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)

Two hundred and sixteen patients, presenting with a suspicious digital examination (stage T3 excluded) or a level of prostate-specific antigen (PSA) greater than or equal to 2.5 ng/ml, assessed by radioimmunoassay, underwent a transrectal ultrasound examination. Prostate volume was systematically calculated and correlated to PSA level. Biopsies were performed: (1) on suspicious peripheral hypoechoic areas; ultrasound-guided biopsies; (2) systematically on the 2 prostate lobes, whatever the result of transrectal ultrasound imaging:random systematic ultrasound-guided biopsies. In the 186 patients who had never undergone prostate surgery, ultrasound-guided biopsies showed 42 prostate cancers and random systematic ultrasound-guided biopsies showed 75; 14 of the 76 patients with normal digital rectal examination and transrectal ultrasound imaging had a prostate cancer. In the 30 patients who had previously undergone surgery for benign prostatic hypertrophy, random systematic ultrasound-guided biopsies showed 18 prostate cancers, 13% more than ultrasound-guided biopsies; 75% of patients with a serum PSA greater than 5 ng/ml had a prostate cancer. A very significant correlation was found between PSA level and prostatic volume (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Advantage of systematic random ultrasound-guided biopsies, measurement of serum prostate-specific antigen level and determination of prostate volume in the early diagnosis of prostate cancer. 137 93

The serum half-life of prostate-specific antigen (PSA) after radical prostatectomy is about 3 days; to the authors' knowledge, the PSA half-life during radiation therapy (RT) has not been investigated with weekly serial measurements. To determine the rate of decline and the half-life of PSA, serial measurements were obtained during 6-8 weeks of external-beam RT for localized prostate cancer. PSA values were determined immediately before and approximately 24 hours after the first dose of RT; thereafter, weekly measurements were made. There was a downward trend in PSA levels in 19 patients, with a median half-life of 58.5 days; the mean decline was 1.6% per day. However, in four patients, PSA levels either rose and fell to pre-RT values or increased steadily. The effect of digital rectal examination (DRE) on PSA levels was also analyzed. When the dates of DRE and subsequent PSA levels were inspected, no increase in PSA levels subsequent to DRE was found, although three of the four patients in whom PSA levels did not decrease underwent multiple DREs. The authors found a statistically significant (P = .023) transient elevation in the mean PSA values after the first fraction of RT (2 Gy) was administered; the mechanism and importance of which are not known.
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PMID:Localized prostate cancer: use of serial prostate-specific antigen measurements during radiation therapy. 137 33

Despite development of new technology for the diagnosis and treatment of prostate cancer, the age-adjusted mortality rate for the disease has not declined for nearly half a century. Physicians now have the ability to diagnose very small tumors in asymptomatic patients, but it remains to be determined which subset of patients would benefit most from early identification and treatment. Studies that are currently under way hopefully will clarify what screening protocols, if any, actually reduce the mortality and morbidity that are associated with prostate cancer and its treatment. Until such evidence becomes available, screening measures for the general population are unwarranted, with the possible exception of digital rectal examination performed as part of other healthcare services. Prostate-specific antigen (PSA) determination may have a place in screening patients whose family history puts them at increased risk. In patients with symptoms or findings suggestive of prostate cancer, diagnosis and staging can be accomplished more accurately and easily than ever before with a combination of PSA determination, transrectal ultrasound, ultrasound-guided tissue sampling using a biopsy gun, and the judicious use of imaging techniques such as bone scans, magnetic resonance imaging, and computed tomography. New treatment methods are being studied, and the options available, especially for management of disease progression, are expected to increase. Monitoring of treated patients has been greatly facilitated by determination of PSA levels, which are predictive of both long- and short-term prognosis. Although much work remains to be done, we may finally be on the verge of making real progress in control of prostate cancer.
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PMID:Prostate cancer. Finding and managing it. 137 86

