Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.5.4.4 (adenosine deaminase)
5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In highly malignant Gelshtein 22A hepatcma and ascites Ehrlich carcinoma adenosine deaminase activity was found to be reduced 3-fold as compared with that of the normal mouse liver. In less malignant hepatomas adenosine deaminase activity drops only by 20%. A certain reduction of adenosine deaminase activity was also noted in the liver to tumour-bearing mice.
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PMID:[Adenosine deaminase activity in hepatomas of varying degrees of malignancy]. 20 52

Deamination of many analogs of adenine nucleosides results in the loss of their chemotherapeutic efficacy. Two approaches have been used in this study to overcome this problem. First, some adenine nucleotides, which are resistant to mammalian adenosine deaminase, are more toxic to animal cells than are the respective nucleosides. For toxic to animal cells than are the respective nucleosides. For example, 9-beta-D-arabinofuranosyladenine 5'-phosphate, a molecule that penetrates the cell without degradation, has a more sustained toxicity against mouse fibroblasts (L-cells) than does 9-beta-D-arabinofuranosyladenine (ara-A). Furthermore, L-cells treated with 2',3'-dideoxyadenosine 5'-phosphate are extensively killed after 48 hr, whereas 2',3'-dideoxyadenosine is almost nontoxic to L-cells. Specific inhibition of adenosine deaminase by nontoxic concentrations of erythro-9-(2-hydroxy-3-nonyl)adenine greatly potentiates the biological activity of both ara-A and 3'-deoxyadenosine (cordycepin). Simultaneous administration of cytostatic concentrations of ara-A and the inhibitor of adenosine deaminase to L-cells killed greater than 99.9 percent of cells in 36 hr. A similar concentration of ara-A plus the deaminase inhibitor also markedly extended the mean survival of mice bearing Ehrlich ascites carcinoma as compared to ara-A alone. A cytostatic concentration of cordycepin 1 x 10-4 M), administered in the presence of deaminase inhibitor, killed greater than 99.9 percent of cultured L-cells in only 8 hr. During the latter incubation, accumulation of uridine in acid-insoluble material reached a maximum after 30 min, and incorporation of thymidine into acid-insoluble material was almost totally arrested after 2 hr.
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PMID:Two approaches that increase the activity of analogs of adenine nucleosides in animal cells. 107 75

YK-176 is a newly isolated 2'-deoxycoformycin (DCF), a potent inhibitor of adenosine deaminase, produced by Aspergillus nidulans. In a cooperative phase I study, YK-176 was administered to 22 patients, comprising 18 with adult T-cell leukemia-lymphoma (ATL), two with cutaneous T-cell lymphoma (CTCL), one with lymphoblastic lymphoma of T-cell type and one with carcinoma of the uterine cervix. Doses of YK-176 ranged from 3.0 to 9.0 mg/m2 and were given intravenously for three consecutive days. General malaise, anorexia, nausea, vomiting and low grade fever were frequently encountered, but were transient and not dose-related. At all dose levels hematological toxicities were mild. Two of seven patients receiving 7.0 mg/m2 for three consecutive days developed hepatocellular enzyme elevations (grade 2) and one patient, proteinuria (grade 2). One of two patients given 9.0 mg/m2 for three consecutive days manifested a life-threatening (grade 4) disturbance of consciousness and dyspnea, presumably ascribable to the drug-related toxicity of YK-176. The results suggest that 7.0 mg/m2 i.v. for three consecutive days is the maximum acceptable dose of YK-176. Central nervous system, pulmonary and possibly renal toxicities appeared to be dose-limiting. Out of the 20 patients evaluable for therapeutic response, partial remissions were observed in four, three with ATL and one with CTCL, who received less than 7.0 mg/m2 for three consecutive days. We conclude that YK-176 is an active agent against ATL at doses that may not be associated with prohibitive toxicity. A starting dose of 5.0 mg/m2 for three consecutive days is recommended for further phase II studies on ATL.
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PMID:Phase I study of YK-176 (2'-deoxycoformycin) in patients with adult T-cell leukemia-lymphoma. The DCF Study Group. 151 64

The expression of the adenosine deaminase complexing protein (ADCP) was investigated by immunohistochemistry in the normal and hyperplastic human prostate, in 30 prostatic adenocarcinomas, and in seven human prostatic adenocarcinoma cell lines grown as xenografts in athymic nude mice. In the normal and hyperplastic prostate, ADCP was localized exclusively in the apical membrane and the apical cytoplasm of the glandular epithelial cells. In prostatic adenocarcinomas, four distinct ADCP expression patterns were observed: diffuse cytoplasmic, membranous, both cytoplasmic and membranous, and no ADCP expression. The expression patterns were compared with the presence of metastases. We found an inverse correlation between membranous ADCP immunoreactivity and metastatic propensity. Exclusively membranous ADCP immunoreactivity occurred only in non-metastatic tumours. In contrast, the metastatic tumours showed no or diffuse cytoplasmic ADCP immunoreactivity. This suggests that immunohistochemical detection of ADCP might predict the biological behaviour of prostatic cancer. However, the occurrence of membranous ADCP immunoreactivity in the xenograft of a cell line (PC-EW), derived from a prostatic carcinoma metastasis, indicates that not only the tendency to metastasize modulates ADCP expression.
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PMID:Adenosine deaminase complexing protein (ADCP) expression and metastatic potential in prostatic adenocarcinomas. 169 38

