Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A dose of 10 or 20 mg of N-butylnitrosourea (BNU) dissolved in 50% ethanol was administered by a gastric tube to 6-week-old male ICR/JCL strain mice and they were sacrificed 15 months later. One of 18 animals developed a hepatoma, but none of the mice given CCl4 in 0.1 ml of 50% oliver oil subcutaneously at the right thigh developed hepatoma. However, a marked enhancement of hepatoma induction was observed in mice injected with CCl4 one day before the single intragastric administration of BNU, with 12 out of 28 mice developing one or more hepatomas (average 3.2/mouse) ranging in diameter from 0.5 to 1.5 cm. By extending the administration interval between CCl4 and BNU to 1 week or 1 month, or by reversing the order of administration, the hepatotumorigenic action was virtually lost. There was no occurrence of hepatoma but a predominant development of leukemia, of either thymic or nonthymic origin, was observed in mice of younger age treated with CCl4 one day before continuous oral administration of BNU (1 mg/day/mouse). It is thus concluded that the preparative (cocarcinogenic) action of CCl4 is indispensable for hepatotumorigenesis with a single large dose of BNU.
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PMID:Preparative action of carbon tetrachloride in liver tumorigenesis by a single application of N-butylnitrosourea in male ICR/JCL strain mice. 17 59

The effect of chalone-containing ethanol extract of rat skin (CCE) on the growth in mice of transplanted uterine cervix and skin carcinomas, hepatoma-22a, sarcoma-180 and leukemia L-1210 was studied. When CCE is added to the suspension of tumour cells (10 mg CCE/100 mg tumour tissue/ml saline) the most obvious retention of tumour growth is observed on squamous-cell carcinoma of uterine cervix (72.6%; p less than 0.01). The effect of CCE on the growth of other transplanted tumours, including the skin carcinoma, is not significant. As compared to the uterine cervix carcinoma, the skin carcinoma lacked its primary squamous-cell structure during the tumour progression. The possibility of applicative use of chalones for cancer control is discussed.
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PMID:Study of antiblastomogenic action of epidermal chalones. I. The effect of epidermal chalones on some transplantable mouse tumours. 21 Oct 47

The RNA components of two C-type RNA viruses, avian myeloblastosis virus and Friend leukaemia virus, have been isolated by treatment of the viruses with 6 M-guanidine-HCl and precipitation with ethanol. The virus proteins were recovered by lyophilization of the guanidine-HCl-ethanol supernatant after thorough dialysis against 0.5 mM-dithiothreitol. This simple method yielded RNA of similar quality to the phenol and sodium dodecyl sulphate (SDS) extraction methods, and the same amount of 60-70S RNA, although a fraction of the smaller (4S) species remained in the protein fraction. The sedimentation patterns of heat-denatured RNA extracted by either method were similar. Electrophoretic analyses of the extracted proteins in polyacrylamide gel gradients containing SDS gave patterns that were very similar to those obtained by direct analysis of SDS disrupted viruses.
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PMID:The use of guanidine-HCl for the isolation of both RNA and protein from RNA tumour viruses. 21 Nov 81

The pharmacological and therapeutic effects of the daunomycin (DNM):DNA complex were compared with those of free DNM in mice. A complex formation between dnm and DNA (1:11.7, w/w) resulted in a 79% decrease in DNM complex was dialyzable. The DNM fluorescence was completely recovered from the complex in 0.3 N HCl and 50% ethanol solution, and a short contact with biological tissues studied did not quench DNM fluorescence after extraction. The plasma fluorescence (DNM equivalent) 5 min after the i.v. injection of DNM:DNA complex at a dose of 20 mg/kg was 60-fold higher than that of an equivalent amount of free DNM. The complex was cleared for plasma with an initial half-life of 20 min. In spite of an initally higher blood generally similar except in liver and spleen, where DNM equivalent were significantly higher than those of free DNM. The uptake of DNM:DNA into L1210 cells in vitro was low and, at 1 hr, was about one-twentieth of that from DNM. Treatment of DBA/2 mice bearing i.p. L1210 leukemia transplant (initial cell number, 10-3) with DNM:DNA complex resulted in identical increases in life-span as occurred with free DNM. When routes of cell transplant and treatment were different, no therapeutic advantage of DNM:DNA over DNM was seen.
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PMID:Pharmacological and therapeutic efficacy of daunomycin:DNA complex in mice. 113 31

