Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.26.9 (ribonuclease)
6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum ribonuclease levels were determined in 54 patients with lung carcinoma, 74 long-term cigarette smokers, and 172 nonsmokers. The mean serum ribonuclease level was significantly higher in patients with lung carcinoma and long-term smokers compared with healthy nonsmokers (P less than .001). The serum ribonuclease activity level was not related to chronological age, sex, or race of the smoker or nonsmoker population. Forty (75%) of 53 patients with lung cancer and 49 (66%) of 74 smokers had elevated serum ribonuclease levels compared with 13 (7%) of 179 nonsmoker healthy controls (P less than .001). The highest incidence of elevation was noted in patients with epidermoid carcinoma (95%).
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PMID:Carcinoma of the lung and cigarette smoking. Effect on serum ribonuclease activity. 20 37

Fifty-one previously untreated cases of lung carcinoma and 7 normal healthy controls were evaluated with respect to serum ribonuclease (S-RNase) levels. Cellular immunity was tested in 22 of these 51 cases by leukocyte migration inhibition test (MIT) using extract of culture cell line of lung carcinoma. S-RNase levels in lung carcinomas were significantly elevated. There appeared to be no difference in S-RNase levels by histological classification. More striking was high S-RNase level in disseminated versus localized cases. MIT results indicated impairment of cellular immunity in those cases of more elevated S-RNase. S-RNase may be implicated in blocking phenomenon associated with neoplastic disease.
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PMID:Serum ribonuclease in patients with lung carcinoma. 99 11

Infusion of cycloheximide i.v., an antibiotic known to inhibit synthesis of protein, at a rate of 0.2 mg/kg/hr, reliably caused lysis of fever in 15 chronically febrile patients with Hodgkin's disease who did not have detectable bacterial, fungal, or viral infection. Antipyretic effects were also seen in some patients with reticulum cell sarcoma, lymphosarcoma, acute leukemia, histiocytic medullary reticulosis, plasma cell myeloma, carcinoma of the lung, and carcinoma of the cervix. The drug failed to produce defervescence in four patients with normal granulocyte reserves, who were febrile due to bacterial infection. When infused at a rate of 0.2 mg/kg/hr, the drug apparently caused an acute alteration of protein metabolism in man in that plasma amino acid nitrogen rose acutely while plasma levels of muramidase and ribonuclease fell during the period of the infusion. The data suggest that continuing synthesis of protein may be involved in nonbacterial fever of neoplastic disease. Mammalian granulocytes and monocytes are known to elaborate a pyrogenic protein following appropriate stimulation; it is suggested that in some types of neoplastic disease, particularly Hodgkin's disease, tumor cells may produce and release a pyrogenic protein and that drug-induced inhibition of its synthesis is responsible for the observed lysis of fever.
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PMID:Antipyretic effect of cycloheximide, and inhibitor of protein synthesis, in patients with Hodgkin's disease or other malignant neoplasms. 109 49

The expression of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in the catabolism of polyamines, is highly regulated by a number of factors including the natural polyamines and their analogues. The phenotype-specific cytotoxicity that occurs in response to a class of polyamine analogues, the diethylpolyamines, is associated with a phenotype-specific superinduction of SSAT in human non-small-cell lung carcinomas, whereas in non-responding cell types, including the small-cell lung carcinomas, the superinduction of SSAT does not occur. In this study, we have investigated the molecular basis of this phenotype-specific SSAT induction in human lung carcinoma cells in response to N1,N12-diethylspermine (BESpm). To facilitate the study of transcriptional regulation, we have cloned and characterized 11 kb of the human SSAT locus, including 3500 bp of the 5' promoter region. Nuclear run-on transcription studies suggest that the initial induction of SSAT results from an increase in the rate of gene transcription. Results from Northern blot analysis and ribonuclease protection assays indicate a differential expression of SSAT mRNA between the analogue-responsive H157 and non-responsive H82 cells. There is no detectable SSAT mRNA in H82 cells, even after a 24-h analogue treatment, whereas SSAT mRNA in H157 cells was detectable by Northern blot analysis and increased more than 100-fold following drug exposure. Furthermore, nuclear run-on transcription assays do not detect any active transcription of SSAT gene in either treated or untreated H82 cells. These results indicate that at least one component of the phenotype-specific induction of SSAT appears to be due to differences in transcriptional regulation of the gene. In addition, mapping of DNase I-hypersensitive sites of the SSAT gene suggest that the cell type-specific promoter/enhancer utilization may control the expression of the SSAT gene in differentially sensitive cell types in vivo.
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PMID:Differential transcription of the human spermidine/spermine N1-acetyltransferase (SSAT) gene in human lung carcinoma cells. 857 11

