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)

Serum-acid phosphatase as measured by nine different methods, serum prostate-specific antigen, cancer antigen CA-50, and creatine kinase BB isoenzyme have been evaluated and compared with respect to efficiency in differentiating between prostate cancer and benign hyperplasia. The patient material consisted of 92 prostate cancer patients (59 untreated, and 33 previously treated), 106 patients with benign hyperplasia and 66 patients with non-prostatic urological diseases. The cancer group was classified according to the TNM-system, and also graded according to histopathological findings. The following main conclusions were drawn. Acid phosphatase activity, when measured with continuous monitoring procedure (substrate: alpha-naphthyl phosphate), showed on the average slightly, but statistically not significant higher diagnostic efficiency than when measured with conventional two-point discontinuous monitoring method (substrate: p-nitrophenyl phosphate). There was no or only marginal differences in diagnostic efficiency between activity measurements of the total acid phosphatase and the tartrate-labile fraction, and also between activity measurements and immunological measurements (PAP-RIA and PAP-IEA). Prostate-specific antigen was found to have statistically significant higher diagnostic efficiency than acid phosphatase, the former being positive in 17 of 25 patients with prostate cancer without distant metastases, and in six of 11 patients classified as T0-2 M0. Cancer antigen CA-50 and creatine kinase BB isoenzyme appeared to be of little diagnostic value. From a cost-effective point of view, total or tartrate-labile prostatic acid phosphatase activity, as measured by continuous monitoring technique with alpha-naphthyl phosphate as substrate, is suggested suitable as a first-choice parameter both for diagnostic and monitoring purposes with respect to prostate disease. Prostate-specific antigen may give additional information, and should be considered analysed on special request.
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PMID:Diagnostic efficiency of biological markers in blood serum on prostate cancer: a comparison of four different markers and 12 different methods. 242 93

Small cell lung cancers are neuroendocrine tumours and therefore produce a lot of peptide hormones (calcitonin, ACTH, ADH), as well as the neuropeptide chromogranin A, which are all useful tumour markers. Furthermore, the tumour-associated antigens CEA and TPA, as well as the enzymes neuron specific enolase (NSE) and creatine kinase BB are used as markers in small cell lung cancer. At present, NSE appears to be the best marker for small cell lung cancer; elevated serum NSE levels are found in 65 to 85% of the patients. The serum level of the tumour markers is related to the stage of the tumour. When tumour regression occurs following therapy, elevated pretreatment levels decrease to the normal range. If the marker level increases again, tumour progression is indicated and this can be an early and sensitive sign denoting recurrence. Metastases in the central nervous system can be detected early by marker determination in the cerebrospinal fluid. At present, CEA appears to be the most valuable tumour marker for non-small cell lung cancer, but TPA may also be a useful marker.
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PMID:[Tumor markers in bronchus cancer]. 254 31

To determine whether creatine kinase-BB isoenzyme would be useful in detecting central nervous system metastases secondary to breast cancer, we measured the cerebrospinal fluid (CSF) activity of creatine kinase (CK) and its BB isoenzyme (CK-BB) in 65 consecutive patients suspected of having CNS involvement. All patients underwent neurological evaluation, computer tomography (CT) scan and/or radionuclide scintigraphy and lumbar puncture with CSF examination. Thirty patients had CNS metastases, of whom 18 had parenchymal brain metastases (MET). Twelve had leptomeningeal carcinomatosis (MC), of whom four also had parenchymal brain metastases. Thirty-four patients were concluded not to have CNS involvement, whereas one was considered equivocal. CK-BB activity was significantly higher in patients with CNS metastases than in those without (P less than 0.05). This difference was primarily related to the fact that patients with MC had a significantly higher CK-BB activity than patients without CNS metastases or patients with parenchymal brain metastases only (P less than 0.01 and P less than 0.05, respectively). Taking 0.20 U/l as a tentative cut-off value (the upper limit range of patients without CNS metastases being 0.19 U/l), 10 out of 12 patients with MC had activities above this level. The sensitivity and specificity for having MC were 83% and 87%, and the positive and negative predictive values 60% and 96%, respectively. The sensitivity and negative predictive value for having any CNS metastases were 57% and 72%. Specificity and positive predictive value: 100%. The CSF activity of CK-BB appears to be a contribution in the diagnosis of MC secondary to breast cancer and seems superior to protein and LDH.
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PMID:Creatine kinase-BB in the cerebrospinal fluid as a marker of CNS metastases and leptomeningeal carcinomatosis in patients with breast cancer. 263 53