High affinity receptors (VDR) for 1,25-dihydroxycholecalciferol (calcitriol) are expressed in HL60 human leukemia cells and in low numbers in peripheral blood lymphocytes (PBL). HL60 cells, expressing some characteristics of promyelocytes, can be induced to monocytoid differentiation by calcitriol. Specific nuclear translocation of [3H]calcitriol/VDR was examined after exposure of whole cells to 10(-9) M/l calcitriol in the presence and absence of a 500-fold excess of unlabeled ligand and subsequent isolation of nuclei. Specific nuclear translocation of [3H]calcitriol/VDR was found to be time dependent reaching a maximum of approximately 2100 binding sites/nucleus after 3 h of incubation in HL60 cells, whereas a maximum of approximately 310 binding sites/nucleus was found after 3 h in PBL. Pulse exposure of HL60 to radiolabeled hormone for 3 h followed by culture in medium without serum and calcitriol lead to nuclear retention of approximately 1600 radiolabeled VDR by 8 h and approximately 1000 VDR by 24 h. Radiolabeled VDR disappeared from the nuclear compartment with a halflife of approximately 30 min if cells were cultured with identical concentrations of unlabeled hormone after the pulse (pulse/chase-experiments). No difference of VDR retention in pulse and pulse/chase-experiments was seen in PBL, where VDR halflife was approximately 30 min. No specific translocation into the nuclear compartment was seen when isolated nuclei were incubated in [3H]calcitriol. Radiolabeled hormone/receptor complexes of nuclei isolated from cells exposed for 3 h to radiolabeled hormone--in contrast to identical experiments with intact cells--did not disappear from the nuclear compartment upon incubation of nuclei with identical concentrations of the unlabeled compound. The activity of DNA relaxing enzymes (e.g. topoisomerases I and II) in nuclear extracts was measured using a PBR 322-relaxation-assay. Enhanced overall enzyme activity was found in nuclear extracts by 1 h after incubation with calcitriol (final ethanol concentration 0.0001% v/v) in HL60 and PBL. The enhanced activity disappeared after 2 h in PBL, whereas it was still enhanced by 4 h in HL60. No effect was seen in ethanol treated controls. We conclude that a specific nuclear translocation mechanism exists for calcitriol in both cell types examined, most likely due to translocation of receptor proteins after hormone binding. Translocated hormone/receptor complexes compete for a limited number of specific nuclear binding sites. Enhanced activity of topoisomerases in nuclear extracts upon translocation of VDR might reflect interaction of both within the nuclear compartment, thus initiating DNA-unwinding, a prerequisite of transcription initiation.
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PMID:Kinetics of nuclear translocation and turnover of the vitamin D receptor in human HL60 leukemia cells and peripheral blood lymphocytes--coincident rise of DNA-relaxing activity in nuclear extracts. 131 93

The relatively high incidence of infectious disease in alcoholics is attributed to the immunosuppressive effects of alcohol. The potential role of alcohol as cofactor in HIV infection and in the development and expression of AIDS is suggested but unknown. In order to understand better the contribution of alcohol to immune dysfunction following HIV infection, we assessed the presence of specific markers on thymus and spleen cells in C57B1/6 mice infected with LP-BM5 murine leukemia virus and fed ethanol-containing diets. In the first experiments, mice were fed diets containing 0, 4.5, 5.5, and 6% (v/v) ethanol for 14 weeks. High ethanol exposure (6%) resulted in severe dehydration and death after 7 weeks. Although moderately low intakes of ethanol did not significantly modify percentages of T and B cells, they increased the absolute number of mature T, B, and CD4+ cells and decreased percentages of Thy 1.2+ cells. In the second experiment, mice were infected with LP-BM5 murine leukemia retrovirus and fed diets containing 5% ethanol in a regimen of 5 days of ethanol diet and 2 days of diet without alcohol for 12 weeks. Ethanol exposure in the retrovirally infected mice showed a marked decrease in Thy 1.2+ (P < 0.05). Moderate decreases in percentages of CD4+, CD8+, CD5+ cells and an increase in Ia+ cells were also observed in the retrovirus/infected ethanol-treated mice. Moderate ethanol consumption during retroviral infection induced mild/moderate changes on lymphoid cells. Ethanol consumption may accelerate the progression of murine AIDS through such changes in the lymphoid cells of the spleen.
Alcohol Alcohol 1992 Jul
PMID:Modification of lymphoid subsets by chronic ethanol consumption in C57Bl/6 mice infected with LP-BM5 murine leukemia virus. 135 81

Extracts of human MCF 7 mammary carcinoma cells, the human lymphoblastoid cell lines AEH 1 and IM 9, T-cell derived CCRF cells, HL 60 myeloic leukaemia cells and murine myeloma cells SP 0 and NS I were analysed for immunoreactivity with polyclonal goat antibodies raised against homogeneous preparations of C-terminal fragments (32 kDa) of porcine uterine oestradiol receptor (ER). Whole cells and low speed cytosols were analysed for specific oestradiol-binding activity. ERs were enriched from cell extracts by either fractionated ethanol precipitation (0-25% (v/v) ethanol) and/or microscale-immunoaffinity chromatography. Immunoreactive proteins of identical molecular weight (approximately 65 kDa) were detected in all cell lines examined. Whole cell binding assays showed specific oestradiol-binding activity in MCF 7, IM 9 and CCRF cells. Borderline binding was found in HL 60 myeloid cells. No specific binding could be detected in AEH 1, NS I and SP 0 cells. Identical results were obtained using agar-electrophoresis after dextran-coated charcoal treatment. Immunoaffinity purified ERs from MCF 7, AEH 1 and HL 60 cells were subjected to limited proteolysis, where identical tryptic fragments were generated. In conclusion, we have confirmed by immunological methods that ERs are expressed in a variety of cell lines derived from the immune system and the haematopoietic system. The lack of specific hormone binding or very low-affinity hormone binding in some of the cells examined may be due to post-translational events or point mutations.
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PMID:Immunological detection of the oestradiol receptor protein in cell lines derived from the lymphatic system and the haematopoietic system: variability of specific hormone binding in vitro. 140 47

