Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Staging in prostate cancer, as in any other cancer has significant ramifications in management. Currently, prostate-specific antigen (PSA) determination and the bone scan are two important procedures in the pretreatment staging workup of prostate cancer. PSA is a very useful serum tumor marker in the management of prostate cancer patients. We retrospectively evaluated 90 patients at the time of initial diagnosis of prostate cancer, all of whom had initial PSA levels measured, as well as bone scans obtained. In addition to the PSA level, we considered clinical stage and pathologic grade in the prediction of bone scan for metastases, at the time of initial diagnosis of prostate cancer. Negative predictive value for PSA values < 10 ng/ml (27 patients), clinical stage A (9 patients) and pathologic grade 1 (19 patients) was 100%. The number of patients with bone scan evidence of metastasis with < 10 ng/ml and > 10 ng/ml PSA levels were 0% (0/27 patients) and 27% (17/63 patients) (p = .0022 [Fisher's Exact test]; p = .003 [chi-square test]). In patients with higher stage (p = .688), grade (p = .039), or PSA levels (p = .0001), the incidence of bone metastases increased. However, none of these three parameters can predict reliably bone scan evidence of metastases (i.e., positive predictive value). The negative predictive values did not improve when a combination of the two or three of the above parameters were used.
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PMID:Can prostate-specific antigen levels predict bone scan evidence of metastases in newly diagnosed prostate cancer? 752 94

Prostate-specific antigen is the most important, accurate, and clinically useful biochemical marker in the prostate. It is manufactured by the secretory epithelial cells and drains into the ductal system, where it catalyzes the liquefaction of the seminal coagulum after ejaculation. Serum levels are normally less than 4 ng/mL (monoclonal) but vary according to patient age and race; any process that disrupts the normal architecture of the prostate allows diffusion of prostate-specific antigen into the stroma and microvasculature. Elevated serum prostate-specific antigen levels are seen with prostatitis, infarcts, hyperplasia, and transiently after biopsy, but the most clinically important increases are seen with prostatic adenocarcinoma. Cancer produces less prostate-specific antigen per cell than benign epithelium, but the greater number of malignant cells and the stromal disruption associated with cancer account for the increased serum prostate-specific antigen level. Serum prostate-specific antigen level correlates positively with clinical stage, tumor volume, histologic grade, and the presence of capsular perforation and seminal vesicle invasion; despite these strong correlations, its value is limited in predicting stage for individual patients. It may also predict the presence of lymph node metastases, bone metastases, and survival after androgen-deprivation therapy. The use of prostate-specific antigen has resulted in an increase in the early detection rate of cancer, and it is now advocated for annual routine use in men older than 40 years who are at increased risk and in all men older than 50 years. It is a test with high sensitivity and specificity that is rapid, inexpensive, minimally invasive, and acceptable to patients. In addition to serum prostate-specific antigen level, five derivatives of serum prostate-specific antigen were recently described that may increase the predictive value by accounting for confounding variables such as patient age, prostate volume, and cancer volume: age-specific reference ranges, prostate-specific antigen density, prostate-specific antigen velocity, prostate-specific antigen cancer density, and prostate-specific antigen doubling times. Serum prostate-specific antigen detects a heterogeneous group of cancers (clinical stage T1c) that are clinically important and potentially curable. Immunohistochemical expression of prostate-specific antigen in tissue sections allows determination of the prostatic origin of some metastatic adenocarcinomas, although extraprostatic expression of prostate-specific antigen has been reported in several tissues and tumors, including periurethral gland adenocarcinoma in women, rectal carcinoid, and extramammary Paget disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prostate-specific antigen. Current role in diagnostic pathology of prostate cancer. 752 5

The use of the serum marker prostate-specific antigen (PSA) has altered drastically the follow-up after prostate cancer. PSA is far superior to any other method of detecting recurrences after either radiation therapy or radical prostatectomy. Once the PSA reaches a nadir level after radiation therapy or becomes undetectable after radical prostatectomy, it should remain at that level. PSA provides a lead time of approximately 3 to 7 years prior to identification of recurrence or metastases by other traditional methods. The yield of diagnostic studies to identify the site of recurrence in patients with very low levels of PSA after radical prostatectomy is quite low. A substantial dilemma remains about optimal therapy once a rising PSA is identified.
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PMID:Follow-up after radical prostatectomy or radiation therapy for prostate cancer. 752 13