Four patients with metastatic small cell carcinoma of the lung who had initial chest x-rays that did not reveal the cancer showed striking elevations of serum creatine kinase BB isoenzyme, which suggested the diagnosis and directed the subsequent evaluation. Creatine kinase BB isoenzyme elevation with widespread small cell carcinoma of the lung is probably more common than currently recognized, and is a useful diagnostic indicator for extensive stage small cell lung cancer, even in the absence of central nervous system metastases.
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PMID:Serum creatine kinase BB isoenzyme as a diagnostic aid in occult small cell lung cancer. 298 48

Creatine kinase (CK) and its BB isoenzyme (CK-BB) were measured in CSF in 65 evaluable patients suspected of CNS metastases secondary to small-cell lung cancer (SCLC). In addition, CSF and plasma levels of beta-2-microglobulin (beta-2-m) were measured in a group of 73 evaluable patients. Of the 65 patients analysed for CK-BB, 17 had meningeal carcinomatosis (MC), 26 had parenchymal metastases only, and 22 had no CNS disease. Patients with MC had a significantly higher CK-BB concentration in CSF than did patients belonging to the other two groups (P less than .01). Taking 0.4 U/L (upper limit in patients without CNS disease) as a cut-off point, 15 patients (88%) with MC had elevated CSF concentrations of CK-BB. Patients without CNS metastases had no CSF levels exceeding this value, whereas five patients with multiple CNS metastases did. Receiver operating characteristic (ROC) analysis suggests that CK-BB may be useful in distinguishing MC among patients suspected of having CNS metastases, and CK-BB appears superior to total CK, CSF protein, and CSF lactic dehydrogenase (LDH). In 12 patients with MC at autopsy, CK-BB was, with the above cut-off point, elevated in six patients with a false negative cytology. Of the 73 patients examined for beta-2-m, 18 had MC, 30 had parenchymatous metastases only, and 25 patients had no CNS metastases. The CSF concentrations in the three groups were not significantly different. The median concentrations in the groups were 133 nmol/L, 125 nmol/L, and 107 nmol/L, respectively. The ratios between beta-2-m in CSF and plasma were also not significantly different between the three groups. Thus, the data on CK-BB are promising, and further studies are warranted to see if the usefulness of CK-BB can be more firmly established. By contrast, beta-2-m has no role as a marker of CNS disease secondary to SCLC.
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PMID:Creatine kinase BB and beta-2-microglobulin as markers of CNS metastases in patients with small-cell lung cancer. 299 99

Many biological substances are commonly used as markers for malignant neoplasms, but no single marker with high specificity and sensitivity has been found for cancer to date. In this study we evaluated simultaneously the serum levels of five biomarkers of malignancy: phosphohexose-isomerase (PHI), creatine kinase isoenzyme BB (CK-BB), alpha 1-acid glycoprotein (AAG), beta 2-microglobulin (BMG), and ferritin. In 89 female patients with breast lesions, we identified 30 benign lesions, 32 primary breast cancers, and 27 metastatic breast cancers (pulmonary and/or bone metastases). Each marker was assayed individually and in a combination and was compared with other markers. The results revealed that in benign lesions only 7% had PHI values higher than our cut-off limit value, while 3% had elevated values of AAG, BMG, and ferritin. In primary breast cancer we discovered pathological values of CK-BB and AAG in 71%, of PHI in 69%, of BMG in 50%, and of ferritin in 47%. Metastatic disease was associated with elevated values in 88% of CK-BB, in 70% of PHI and AAG, and in only 55% of BMG and ferritin. Combined pathological values for primary and metastatic breast cancer were 79% for CK-BB, 71% for AAG, 70% for PHI, and only 55% for BMG and ferritin. These data were assessed by the Student t test, which revealed for each marker a significant capacity (P less than 0.01) to discriminate between benign lesions and neoplastic diseases. The same capacity to distinguish between primary and metastatic cancer was obtained by the simultaneous use of three markers (CK-BB, PHI, and AAG).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical utility of the combined use of plurime tumor markers in human breast cancer. 307 81