Chronic ethanol consumption impairs cellular immune functions. This may explain the increased occurrence of various opportunistic infections in heavy ethanol users. Immunological alterations associated with Acquired Immune Deficiency Syndrome (AIDS) also permit more opportunistic infections. In this study, we used a murine model of retrovirus infection induced by LP-BM5 murine leukemia virus. The combined effects of ethanol use and early retroviral infection (prior to the development of AIDS) on resistance to Streptococcus pneumoniae were investigated. Consumption of ethanol by non-retrovirus-infected mice resulted in decreased resistance to S. pneumoniae. However, retrovirus-infected mice fed a diet containing high concentrations of ethanol (6 and 7% v/v) exhibited a greater resistance to S. pneumoniae infection than retrovirus-infected mice fed diets with lower concentrations (5%) or no ethanol. The total number of white blood cells also decreased as serum ethanol levels increased. There were also fewer lymphocytes and more neutrophils and monocytes in retrovirus-infected mice fed ethanol. Diet consumption decreased as the concentration of ethanol increased in the diet. Consumption was dependent upon the dark-light cycle. The highest diet consumption was observed during the first 4 hr of the dark period. The level of ethanol in serum was influenced by the amount of the diet consumed and its ethanol concentration. Both retrovirus infection and ethanol consumption effected survival after S. pneumoniae infection.
Alcohol Alcohol 1992 Jul
PMID:Influence of the level of dietary ethanol in mice with murine AIDS on resistance to Streptococcus pneumoniae. 141 8

The effects of acute and chronic ethanol administration on tumor progression and metastasis were studied in rat models of leukemia and breast cancer, respectively. Acute administration of 1.5-3.5 g of ethanol/kg body weight significantly reduced survival of rats injected with CRNK-16 leukemia cells in a dose-related manner. Acute administration of 2.5-3.5 g of ethanol/kg body weight, one hour before tumor inoculation, or chronic consumption of liquid diet containing ethanol for two weeks before and three weeks after tumor inoculation, significantly increased the number of lung metastases of MADB106 mammary adenocarcinoma. The ethanol-induced increase in the number of metastases was not correlated with plasma levels of corticosterone and was not altered by the opiate antagonist naltrexone. Incubation of spleen cells in vitro in the presence of ethanol, at concentrations comparable to those measured in the blood of ethanol-treated rats, significantly suppressed natural killer (NK) cell activity against MADB106 cells in a standard chromium-release assay and decreased the binding of effector to MADB106 tumor cells. However, neither acute nor chronic ethanol administration in vivo altered splenic NK activity against this tumor in the same in vitro assay, in which the ethanol would have been washed away. These results suggest that, in the presence of ethanol, tumor progression is facilitated. The possibility that this facilitation is related to ethanol-induced impairment of the normal tumoricidal interaction between NK and tumor cells is discussed.
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PMID:Ethanol increases tumor progression in rats: possible involvement of natural killer cells. 157 4

1. The effect of n-alcohols (methanol and ethanol) and anesthetics (lidocaine, thiopental, methohexital and thiamylal) on procoagulant activity (PCA) in human peripheral-blood monocytes and non-adherent cultured leukemia promonocytic U937 and THP-1 cells was examined herein. 2. Exposure of whole blood to ethanol showed no effect on PCA in human monocytes. However, ethanol dose-dependently inhibited LPS-induced PCA in isolated human monocytes. 3. In THP-1 cells, ethanol had no significant effect on PCA in either non-challenged or LPS-induced status. However, the induction of PCA by LPS was substantially inhibited when cells were pretreated with 1% ethanol (v/v) for 72 hr. 4. In U937 cells, n-alcohols and anesthetics resulted in dose-dependent depressions in PCA. Importantly, the percent reduction in LPS-induced PCA was much more pronounced than that in non-challenged PCA. 5. These data clearly suggest that n-alcohols and anesthetics readily inhibit the LPS-stimulatory action on monocytic PCA.
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PMID:Inhibition of endotoxin-induced monocytic procoagulant activity by n-alcohols and anesthetics. 168 19


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