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)

We studied the creatine kinase (CK) isoenzyme pattern in sera from 332 patients affected by hepatic cirrhosis and several neoplastic diseases (102 cirrhosis, 36 hepatocarcinoma, 16 metastatic liver tumor, 40 breast cancer, 18 other neoplastic diseases and 120 cases of leukemia or lymphoma) to evaluate both its diagnostic utility for cancer diagnosis and its power as a prognostic index. Type-2 macro CK (mitochondrial creatine kinase) was detected, with no statistical difference in cirrhosis (14%), hepatocarcinoma (16%), metastatic liver tumor (31%), breast cancer (5%) and other tumors (6%). It was not detected in any patient with leukemia or lymphoma. The presence of type-2 macro CK was unrelated to the stage of either cirrhosis or hepatocarcinoma, according to Child and Okuda, respectively, nor was it correlated to serum cytolytic enzyme levels or to gamma-globulin levels. In cirrhotics, type-2 macro CK was not linked to serum levels of the following tumor markers: alpha-fetoprotein, pseudouridine and gamma-glutamyltransferase isoenzymes complexed to low-density lipoprotein. In addition, the atypical band persisted in several patients with cirrhosis monitored for six months who did not show any evidence of evolution toward hepatocarcinoma. Thus, type-2 macro CK has poor diagnostic sensitivity for neoplastic diseases, and lacks prognostic value both in cirrhosis and neoplastic diseases.
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PMID:Serum type-2 macro-creatine kinase isoenzyme is not a useful marker of severe liver diseases or neoplasia. 228 11

Twelve cases of alveolar soft part sarcoma (ASPS) were reviewed. Seven of them arose primarily in the lower extremities, three in the head and neck region, and two in other parts. ASPSs in the head and neck region occurred in children before 10 years of age, whereas ASPSs in the other regions occurred in rather older patients. Moreover, ASPSs of the head and neck were relatively small in size, and were diagnosed earlier than those in other regions. Histologically, six cases (including all the head and neck cases) contained considerable area of small and indistinct alveolar structures. Four cases showed remarkable cellular pleomorphism. Immunohistochemical demonstration of vimentin, desmin, the beta-subunit of enolase and the MM isozyme of creatine kinase, together with the absence of immunoreactive cytokeratin, supported the myogenic nature of this rare tumor. A small number of S-100 protein-positive tumor cells were also observed. Follow-up data for these cases disclosed that the tumors containing considerable area of small alveoli and uniform small tumor cells formed distant metastases at an early stage.
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PMID:Alveolar soft part sarcoma. A clinicopathologic and immunohistochemical study of 12 cases. 236 Apr 59

The serum levels of the BB isozyme of creatine kinase (CK-BB) and neuron-specific enolase (NSE) were measured before therapy in 35 patients with neuroblastoma. Sixty percent (21 of 35) of neuroblastoma patients had CK-BB levels higher than 11 ng/ml. The extent of disease was associated with an increased incidence of elevated serum CK-BB levels. The highest pretreatment serum CK-BB titers were found in patients with Stage IV disease. A strong correlation between the pretreatment CK-BB level and the outcome in patients with neuroblastoma was observed. Eleven (79%) of 12 patients who had a serum CK-BB level greater than 15 ng/ml died, and eight of ten (80%) who had a serum level less than 11 ng/ml were alive and tumor free after 2 years. A positive linear correlation between the pretreatment CK-BB and NSE (n = 35, r = 0.695) levels was found.
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PMID:The diagnostic and prognostic value of pretreatment serum creatine kinase BB levels in patients with neuroblastoma. 237 68

