Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concentrations of creatine kinase (CK) B subunit (CK-B) in tumor tissues and in sera of patients with various lung carcinomas were determined, together with the concentrations of neuron-specific gamma-enolase (gamma subunit of a gamma and gamma gamma enolases), by the use of a sensitive enzyme immunoassay method. The CK-B and gamma-enolase levels were enhanced in tissues of small cell carcinoma of the lung. The average tissue contents of CK-B in small cell carcinoma (SCCL), adenocarcinoma (ADCL) and squamous cell carcinoma (ECCL) of the lung, and normal lung were 2320, 308, 163, and 372 ng/mg protein, respectively. The contents of gamma-enolase in those tissues were 1460, 276, 225, and 42.7 ng/mg protein, respectively. Serum CK-B concentrations in healthy adults (n = 100) were 0.53 +/- 0.22 ng/ml and ranged from 0.25 to 1.44 ng/ml, but they were significantly increased (greater than 1.5 ng/ml) in some patients with SCCL (26/42 cases, 62%), ADCL (7/36, 19%), ECCL (7/37, 19%), and large cell carcinoma of the lung (LCCL, 4/13, 31%). Serum CK-B was also enhanced in some patients with breast carcinoma and in a few cases in carcinomas of the stomach, colon and pancreas. Serum concentrations of CK-B were well correlated with those of gamma-enolase in patients with SCCL (r = 0.667, n = 83, P less than 0.01) and LCCL (r = 0.689, n = 20, P less than 0.01), but poorly in patients with ADCL and ECCL. Since serum CK-B concentrations in patients with SCCL changed in parallel with the clinical course during treatment, serum CK-B may also be a useful biomarker, as well as neuron-specific gamma-enolase, for monitoring the clinical course of patients with SCCL.
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PMID:Creatine kinase B subunit as a biomarker for small cell carcinoma of the lung: comparison with gamma-enolase. 300 8

The specificity of neuron-specific enolase (NSE) and creatine kinase BB (CK-BB) for small cell lung cancer (SCLC) was determined by biological and immunohistochemical procedures in lung cancer tissues and cultured cell lines. Average values of extractable NSE and CK-BB of SCLC tissues were significantly higher than those of non-SCLC and normal lung tissues. A large amount of NSE and CK-BB was demonstrated in SCLC cell lines. Immunohistochemical examination showed positive staining for NSE and CK-BB in most cases of SCLC and in a few cases of non-SCLC. From these data NSE and CK-BB should be considered to be highly specific for SCLC. In a clinical study serum values exceeding 10 ng/ml for NSE and 1.5 ng/ml for CK-BB were set as positive for the enzymes. Positive rates in SCLC were 71.4% for NSE and 65.3% for CK-BB, which were significantly higher than those in non-SCLC. All positive cases were in an advanced stage. Consecutive daily NSE determinations during induction chemotherapy showed transient elevation immediately after the initiation of drug administration (tumor lysis syndrome), followed by a decline to normal range in responders. This phenomenon seems to indicate tumor sensitivity to cytotoxic drugs. NSE positive non-SCLC was as sensitive to cytotoxic drugs as SCLC. These findings indicate that lung cancer with elevated serum NSE and CK-BB levels at diagnosis should be strongly suspected of being SCLC in the advanced stage.
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PMID:Biological and clinical implication of neuron-specific enolase and creatine kinase BB in small cell lung cancer. 302 31