A highly sensitive nested reverse transcriptase-PCR assay, with primers derived from the prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSM) cDNA sequences, has been used to detect occult hematogenous micrometastatic prostate cells. In 77 patients with prostate cancer, PSM and PSA primers detected circulating prostate cells in 48 (62.3%) and 7 (9.1%) patients, respectively. In treated stage D disease patients, PSM primers detected cells in 16 of 24 patients (66.7%), while PSA primers detected cells in 6 of 24 (25%). In post-radical prostectomy patients with negative serum PSA values, PSM primers detected metastases in 21 of 31 patients (67.7%), whereas PSA primers detected cells in only 1 of 33 (3.0%), indicating that micrometastatic spread may be a relatively early event in prostate cancer. The analysis of 40 individuals without known prostate cancer provides evidence that this assay is highly specific and suggests that PSM expression may predict the development of cancer in patients without clinically apparent prostate cancer. Using PSM primers, we detected micrometastases in 4 of 40 controls, 2 of whom had known benign prostatic hyperplasia and were later found to have previously undetected prostate cancer. The clinical significance of detection of hematogenous micrometastic prostate cells using PSM primers and potential applications of this molecular assay, as well as the assay for PSA, merit further study.
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PMID:Sensitive nested reverse transcription polymerase chain reaction detection of circulating prostatic tumor cells: comparison of prostate-specific membrane antigen and prostate-specific antigen-based assays. 752 94

We compared tumor grade and DNA content with expression of E-cadherin (E-CD), a cell adhesion molecule associated with cell-cell and cell-matrix interaction, leukocyte function, and tumor invasion and metastases, on 56 prostate carcinoma needle biopsies. The findings were correlated with final pathologic stage at subsequent prostatectomy, preoperative serum prostate-specific antigen level and further development of metastases during an initial 2.4-yr mean clinical follow-up period (range 0.5 to 5.5 yr). E-CD expression (uvomorulin, L-CAM, cell CAM 80/120, ARC-1, Sigma, St. Louis, MO) was measured by double-linked immunoalkaline phosphatase immunohistochemistry quantified with a the Roche RPW image analyzer (Roche Image Analysis Systems, Elon College, NC). DNA ploidy was determined on formalin-fixed, paraffin-embedded Feulgen-stained 5-microns tissue sections of the narrow-bore initial prostate carcinoma biopsies with the Roche RPW image analyzer. The 51% mean positive area E-CD expression in the group of 56 adenocarcinomas was significantly less than the 76% expression level for 15 normal control prostate tissues (P < 0.001). E-CD expression was also decreased in aneuploid (39%) versus diploid tumors (54%, P < 0.001); and in high-grade (44%) versus low-grade lesions (54%; P < 0.01). The 44% E-CD expression level in patients with metastases was lower than the 52% level in the nonmetastatic cases, but this finding was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:E-cadherin expression in prostatic carcinoma biopsies: correlation with tumor grade, DNA content, pathologic stage, and clinical outcome. 753 Aug 50

We have studied the expression of prostate-specific antigen (PSA) mRNA by reverse transcriptase-polymerase chain reaction in peripheral blood of 25 patients with cancer of the prostate (CAP), four with benign prostatic hyperplasia (BPH), two with renal stones, three with other types of cancer, and six healthy male and three female controls. Expression of mRNA specific for a certain tissue in peripheral blood is thought to indicate the presence of circulating cancer cells and metastatic spread of a tumor originating from this tissue. We detected PSA mRNA in 9 of 18 CAP patients with metastatic disease but in none of 7 patients without metastases. Negative results in patients with metastatic disease were associated with successful endocrine therapy and low concentrations of serum PSA, and the correlation between serum concentrations of PSA and the presence of PSA mRNA in peripheral blood was statistically significant. PSA mRNA was not found in patients with BPH, other types of cancer, or in healthy controls. Thus the occurrence of PSA mRNA in peripheral blood is associated with metastatic CAP.
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PMID:Detection of prostatic cells in peripheral blood: correlation with serum concentrations of prostate-specific antigen. 753 61

Prostate cancer is the most common noncutaneous malignancy diagnosed in American men, and in 1994 it will pass lung cancer as the most common cancer diagnosed in the United States, with an estimated 200,000 new cases. The molecular biology of prostate carcinogenesis is rapidly advancing, and it is clear that, to a degree, prostate cancer is a heritable disease. The use of serum prostate-specific antigen (PSA) as a screening tool has been widely accepted by the medical community, although the evidence to support the efficacy of screening is not yet available. The curative approaches to organ-confined, clinically localized prostate cancer include radiation therapy, radical prostatectomy, and close observation in selected patients. The absence of well-designed clinical trials contributes to the confusion surrounding which curative treatment is the best option in individual patients. The standard approach to patients with evidence of extracapsular spread without distant metastases has been external-beam radiotherapy, although the results with radiation therapy alone in these patients has left considerable room for improvement. Innovative combined-modality approaches are currently being investigated at a number of institutions for these poor-prognosis patients. Three-dimensional conformal radiation therapy is currently being investigated at multiple institutions and offers some hope for improved results. The treatment of metastatic disease remains hormonal manipulation, although the exact nature of optimal androgen deprivation is currently a matter of considerable debate. In patients with hormone-refractory disease newer regimens using novel chemotherapy regimens offer some promise.
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PMID:Prostate cancer. 753 41