Magnetic resonance spectroscopy (MRS) uniquely provides noninvasive access to chemistry in vivo. 31P MRS can be used to monitor the high energy phosphates--phosphocreatine (PCr) and ATP, and their breakdown product--Pi, in situ in animals or patients. In several experimental tumor lines in animals it has been shown that the PCr/ATP and other related ratios steadily decline as the tumor increases in size, and that this effect is reversed when the tumor is treated with a therapeutic modality to which it responds. Acid extracts of freeze-clamped tumors at different stages of growth have confirmed these MRS observations and give additional information on related compounds such as creatine and ADP. Results show that, in the tumors studied, at least 80% of the ADP and about 40% of the Pi are bound and not in solution in the cytosol. Histological sections have indicated that the MRS response to endocrine therapy, in an NMU-induced estrogen-sensitive mammary tumor model, precedes any histological changes or any measurable regression. If these findings can be translated into a clinical setting, this may mean that MRS can be used in the clinic as an early predictor of tumor responsiveness to treatment. In untreated tumor growth, the cause of the decrease in PCr and ATP relative to Pi is probably due to the tumors outgrowing their blood supply and the cells becoming increasingly hypoxic. The PCr is lost more rapidly than ATP, indicating that the equilibrium in the creatine kinase reaction is maintained in these tumors. When the tumor is treated, cellular growth ceases and the requirement for oxygen and other nutrients is greatly reduced. This would allow the cellular energy reserves to be repleted and thus lead to the paradoxical improvement in the high energy phosphate status of a tumor that is about to regress.
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PMID:Monitoring tumor growth and regression by 31P magnetic resonance spectroscopy. 240 32

The objective of this study was to determine the distribution of creatine phosphokinase (CPK) into its three isoenzymes, MM, MB, and BB, in human prostatic tissue, in patients with benign hyperplasia (BPH) and adenocarcinoma. Specimens were obtained from 23 patients with adenocarcinoma of the prostate and 25 patients with benign hyperplasia. We also had the opportunity to analyze the CPK content in two normal prostates, the first from a 16 1/2-year-old boy and the second from a 9 1/2-year-old child. Our results showed prostate tissue to contain almost exclusively the BB isoenzyme with traces of the MB and MM dimers in both cancer and BPH as well as the specimen of normal prostate from the 16 1/2-year-old boy. As for the 9 1/2-year-old child, we found the following distribution: 39% MM, 21% MB, and 40% BB dimer. A comparison of the CPK-BB content in benign hyperplasia and adenocarcinoma revealed no significant difference between the two groups. Furthermore, we tried to correlate prostatic tissue CPK-BB levels with another possible tumor marker of the prostate, prostatic acid phosphatase (PAP) measured in the cytosol. No correlation was found between these two markers. We also studied the relationship of CPK-BB and PAP content in prostatic tissue to nuclear and cytosolic androgen receptor content in human prostatic tissue. We found some correlation between CPK-BB and androgen cytosolic receptors as well as between PAP content and androgen cytosolic receptors in patients with benign hyperplasia. No such correlation was found in the group with adenocarcinoma. In conclusion, this study does not show that the measurement of CPK-BB in the prostatic tissue could be used as an index of tissue malignancy.
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PMID:Creatine phosphokinase isoenzymes in human prostatic tissues: a comparison between benign hyperplasia and adenocarcinoma. 241 30