Two small cell lung cancer (SCLC) cell lines were established from pericardial and pleural effusions of a patient with histopathologically proven SCLC of the oat cell type. Chemotherapy was administered without response during the 148-day period prior to the establishment of the first cell line, SCLC-22H, and some of the same drugs were administered in the 15 days prior to the establishment of the second cell line, SCLC-21H. Both cell lines differed markedly in their biochemical, kinetic, and morphological properties. Although the biomarkers L-Dopa decarboxylase, bombesin, carcinoembryonic antigen, and neurotensin were detectable in SCLC-22H, they were undetectable or low in SCLC-21H. The population doubling time was twice as fast and the colony forming efficiency higher in SCLC-21H than in SCLC-22H. They both expressed high concentrations of the SCLC marker enzymes neuron-specific enolase and the creatine kinase isoenzyme BB and showed no significant differences in their chromosomal characteristics. c-myc was amplified and expressed in both cell lines, and SCLC-21H had an additional rearranged and amplified EcoRI c-myc fragment. Morphological differences were apparent in liquid culture, cytology, and xenograft histology; SCLC-21H grew much more loosely than SCLC-22H, and had more prominent nucleoli and more abundant cytoplasm. Ultrastructurally dense core granules were present in both cell lines. SCLC-21H thus expressed properties of the variant cell type of SCLC, whereas SCLC-22H had mixed classic/variant features. An in vivo progression of the patient's tumor from a pure small cell to a mixed small cell/large cell morphology could be demonstrated, which suggests that cell line SCLC-22H represents a cell type characteristic for the transitional phase of the tumor. The features of this cell line therefore define a new subclass of SCLC called transitional cell type. SCLC-22H may be of use to study the mechanisms involved in the classic to variant transition, which probably has a considerable impact on the prognosis and response to therapy.
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PMID:Characterization of two cell lines with distinct phenotypes established from a patient with small cell lung cancer. 302 17

Pleomorphic rhabdomyosarcoma in adults over 30 years of age was a diagnosis frequently made in the 1960s and 1970s. Since the general acceptance of malignant fibrous histiocytoma (MFH) as a tumor entity at the end of the 1970s, however, it has become a very rare tumor in adults. Therefore, 21 cases originally diagnosed on the basis of histology and clinical data as pleomorphic rhabdomyosarcoma in the 1960s and 1970s were reexamined immunohistochemically. Other types of pleomorphic sarcomas involved in the differential diagnosis were also studied. Specific antibodies against vimentin, desmin, creatine kinase subunit M, skeletal muscle actin and myosin, and myoglobin, and the avidin-biotin-peroxidase complex technique were used. The immunohistochemical findings indicate that rhabdomyosarcoma occurs only rarely in adults over 30 years of age and that the majority of the tumors have to be reclassified as MFH or leiomyosarcoma. On the other hand, several pleomorphic sarcomas were found to be diagnosed incorrectly as MFH or liposarcoma by routine histologic stains and electron microscopy. The revised diagnosis was pleomorphic rhabdomyosarcoma for one case and pleomorphic leiomyosarcoma for the other cases. Thus, this study clearly shows the usefulness of immunohistochemistry as a technique in the diagnosis of pleomorphic sarcomas in adults.
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PMID:Pleomorphic rhabdomyosarcoma in adults: immunohistochemistry as a tool for its diagnosis. 302 31

Three creatine kinase isozymes (CK-BB, CK-MB and CK-MM) were estimated by immunoassay in tumor tissues and in sera of patients with various lung carcinomas. CK-BB was increased in small cell carcinoma, but not in other lung carcinomas. CK-MM and CK-MB were not increased in any types of carcinoma. Serum CK-BB was increased in all types of lung carcinoma examined, while serum CK-MM and CK-MB were within normal limits in all patients. Serum CK-BB of healthy adults was estimated as 0.32 +/- 0.14 (mean +/- SD) ng/ml, ranging from 0.11-0.68 ng/ml. If CK-BB values above 1.0 ng/ml were considered abnormal, elevation occurred in 28/40 (70%) of patients with small cell carcinoma, 25/67 (37%) with adenocarcinoma, 21/51 (41%) with squamous cell carcinoma, 4/11 (36%) with other carcinoma of the lung and 10/42 (24%) with lung tuberculosis. Since serum CK-BB with lung cancer changed in parallel with the clinical course, this isozyme may be a marker for monitoring the clinical course, especially in small cell carcinoma of the lung.
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PMID:Determination of creatine kinase isozymes in sera and tissues of patients with various lung carcinomas. 303 55