The mechanism by which the murine fibrosarcoma clone PAK 17.15 induces platelet aggregation [tumor cell-induced platelet aggregation (TCIPA)] was studied because platelet activation by this clone is necessary for metastasis to the lungs. PAK 17.15 TCIPA was completely inhibited by ADP-clearing enzymes, such as apyrase, or a mixture of creatine phosphate and creatine phosphokinase. Thrombin and collagen were not involved in PAK 17.15 TCIPA. Further studies showed that ADP is most likely secreted from activated platelets and that membrane protein(s) on PAK 17.15 cells are responsible for platelet activation. Inasmuch as ADP-dependent platelet aggregation requires fibrinogen and can be inhibited by the Gly-Arg-Gly-Asp-Ser (GRGDS) synthetic peptide, the effect of this peptide on PAK 17.15 TCIPA was studied. PAK 17.15 TCIPA was completely inhibited by the GRGDS peptide (0.4 mM) but not by a control peptide, Gly-Arg-Gly-Glu-Ser (0.8 mM). In addition, the GRGDS peptide inhibited adhesion of PAK 17.15 cells to immobilized fibronectin. As expected, the GRGDS peptide almost completely inhibited lung colonization by iv injected PAK 17.15 cells in C57BL/6 mice. Our results indicate that GRGDS may inhibit pulmonary metastases by interfering with TCIPA as well as with tumor cell adhesion to extra-cellular matrix components in the host.
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PMID:Inhibition of tumor cell-induced platelet aggregation and experimental tumor metastasis by the synthetic Gly-Arg-Gly-Asp-Ser peptide. 318 95

Concentrations of total serum N-acetyl-neuraminic acid, carcinoembryonic antigen, ferritin, lactate dehydrogenase, creatine phosphokinase and total proteins were measured in both tumor drainage blood (axillary vein) and in peripheral blood taken during surgery from 44 breast cancer patients. There were no significant differences in any of the markers between mean values in peripheral and tumor drainage blood, between cancer patients and healthy controls, between patients with or without axillary lymph node metastases, or according to the site of breast mass.
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PMID:Sialic acid, ferritin and CEA levels in peripheral blood and blood draining from the tumor in breast cancer. 323 52

We conducted a trial of a murine monoclonal antimelanoma antibody-ricin A chain immunotoxin (XOMAZYME-MEL) in 22 patients with metastatic malignant melanoma. The dose of immunotoxin administered ranged from 0.01 mg/kg daily for 5 days to 1 mg/kg daily for 4 days (total dose: 3.2 to 300 mg). Side effects observed in most patients were a transient fall in serum albumin with an associated fall in serum protein, weight gain, and fluid shifts resulting in edema. In addition, patients experienced mild to moderate malaise, fatigue, myalgia, decrease in appetite, and fevers. There was a transient decrease in voltage on electrocardiograms without clinical symptoms, change in serial echocardiograms or elevation of creatine phosphokinase MB isozyme levels. Symptoms consistent with mild allergic reactions were observed in three patients. The side effects were related to the dose of immunotoxin administered and were generally transient and reversible. Encouraging clinical results were observed, even after a single course of a low dose of immunotoxin. In addition, localization of antibody and A chain to sites of metastatic disease was demonstrated by immunoperoxidase staining of biopsy specimens. Additional studies are being conducted to continue the evaluation of safety and efficacy of immunotoxin therapy for malignancy.
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PMID:Therapy of patients with malignant melanoma using a monoclonal antimelanoma antibody-ricin A chain immunotoxin. 349 66

Blood platelets have been suggested to play an important role in modulating the development of experimental metastases. Tumour cells can induce platelet aggregation in vitro and a number of mechanisms have been proposed to explain the in vivo and in vitro observations. In the present study, we used tumour cells cloned from B16 melanoma and mouse mammary tumour virus (MMTV) carcinoma polyclonal populations to check whether tumour cells with low- and high-metastatic behaviour in vivo had different quantitative and qualitative platelet-aggregating activity in vitro. We found no significant quantitative difference between platelet aggregation induced by the low- and the high-metastatic clones. Indeed both the high and the low metastatic B16 melanoma clones poorly aggregated platelets, while both the high and low metastatic MMTV carcinoma clones efficiently aggregated platelets. Both the B16 melanoma and the MMTV carcinoma parental cell lines, which can be classed as intermediate metastatic, aggregated platelets well. However, based on the results with heparin and creatine phosphate/creatine phosphokinase, it appeared that qualitative differences might exist in the mechanism of platelet aggregation by tumour cells. For the parental lines and highly metastatic clone C1 a thrombin-linked component was more important than an ADP-like component, which was nevertheless present, to promote platelet aggregation. For the low-metastatic clone C2, the ADP-like component appeared to be the most important.
Invasion Metastasis 1987
PMID:Tumour-cell-induced platelet aggregation: studies with cloned metastatic and non-metastatic variants. 367 44


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