Permanent human small cell lung cancer (SCLC) cell lines established in our laboratory were investigated for their expression of the enzymatic neuroendocrine markers L-DOPA decarboxylase (DDC), neuron-specific enolase (NSE), and creatine kinase (CK), including its BB isoenzyme (CK-BB), the classical tumor markers carcinoembryonic antigen (CEA), the alpha and beta subunits of human chorionic gonadotropin (alpha-HCG, beta-HCG), and alpha-fetoprotein (alpha-FP), and their chromosomal characteristics. DDC activities were detectable in 5/6 SCLC cell lines and absent in non-SCLC. NSE levels ranged from 160 to 1422 ng/mg soluble protein and were less than 290 ng/mg soluble protein in non-SCLC. Activities of CK and levels of CK-BB clearly distinguished SCLC from non-SCLC with CK activities greater than 1000 munits/mg soluble protein and CK-BB levels greater than 3000 ng/mg soluble protein in SCLC and less than 300 munits/mg soluble protein and less than 2000 ng/mg soluble protein in non-SCLC. CEA was detectable in 5/6 SCLC cell lines but absent in non-SCLC, and its level seemed to correlate with those of DDC, NSE, and CK. One cell line, SCLC-16H, lost some of its neuroendocrine properties and CEA after 1 year of in vitro cultivation. Generally, marker levels were low in fast growing cell lines and high in slow growing cell lines. HCG alpha and beta subunit and alpha-FP were not detectable in SCLC cell lines. All SCLC cell lines examined had near diploid DNA indices and modal chromosome numbers. Double minute chromosomes and homogeneously staining regions were found in 2/5 and 4/5 SCLC cell lines respectively. With respect to chromosomal aberrations, we found a deletion of the short arm of at least one chromosome 3 in all SCLC cell lines (5/5). These data show that SCLC expresses neuroendocrine markers and CEA; CK is the most sensitive marker, and DDC and CEA are the most specific markers for SCLC in vitro; individual marker levels correlate with each other and the in vitro malignancy of SCLC; and SCLC cell lines have relatively uniform chromosomal characteristics. Our results suggest that patients whose tumors have high levels of DDC, NSE, CK-BB, and CEA have a better prognosis than those with low marker levels. This hypothesis could be proved by comparing pairs of patients that are matched for all known prognostic parameters, in particular tumor spread, for their serum and tumor marker levels with respect to the patients' outcome and prognosis.
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PMID:Markers and characteristics of human SCLC cell lines. Neuroendocrine markers, classical tumor markers, and chromosomal characteristics of permanent human small cell lung cancer cell lines. 243 85

We determined serum CK-BB mass concentration using a specific RIA method, in 267 patients with carcinoma confirmed histologically distributed as follows: 46 prostatic adenocarcinoma, 52 lung neoplasies, 70 colon carcinoma, 52 breast carcinoma and 41 gastric carcinoma; and also in 135 patients with histologically proved non-neoplastic diseases distributed as follows: 28 prostatic hyperplasy, 31 lung tuberculosis, 29 inflammatory bowel disease, 27 fibrocystic mastopathy and 20 gastroduodenal ulcer. Reference values in healthy subjects (n = 360) were 5.46 +/- 2.68 (SD) ng/ml. We found that serum CK-BB mass concentration is not a specific tumor marker but it is a valuable indicator of responsing to therapy and metastatic widespread. However, in prostatic carcinoma--prevalence 0.25, predictive positive value (PPV) 0.51 and predictive negative value (PNV) 0.88--and breast carcinoma--prevalence 0.32, PPV 0.60 and PNV 0.87--serum CK-BB can be used as a tumor marker. Only 12 over 268 patients with different neoplastic disease (4.47%) showed detectable serum CK-BB catalytic concentrations.
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PMID:Serum CK-BB as a tumor marker in patients with carcinoma confirmed histologically. 247 65