Creatine kinase (CK, ATP: creatine N-phosphotransferase, EC 2.7.3.2) and immunoglobulin complexes were detected in 27 of 234 (11.5%) patients with malignant tumors. The complexes electrophoresed between CK-MM and the sample application point. The positive rate was significantly higher than rates in patients with benign diseases, or in healthy adults (p less than 0.001). Primary malignancies of the 27 patients were colon 8, gastric 6, pancreatic 4, liver 5, pulmonary 3 and mammary 1. As 22 of the 27 patients had a recurrence or a metastasis and the mortality rate of the positive group 6 mth after the tests was high (85%), most of the 27 patients had advanced tumors. Thus, the CK-immunoglobulin complexes seem to be a prognosticator of patients with advanced tumors. The classes and types of immunoglobulins in the complexes were IgA lambda, 7; IgA kappa lambda, 5; IgA (types of the light chain were not identified), 4; IgA/G kappa, 1; IgA/G lambda, 3; and IgA/G kappa lambda, 7. The molecular sizes of the complexes were 384,000 +/- 22,000 (mean +/- 1 SD). The results of recombination assays using IgA isolated from the complexes of 4 patients suggested that the complexes in the patients' sera were mitochondrial CK-IgA. Non CK-M subunit activities of the positive group were 58 +/- 40 U/l (mean +/- 1 SD) and they were significantly higher than those of the complex negative group of tumor patients (p less than 0.01). This is probably the first report of detection of mitochondrial CK-IgA complexes.
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PMID:Clinical significance and characteristics of creatine kinase-immunoglobulin complexes in sera from patients with malignant tumors. 309 3

In an effort to identify enzymatic activities in primary prostatic carcinomas that might be complementary to histological and other clinical techniques for the prediction of prognosis, we have assayed several enzymatic activities extracted from prostatic carcinomas. We reported previously that, for each of the studied enzymes, tissues with benign prostatic hyperplasia and prostatic carcinoma showed significantly different activities. With additional patients now included and a longer interval since resection of these tumors, we have found that the histological grade (Gleason's system for grading) of the sample (prostate chip) analyzed is related to several activities extracted from the cancers including arginase (r = -0.81, p less than 0.0001), glucose-6-phosphate dehydrogenase (r = 0.72, p less than 0.0001), and the B isoenzyme of N-acetyl-beta-D-glucosaminidase (r = -0.58, p = 0.0369). Acid phosphatase (r = 0.15, p = 0.5530) and the BB isoenzyme of creatine kinase (r = -0.13, p = 0.5221) are not significantly related to histological grade. In a large series, Gleason grade is related to survival. In our series of 27 patients followed for 20 to 46 months, the Gleason grade (p = 0.22) is not related to survival, but arginase activity is related (p = 0.0392) to survival. In this small series, arginase is more valuable than the best currently proven predictor of survival, Gleason grade. Hexosaminidase B activity approaches being significantly (p = 0.0575) related to survival. Of the 11 patients whose tumors contained the lowest arginase activities, eight are dead. Of the 11 with the highest activities, only one is dead. Several of the enzyme activities in this series of 27 patients complemented each other for the prediction of Gleason grade; for example, glucose-6-phosphate dehydrogenase, arginase, and the BB isoenzyme of creatine kinase were more closely correlated (multiple correlation coefficient, r = 0.77) with the Gleason grade for all chips than was any single enzyme: arginase, r = -0.67; glucose-6-phosphate dehydrogenase, r = 0.67; creatine kinase, r = -0.16. It seems likely that enzymatic analysis may provide an approach that is qualitatively different from and complementary to histological evaluation for the prediction of prognosis in prostatic carcinoma. Verification of this hypothesis will require more patients followed over a longer period of time and will probably be facilitated by analysis of several samples from different locations in each tumor.
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PMID:Enzyme activities in prostatic carcinoma related to Gleason grades. 315 94

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

A 37-year-old man with metastatic immature (malignant) teratoma with prominent rhabdomyosarcomatous elements had markedly increased activity of creatine kinase (EC 2.7.3.2) MB in serum. There was no electrocardiographic evidence of infarction or ischemia, and autopsy revealed no myocardial infarction, significant coronary atherosclerosis, myocarditis, or invasion of the heart by tumor. A high proportion of the creatine kinase activity in a homogenate of the tumor was attributable to the MB isoenzyme. Persistent increases of creatine kinase-MB and an unusually high MB isoenzyme activity, out of proportion to total creatine kinase activity, may indicate a nonmyocardial origin of this isoenzyme.
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PMID:Secretion of creatine kinase MB isoenzyme by an immature teratoma with predominant rhabdomyosarcomatous elements. 272 Sep 94

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


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