Carcinoma of the prostate is the commonest malignancy of the genitourinary tract in the male and is frequently associated with metastatic bone disease. Serial isotope bone scans for screening secondary deposits are not cost-effective. We have evaluated the serum prostate markers prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) as an alternative to conventional serial bone scanning in 129 patients with newly diagnosed prostate cancer over a period of 3 years. Although serum PSA did not reflect local tumour burden at presentation, it was significantly elevated in those who presented with stage D disease (p < 0.01). 45 patients presented de novo with metastatic bone deposits and a further 18 patients developed metastases during the study period. The sensitivity of PSA in detecting secondary deposits at presentation for levels in excess of 100 micrograms/l was 93.75%, the positive predictive value 95.7% and the negative predictive value for levels less than 5 micrograms/l was 90.6%. During the follow-up period the sensitivity was 94.4%, the positive predictive value 100% and the negative predictive value 100%, with a median lead time of 3 months in predicting metastases in the 18 patients with progressive disease. When compared with PAP, PSA was found to be a statistically superior marker of bone metastases both at presentation and follow-up (p < 0.05). We recommend that PAP measurements are no longer necessary and should be replaced by PSA, and that serial serum PSA estimations should determine the need for future isotope bone scans in the patient with established prostate cancer.
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PMID:A reappraisal of serial isotope bone scans in prostate cancer. 753 7

Nearly all primary prostatic carcinomas have been found to express the androgen receptor (AR) protein, which is the intracellular mediator of androgen action. To gain a better insight into the mechanisms of androgen independence of advanced prostatic carcinoma, it is important to know whether the AR is also present in metastases of androgen-independent tumors. We have assessed the status of the AR and the prostate-specific antigen in 22 metastases of 18 patients with progressive prostate cancer. In 18 cases, the metastases were localized in bone, in 3 cases in the epidural space, and in 1 case in the periosteum. All but one patient had received some kind of endocrine treatment for prostatic carcinoma. Paraffin-embedded tissue sections were stained for the AR following a streptavidinbiotin-peroxidase protocol with the polyclonal antibody PG-21, which is directed against amino acids 1 through 21 of the rat and the human AR. The percentage of AR-positive cells was evaluated on the basis of an arbitrary 4-point scale. All 22 tumor metastases displayed AR positivity. One AR-positive metastatic lesion did not stain for prostate-specific antigen, but in all other metastases, this protein was detected by means of immunohistochemistry. The present study provides evidence that, unlike androgen-independent prostatic carcinoma cell lines, distant prostatic carcinoma metastases do express the AR. These findings indicate that the AR may be involved in the progression of prostate cancer.
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PMID:Distant metastases from prostatic carcinoma express androgen receptor protein. 754 9

Prostate cancer is the second cause of cancer death in men in the Western world; its medical and social impact is comparable to that of breast cancer in women. Although it is well recognized that early treatment is the only possibility for reducing the high rate of death from prostate cancer, screening and even early treatment are controversial issues due mainly to arguments based upon old literature and lack of awareness of the significant advances recently made in this field. As it is well known that surgical removal of organ-confined prostate cancer cures the disease, and it has been demonstrated that annual screening with prostate-specific antigen coupled with digital rectal examination followed, when indicated, by transrectal ultrasonography of the prostate more than doubles the proportion of organ-confined disease, screening alone offers the possibility of at least doubling the number of patients curable from prostate cancer or the potential for a cure to an estimated 45% of prostate cancer patients compared to a maximum of 20% in the absence of screening. It is important to mention that screening does not detect small and insignificant cancers, especially when random biopsies are not performed routinely. The critical volume of prostate cancer is estimated at 0.3 cm or a tumor 7.5 mm in diameter, if spherical. Such a tumor should increase serum prostate-specific antigen by 0.5 ng/mL. Contrary to the belief that screening detects cancers that are too small, the fact is that screening detects prostate cancer too late or nonorgan- or nonspecimen-confined cancer in 35-50% of cases. There is, thus, a narrow window when prostate cancer can be detected at a curable stage, and even the best available screening techniques cannot succeed in all cases. It should be mentioned that the recent improvements of the technique of radical prostatectomy have markedly improved the acceptability of surgery. Concerning the recent publicity related to watchful waiting, it is essential to indicate that all such reports support the notion that prostate cancer grows slowly, but steadily and irremediably, with increasing malignancy and risk of distant metastases and death if sufficient time is allowed. Another serious limitation of watchful waiting is that the available prognostic factors have a large margin of error and cannot predict with certainty the rate of progression of the tumor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Combination of screening and preoperative endocrine therapy: the potential for an important decrease in prostate cancer mortality. 754


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