Administration of adrenergic agonists induced c-fos mRNA in the salivary glands of the mouse and in the heart of the mouse, rat, and hamster (Barka et al., 1986, Mol. Cell Biol. 6, 2984-2989; 1987; Oncogene 1, 439-443). To further analyze transcriptional and post-transcriptional control of c-fos expression by adrenergic receptors and the putative role of fos in replication and differentiation pathways, we have examined c-fos expression in BC3H1 cells, a tumor-derived nonfusing muscle cell line. BC3H1 cells possess alpha 1- and beta 2-adrenergic receptors as well as receptors for histamine and acetylcholine. Furthermore, rapidly proliferating BC3H1 cells undergo differentiation toward muscle phenotype when exposed to low serum-containing culture media. Both alpha- and beta-adrenergic agonists and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate caused a rapid, transient increase in the steady-state level of c-fos mRNA. This induction was essentially independent of whether the cells were in the proliferative, relatively quiescent, or differentiated state. Protein synthesis inhibitors cycloheximide and anisomycin also increased markedly the concentration of c-fos mRNA, and in the presence of anisomycin c-fos mRNA was superinduced by the alpha-adrenergic agonist norepinephrine. Run-on transcription assays indicated that the c-fos gene is expressed in both proliferating and differentiated cells, although the steady-state levels of c-fos mRNA were low, or even undetectable, in such cells. The adrenergic agonists and the tumor promoter stimulated the transcription of the c-fos gene in both proliferating and differentiated cells. This stimulation, however, was modest, two- to three-fold compared to controls, in contrast to the marked elevation of the level of c-fos mRNA they caused. Neither the proliferation nor the expression of muscle type creatine kinase activity was influenced by adrenergic agonists. It is suggested that activation of the c-fos gene is a consequence of adrenoreceptor stimulation in diverse cell types, and thus it is involved in pleiotropic cellular responses to adrenergic agonists. Catecholamines may be one of the physiologic regulators of the c-fos gene.
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PMID:Adrenergic regulation of c-fos expression in cultured BC3H1 muscle cells. 255 27

Three clonal subpopulations (A, B, C) isolated from the same rhabdomyosarcoma of the rat were tested and compared for their susceptibility to differentiation induction using retinoic acid (RA), dimethylformamide (DMF), and N-monomethylformamide (NMF). These subpopulations differ in that a block to spontaneous differentiation is imposed at different stages which are characteristic for each subpopulation. Whereas tumor cell proliferation was significantly inhibited (P less than 0.001) in all three subpopulations, the effects of RA, DMF, and NMF on tumor cell differentiation were strikingly heterogeneous. The response was most marked in subpopulation C, as evidenced by a significant increase in the number of terminally differentiated myotube-like giant cells (P less than 0.001) and in biochemical differentiation, as indicated by the creatine kinase activity (P less than 0.05). Between 5% (DMF and NMF) and 30% (RA) of the mononuclear cells in subpopulation C exhibited thick and thin myofilaments, which were never observed in the mononuclear cells of the control. In contrast, subpopulation A and B responded to RA, DMF, and NMF quite heterogeneously with an increase in biochemical differentiation, whereas terminally differentiated myotube-like giant cells were never observed. These results demonstrate that the therapeutic potential of differentiation induction in malignant tumors may be impaired by tumor heterogeneity.
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PMID:Heterogeneous response to differentiation induction in different clonal subpopulations of a rat rhabdomyosarcoma cell line (BA-HAN-1). 258 54

We determined the effect of long-term freezer storage and repeated thawing and freezing of serum on concentrations of electrolytes (sodium, potassium, calcium, and phosphate), enzymes (aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, and creatine kinase), total protein, tumor markers (carcinoembryonic antigen and alpha-fetoprotein), and other substances. Vials (1 ml) of frozen serum from a single blood drawing from 40 women with no breast disease and 70 with benign breast disease were analyzed annually from 1983 to 1987. Blood had been obtained from 40 subjects in 1978, 40 in 1980, and 30 in 1983. Thawing and refreezing studies were done in two ways: (1) serum samples from 30 subjects with benign breast disease were thawed at weekly intervals for 6 weeks and (2) serum samples from 30 patients with stage IV breast cancer were analyzed for alpha-fetoprotein and carcinoembryonic antigen, and serum specimens from 23 patients with benign breast disease and 7 control subjects were analyzed for lactate dehydrogenase and creatine kinase after thawing and keeping the samples at room temperature for up to 4 hours and then refreezing them. For measuring laboratory variability, duplicate samples were processed. Long-term storage (up to 10 years) and repeated thawing and refreezing did not affect the results of any tested constituents of serum. Although most measurements showed statistically significant variability over test cycles, these differences were thought to be due to laboratory variability.
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PMID:Effect of long-term freezer storage, thawing, and refreezing on selected constituents of serum. 259 13


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