Blood serum activities of thymidine kinase, thymidine phosphorylase, adenosine deaminase, and 5'-nucleotidase were measured in normal women, women suffering from mastopathies and mammary carcinomas, aged 36 to 70. Blood serum activities of the studied enzymes in mammary carcinoma patients differed from these values in healthy women and those suffering from mastopathies; these differences were age-associated. Measurements of the time course of enzymic activities before and in the course of chemotherapy may be employed as a biochemical test to monitor therapy efficacy.
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PMID:[Use of the study of DNA metabolism enzyme activities as a test system in the treatment of breast cancer]. 205 30

A novel fusion gene has been created in which the expression of a dominant selectable marker, the human multidrug resistance gene, is directly linked to the expression of human adenosine deaminase cDNA. The chimeric gene was inserted between the long terminal repeats of a Harvey murine sarcoma virus expression vector and used to transfect drug-sensitive human KB carcinoma cells. Transfectants were selected in increasing concentrations of colchicine and found to contain multiple copies of the intact fusion gene, which is stably and efficiently expressed. A membrane-associated 210-kDa human P-glycoprotein-adenosine deaminase fusion protein is synthesized which retains function of the multidrug transporter and also exhibits adenosine deaminase activity. The data indicate that the human multidrug resistance gene may be used as a dominant selectable marker to introduce other genes in the form of gene fusions into cultured cells.
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PMID:Expression of a multidrug resistance-adenosine deaminase fusion gene. 256 38

A correlation between reactions of the sympathoadrenal system and the activity of adenosine transformation enzymes in lymphocytes is demonstrated in the dynamics of metastatic Lewis carcinoma development in C57Bl mice. In the period when metastases arise a decrease in the adenosine deaminase activity in lymphoid cells of the thymus and spleen is accompanied by drop in the content of DOPA, noradrenalin and adrenalin in adrenals. At the late stages of the tumour process a decrease in the amount of these compounds in adrenals is accompanied by the diminution of the adenosine deaminase activity and by an increase in the 5'-nucleotidase activity in the thymus. Contrary changes are observed in spleen lymphocytes. The revealed disturbances may stimulate to a considerable extent the appearance and growth of metastases.
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PMID:[Enzymes of adenosine metabolism in lymphocytes and the functional state of the sympatho-adrenal system in tumor processes]. 301 May 22

The antimetastatic action of bacterial endotoxins (BET), E. coli 0111:B4, B in particular, as well as their influence on the adenosine deaminase and 5'-nucleotidase activity were studied in peritoneal macrophages of mice bearing lung Lewis carcinoma. BET inhibition of lung metastasis growth was found to be due to such changes in macrophage adenosine metabolism, that testifies to the rise of their functional activity. The change in the level of macrophage purine metabolism can be considered as an important evidence of the effectiveness of the drugs capable to inhibit the metastasis growth.
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PMID:[Antimetastatic action of bacterial endotoxins and changes in the activity of the enzymes of purine metabolism in macrophages]. 301 30

Surgical operation of metastatic Lewis carcinoma, carried out in male mice of C57B1 strain, which stimulated distinctly the metastases spreading, was accompanied by phase impairments in activities of adenosine deaminase and 5'-nucleotidase in immunocompetent cells correlating with neurochemical stressory reactions. Thus, excessive stressory alterations in activity of symptoadrenal and hypothalamic mediatory systems appear to be among the factors responsible for inhibition of metabolism in lymphoid cells and for stimulation of metastatic spreading.
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PMID:[Adenosine metabolism in lymphocytes and neurochemical stressor reactions in mice with metastatic Lewis carcinoma after surgical removal of the tumor]. 302 90

Peripheral lymphocyte adenosine deaminase (ADA) activity was assessed in a group of 31 patients with gynaecologic malignancies (19 with carcinoma of the portio, 7 with endometrial adenocarcinoma, 3 with ovarian cancer, 1 with adenocarcinoma of the cervix, 1 with liposarcoma myxoide). 30 female subjects, aged 30 to 70 years, were studied as the control group. Lymphocyte ADA activity in the 31 patients ranged from 0 to 7 U/10(7) cells with a mean of 2.3 U/10(7) cells (normal values: range 2-5 U/10(7) cells; mean 2.8 U/10(7) cells). In cases where the enzyme was absent or far below the controls, a faster evolution of the disease was observed. We would point out that lymphocyte ADA activity in the patients under investigations shows a broad range of variability. Our preliminary observations would suggest that lymphocyte ADA assessment in a larger series of cancer patients may add further prognostic informations.
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PMID:Adenosine deaminase activity in peripheral lymphocytes of patients with gynaecologic malignancies. 409 78


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