Changes in prostate-specific antigen (PSA) have been demonstrated to accurately assess response to initial hormone deprivation in metastatic prostate cancer patients. The role of PSA in monitoring response to second-line hormonal treatment has not been documented. In a group of 20 patients with an initial response to androgen deprivation and subsequent relapse, we monitored PSA levels before and after second-line therapy. Ten patients had a clinical response. Four had a more than 90 percent decrease in serum PSA compared with the level at initial progression. This clinical response was maintained for a mean of eighteen months. Six patients had a PSA decrease less than 90 percent; their clinical response was of a mean 5.5 months. Ten patients had no change or increase in PSA. Seven had no clinical response, and 3 responded for an average of four months. Although production of PSA might be under endocrine control, changes in PSA are useful for monitoring response to second-line hormonal therapy.
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PMID:Response to second-line hormonal manipulation monitored by serum PSA in stage D2 prostate carcinoma. 137 47

Prostate-specific antigen (PSA) has emerged as the most useful marker for management of patients with prostate cancer. The regulation of this glycoprotein in vivo has important clinical implications. Indirect evidence indicates that the PSA glycoprotein might be regulated by androgens, and previous studies in this laboratory have demonstrated that PSA mRNA is upregulated by androgens. The current work reports a detailed study of PSA glycoprotein expression as influenced by steroid hormones in a human prostatic adenocarcinoma cell line, LNCaP. First, we have examined the steroid binding specificity of the androgen receptor in this cell line. In comparison with wild-type rat androgen receptor in prostate, the receptor in LNCaP cells has altered affinity for a number of steroids or analogs such as progesterone (R5020), antiprogesterone (RU486), two antiandrogens (cyperoterone acetate and hydroxyflutamide), and an androgen metabolite (epitestosterone). However, its affinity for androgens (mibolerone, dihydrotestosterone, and testosterone) is not changed. The receptor does not bind to the synthetic glucocorticoids (triaminolone acetonide and dexamethasone) nor to a synthetic estrogen DES (diethylstilbestrol). The change of the steroid binding specificity of the receptor is correlated with a single mutation (A----G at nucleotide #876 relative to the initiation codon) of the steroid binding domain of the receptor. The mutation and alteration of steroid-binding specificity of the androgen receptor is also correlated with PSA glycoprotein expression affected by different ligands tested. We have demonstrated that the PSA glycoprotein is upregulated by androgens and is affected by neither epidermal growth factor nor basic fibroblast growth factor. Moreover, PSA glycoprotein could be induced by R5020, estradiol, and epitestosterone; but neither glucocorticoids nor DES had any effect on PSA induction. Interestingly, although the antiandrogen, cyperotone acetate, had the ability to induce PSA, both RU486 and hydroxyflutamide could block androgen and progesterone induction of PSA glycoprotein. Therefore, we conclude that the PSA glycoprotein expression is influenced predominantly by androgens via its receptor, and the mutation of the receptor can affect the expression of this cellular gene by the steroids other than androgens.
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PMID:Hormonal regulation of prostate-specific antigen (PSA) glycoprotein in the human prostatic adenocarcinoma cell line, LNCaP. 137 63

Despite the controversies in management for all stages of prostatic cancer, guidelines are emerging that allow for better selection of treatments for individual patients. For early stage disease, prostate-specific antigen determinations in conjunction with other staging procedures have refined our ability to define truly organ-confined disease. The more widespread use of laparoscopic lymph node dissections has spared many patients needless laparotomies. For patients with metastatic disease, the overall effect of potency-sparing antiandrogens as monotherapy needs to be investigated. Most encouraging is that more groups are using prostate-specific antigen changes to assess disease activity and the rapid translation of recent laboratory investigations into the clinic. As our ability to predict the biologic potential of an individual patient's tumor is improved, more individualized treatment recommendations will be possible.
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PMID:Prostatic cancer: are we closer to rational treatment selection? 137 31

