomenon between both conditions. The better we understand the relationships between benign prostatic hyperplasia and prostate specific antigen, the higher will be the discrimination power of prostate specific antigen measurement as a marker for prostate cancer. Our scope includes a review of the latest published material to date on this subject.
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PMID:Prostate specific antigen and benign prostatic hyperplasia. 1065 May 6

Prostate cancer (PCa) is the most commonly diagnosed cancer in men as well as the second leading cause of cancer death. Age, family history and race are proved risk factors for developing a PCa. Prostate specific antigen (PSA) in combination with the digital rectal examination (DRE) has proven to be an essential element in early prostate cancer detection. Enthusiasm for using transrectal ultrasound (TRUS) alone to identify early prostate cancer has not been demonstrated with longer follow-up. The major role of TRUS today is to ensure accurate wide-area sampling of prostate tissue in men with PCa suspicion. This is best accomplished by targeted biopsy of TRUS-suspicious lesions and systematic biopsy of areas without hypoechoic lesions. Urologists recommend digital rectal examination and a PSA blood test annually starting at age 50.
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PMID:[General features and strategy in the diagnosis of prostatic carcinoma]. 1069 84

Recent studies have provided convincing evidence for the role of soy-isoflavones, particularly genistein, in the inhibition of prostate cancer cell growth. Prostate specific antigen (PSA) is a biological marker used to detect and monitor the treatment of prostate cancer patients. Previous studies have documented that isoflavones can inhibit the secretion of PSA in the androgen-dependent prostate cancer cell line, LNCaP, however, the effects of genistein on androgen-independent PSA expression has not been explored. In this study, we have utilized a prostate cancer cell line, VeCaP, which expresses PSA in an androgen-independent manner, to determine the effects of genistein on cell proliferation and PSA expression. Here we show that genistein inhibits cell growth similarly in both the LNCaP and VeCaP cell lines, but has differential effects on PSA expression. We demonstrate using concentrations of genistein that have been detected in the serum of humans consuming a soy-rich diet, that genistein decreases PSA mRNA, protein expression and secretion. Conversely, only high concentrations of genistein inhibited PSA expression in VeCaP cells. Additionally, we have demonstrated that genistein inhibits cell proliferation independent of PSA signaling pathways, providing further evidence to support the role of genistein as a chemopreventive/therapeutic agent for prostate cancer irrespective of androgen responsiveness.
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PMID:Inhibition of prostate specific antigen expression by genistein in prostate cancer cells. 1081 79

Prostate specific antigen (PSA) is a glycoprotein found in the epithelial cells of the prostatic duct and acini. PSA is elevated in all four stages of prostate cancer as well as in benign prostatic hypertrophy. We evaluated a new chemiluminescent assay for PSA by comparing this assay with the microparticle enzyme immunoassay for PSA (MEIA) on the AxSYM analyzer (Abbott Laboratories, Abbott Park, IL) and a Hybritech Tandem R assay for PSA. The new chemiluminescent assay is recently available from Bayer Diagnostics (Tarrytown, NY) and can be run using the ACS: 180 Plus analyzer. Precision of the new chemiluminescent assay was evaluated using commercially available controls (Bayer Diagnostics). The within-run and total CVs were 6.4 and 8.7% for the low control (mean: 0.43 microg/L), 1.6 and 5.2% for the next level control (mean:1.94 mg/L), 4.3 and 4.9% for the medium control (mean: 2.10 mg/L), 1.2 and 3.9% for the high control 1 (mean: 11.52 mg/L), and finally 3.2 and 6.9% for the high control 2 (mean: 21.52 mg/L). The spike recovery varied from 94.2 to 109.6% for five different specimens we studied. We also observed excellent dilution recoveries. For example, in the specimen supplemented with 3.02 mg/L of PSA, the dilution recoveries were 102. 1, 104.7, and 103.7% for 1:2, 1:4, and 1:8 dilutions, respectively. We analyzed 113 serum specimens from patients with various concentrations of PSA (range 0.5 mg/L-2040 mg/L) using the new chemiluminescent assay and compared our results with the MEIA and Hybridtech (Tandem-R PSA) assays. Using x axis as the PSA concentrations obtained by the Tandem-R assay and the y axis as the PSA values obtained by the new chemiluminescent assay, we observed the following regression equations: y = 1.04 x -0.19 (r = 0.99, n = 112). One specimen with PSA concentrations of 2040 microg/L by the MEIA and 2156 microg/L by the chemiluminescent assay was not used for regression analysis. Similarly using x axis as the PSA concentrations obtained by the MEIA assay and y axis as the PSA concentrations obtained by the chemiluminescent assay, we observed the following regression equation: y = 0.88 + 0.02 (r = 0.99, n = 112). We conclude that the new chemiluminescent assay has excellent precision and the results compared well with the existing assays.
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PMID:Performance evaluation of a new chemiluminescent assay for prostate specific antigen. 1090 69


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