Hel-NI and HuD belong to the elav gene family and have gained recent attention as potential neuroendocrine markers for small-cell lung carcinoma (SCLC). Members of this conserved family normally appear at different stages of neuronal maturation, raising the possibility that their expression patterns in SCLC reflect the degree of neuroendocrine differentiation. I have utilized a ribonuclease protection assay to analyze Hel-NI and HuD expression in cultured SCLC cells with high (classic phenotype) and low (variant phenotype) levels of neuroendocrine differentiation. Hel-NI was detected in both classic and variant SCLC. Although HuD was detected consistently in classic SCLC, it was low to absent in variant SCLC, indicating a significant down-regulation in that phenotype. The expression patterns of Hel-NI and HuD also were analyzed in 9 primary SCLC and 10 non-SCLC lung-tumor samples. In the majority of SCLC samples, either Hel-NI or HuD was detected exclusively or predominantly, indicating a pattern of variable gene expression similar to cultured SC LC. Neither transcript could be detected in the non-SCLC samples. These data indicate that (i) HuD mRNA expression is associated with a higher level of neuroendocrine differentiation in SCLC, (ii) Hel-NI and HuD expressions are variable in both primary and cultured SCLC and (iii) HuD and Hel-NI, in combination, are neurogenetic markers for SCLC.
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PMID:Differential expression of the neuroendocrine genes Hel-N1 and HuD in small-cell lung carcinoma: evidence for down-regulation of HuD in the variant phenotype. 929 25

p21 (Waf1/Cip1) is a downstream target of p53. We evaluated the association between p21 polymorphism (codon 31), p53 polymorphism (codon 72) and their corresponding in vivo mRNA expression. In this study, p21 and p53 genetic polymorphisms (using standard PCR-RFLP techniques) and p21 and p53 gene expressions (using a radiolabelled ribonuclease protection assay (RPA) technique) were evaluated in the peripheral leukocytes of 84 individuals (63 with lung cancer). Log-transformed values of mRNA expression by RPA, which approximated a normal distribution, were analyzed. p53 genotypes did not correlate with p53 mRNA log-expression (P>0.05 for all comparisons), but the Pro allele variants of p53 were associated with a significant decrease in mRNA log-expression of its downstream target, p21. The variant Arg allele of p21 was also associated with a significant decrease in p21 mRNA log-expression. When individuals with at least one variant allele of both p53 and p21 (double-variants) were compared with all other genotype groups, these double-variants had significantly lower log-expression of p21 (P<0.005 by both t-tests (crude) and linear regression analyses (adjusted)). This is translated into an approximate 48% reduction in the geometric mean of the mRNA expression of the double-variants, when compared with all other groups. Results were consistent in both patients with lung cancer (n=63) and in normal controls (n=21). In conclusion, the presence of a p53 Pro allele and/or p21 Arg allele is associated with lower downstream target gene expression of p21.
Lung Cancer 2003 Jun
PMID:P53 (codon 72) and P21 (codon 31) polymorphisms alter in vivo mRNA expression of p21. 1278 24

The successful application of exogenous ribonucleases of different origin to suppress tumor growth allows one to consider them as perspective therapeutics for treatment of oncological diseases. An important aspect of the success of an anti-cancer drug is low hepatotoxicity, which will reduce, if not eliminate entirely the undesirable side effects of treatment. Previously we have shown that ribonuclease from Bacillus intermedius (binase) exhibits high antitumor and antimetastatic activity in tumor models of different histological origin. In this work we studied hepatotoxic action of binase using mouse tumor model of Lewis lung carcinoma. Binase at doses of 0.1-1 mg/kg which produced effective suppression of tumor growth and metastasis, showed positive effect on the liver of tumor-bearing mice expressed in a significant reduction in the volume of destructive changes in the liver parenchyma and return to the normal level of the liver regenerative potential impaired due to endogenous intoxication and tumor burden.
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PMID:Ribonuclease binase decreases destructive changes of the liver and restores its regeneration potential in mouse lung carcinoma model. 2456 11