Prostate-specific antigen (PSA) is used for screening and follow-up of patients with prostate cancer. The effect of certain diagnostic procedures on PSA serum levels is not well defined. Therefore, the effect of digital rectal examination (DRE) on PSA serum levels was investigated. No significant difference was observed in PSA values before and after DRE when blood samples were taken 1-3 min after palpation of the prostate. Kinetic studies demonstrated a significant increase in PSA values up to the factor 3.2 in 14 of 19 patients 2-6 h after DRE. In 9 of 14 cases, PSA was within the initial range 24 h after DRE. That means that a urologist is allowed to take blood samples for the determination of PSA at least within 3 min after palpating a suspicious prostate without getting false-positive results.
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PMID:Effect of digital rectal examination on serum concentration of prostate-specific antigen. 137 26

The goal of this study was to determine if patients with stage D0-3 prostatic adenocarcinoma have detectable hematogenous micrometastasis. Polymerase chain reaction amplification of prostate-specific antigen mRNA, which is exclusively expressed by prostatic epithelial cells, was used to detect circulating prostatic cells. Peripheral venous blood was obtained from 17 control and 12 prostate cancer patients with stage D0-3 prostatic adenocarcinoma. Of the 12 cancer cases, four patients (stage D1-3) tested positive for prostate-specific antigen RNA, indicating the presence of circulating micrometastasis. The 17 negative controls all tested negative. Contrary to a long held hypothesis, these data point to the possibility that hematogenous metastasis may be a relatively early event in the natural history of human prostate cancer. These findings may have an important impact on our understanding and treatment of prostate cancer.
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PMID:Detection of hematogenous micrometastasis in patients with prostate cancer. 138 51

We evaluated a new fully automated procedure for quantitative measurement of prostate-specific antigen (PSA) by the Microparticle Enzyme Immunoassay (MEIA) technology developed for the Abbott IMx automated immunoassay system. The performance characteristics of the Abbott IMx PSA assay (y) were evaluated and compared with those of the Hybritech Tandem-E PSA assay (x), a solid-phase two-site immunoenzymometric assay. PSA values for both assays were well correlated (r = 0.99); regression analysis yielded the equation y = 0.92x - 0.23 micrograms/L. The Abbott assay proved reliable and reproducible, as shown by the intra- and interassay coefficients of variation (2.0-3.4% and 3.1-4.7%, respectively). The assay gave a linear standard curve up to 100 micrograms/L and was very sensitive (detected PSA < 0.1 microgram/L). This analytical sensitivity was comparable with that of the Tandem-E PSA assay. Overall, the IMx PSA assay demonstrated the accuracy, precision, linearity, and intermethod correlation required for monitoring patients with prostate cancer.
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PMID:Abbott IMx evaluated for assay of prostate-specific antigen in serum. 138 93

Insulin-like growth factor binding protein-3 (IGFBP-3), the major serum carrier protein for the IGFs, is absent from Western ligand blots of seminal plasma, but is detectable by RIA. IGFBP-3 protease activity has recently been described in pregnancy serum. We investigated the possibility that seminal plasma contains an IGFBP-3 protease, by incubating seminal plasma with 125I-labeled human IGFBP-3. Seminal plasma was found to have potent IGFBP-3 protease activity with a cleavage pattern different from that of pregnancy serum. Prostate-specific antigen (PSA) is a serine protease found in semen. Autoradiographs measuring IGFBP-3 protease activity demonstrated that purified PSA cleaved IGFBP-3, yielding a cleavage pattern identical to that of seminal plasma. IGFBP-2 and -4 in seminal plasma were not degraded by PSA. Cleavage of IGFBP-3 by PSA resulted in a marked reduction in the binding affinity of the fragments to IGF-I, but not IGF-II. We speculate that PSA may serve to modulate IGF function within the reproductive system or in prostate cancer by altering IGF-IGFBP-3 interactions.
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PMID:Prostate-specific antigen (PSA) is an insulin-like growth factor binding protein-3 protease found in seminal plasma. 138 55


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