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

Damvar, the delta-(2-amino-6-hydroxy-3,4-dihydro-4-oxo-5-pyrimidinyl) valeric acid, administered alone s. c. or i. p., has no effect on L1210 leukemia. In DBA2 mice with L1210, Damvar administered in combination with 5-fluorouracil, or with 6-mercaptopurine, or with cyclophosphamide, in optimal doses, enhances or intensifies the antileukemic effects of the above cytostatics.
 ...
PMID:Combined therapy of L1210 leukemia with Damvar and cytostatics. 52 24

Plasma deoxyribonuclease (E.C.3.1.4.5.) activity was measured in patients suffering from acute non-lymphoblastic leukemia, in blastic phase and in remission, and in DBA2 mice, normal and bearing L1210 leukemia. No difference in enzymic activity could be observed between normal and leukemic states in human beings and mice.
 ...
PMID:Comparison of plasma deoxyribonuclease activity between normal and leukemic states in man and mice. 52 35

Determinations were made of glyoxalase I and glyoxalase II acitivity in the liver of mice (BDF1 and DBA2 strains) bearing sarcoma 180 and L1210 leukemia in ascites form. A progressive decrease in the both glyoxalase I and glyoxalase II activities to about 40--60% of that of the control groups was observed within the developing period 8--9 days. Test results are interpreted in the light of the postulated role of this enzyme system in cell division and in the tumor development process.
 ...
PMID:Further studies on liver glyoxalase I and glyoxalase II. Activity in mice bearing sarcoma 180 and L1210 leukemia. 69 5

Friend leukemia was used as an experimental model to study the action of a ribofuranosyl derivative of nitrosourea : RPCNU. This new product was known to be active in L 1210 leukemia and immunosuppressive. RPCNU significantly decreases the splenomegaly induced in DBA2 mice by Friend virus when it is given at a time ranging from 7 days before to 14 days after virus inoculation. The survival time in leukemic treated groups is also greatly increased. However, viral content of the spleen extracts of the leukemic treated mice is not reduced. Therefore, RPCNU cannot be considered as an antiviral agent. A comparison between survival of leukemic and non leukemic mice treated with different doses show that the effectiveness of RPCNU is correlated with its toxicity. The effect of RPCNU on Friend leukemia by cytotoxicity on hematopoietic stem cells is discussed in this paper.
 ...
PMID:Effect of the nitrosourea derivative rpcnu (ICIG 1163) on the development of Friend leukemia in mice. 89 12

Studies were conducted of the in vivo therapeutic potential of compounds which induce the differentiation of Friend leukaemia cells (FLC) in vitro. DBA2/J mice were inoculated with Friend leukaemia cells grown in tissue culture and at various times thereafter were treated with either N-methylacetamide, dimethylacetamide, or tetramethylurea. While survival was only occasionally prolonged, in every study these agents significantly inhibited leukaemia cell proliferation in the spleen and to a lesser extent in the marrow. These agents had no effect on the rate of proliferation of FLC growing subcutaneously nor on the proliferation of myeloid leukaemia in RFMS mice. These studies indicate that the administration of inducing agents to mice bearing Friend leukaemia can alter the proliferation characteristics of the leukaemia cells and hence suggest that these agents may have therapeutic potential.
 ...
PMID:Inducers of Friend leukaemic cell differentiation in vitro--effects of in vivo administration. 93 12

Rubidazone, the new semi-synthetic benzol hydrazone hydrochloride derivative of dauorubicin, has proved on a molecular weight basis to be less toxic than adriamycin and similar to daunorubicin in cardiac toxicity studies in the hamster as well as in other in vivo and in vitro test systems. It has proven effectiveness against several animal tumours and human acute leukaemias. We have compared the inhibitory effect of rubidazone to that of adriamycin on P388 leukaemia and normal bone marrow colony-forming units (CFU) using the spleen colony assay system in male DBA2 mice. The efficacy ratios (i.e., the ratio of the slopes of the normal bone marrow CFU to leukaemic CFU dose-survival curves) in the spleen colony assay system for rubidazone and adriamycin were 7-8 and 7-5 respectively. This near identity of efficacy ratios fro rubidazone and adriamycin correlated with the results of median survival time studies in the leukaemic mice. Their dose-median survival time curves were almost parallel, having nearly identical slopes. Rubidazone's equal therapeutic index as compared to adriamycin in the spleen colony assay system together with its known decreased toxicity to cardiac muscle cells makes it an extremely promising new anthracycline derivative to study in comparison to adriamycin in human malignancies.
 ...
PMID:Rubidazone vs adriamycin: an evaluation of their differential toxicity in the spleen colony assay system. 95 15

The immunogenicity of murine leukaemias induced by chemical carcinogens or irradiation in C57Bl or (C57Bl times DBA2) F1 hybrid mice has been studied in vivo by transplantation and in vitro by indirect membrane immunofluorescence (IF) using syngeneic immune or allogeneic immune antisera. Two of 5 leukaemias tested for immunogenicity by assessment of the capacity of syngeneic mice specifically immunized with irradiated (3 Krad) cells to reject small challenge inocula (10(3)-10(4) cells) displayed weak neoantigenicity while 3 were non-immunogenic by this criterion. Antibodies directed against cell-surface antigens of the immunizing cells of 7 leukaemias were not detectable by immunofluorescence tests using sera from the respective immunized mice. H-2 histocompatibility antigens readily identified on normal lymphoid cells using reference Balb/c anti-C57Bl (H-2d anti-H-2b) alloantisera could neither be detected on the majority of transplanted leukaemias nor on 9 primary leukaemias in C57Bl mice induced by N-butyl-N-nitrosourea (BNU). Two of the transplanted leukaemias showed greatly diminished capacity for absorption of alloantibody compared with normal spleen cells. Transplantation to H-2 different recipients, in which the leukaemic cells were invariably rejected, generated a strong humoral antibody response, which was demonstrable against normal lymphoid cells. Failure to demonstrate significant antibody binding by indirect immunofluroescence tests with immune sera, or by absorption, is presented as evidency that H-2 antigen expression is substantially modified on BNU induced leukaemia cells. These findings have implications for the detection of tumour neoantigens on chemically induced leukaemias.
 ...
PMID:Cell surface antigen expression on chemically induced murine leukaemias. 117 42

Presumably the coadministration of the uroprotector mesna in cyclophosphamide treatment does not influence the systemic activity of its activated metabolite. This was newly investigated in a mouse model. The LD50 values of i.p. administered mafosfamide, a derivative of act. CP, were increased by the simultaneous i.p. administration of mesna (mafosfamide: mesna 1:2 on a molar weight basis) from 590 mg/kg to 750 mg/kg, and after i.v. injection of cytostatic and thiol from 505 mg/kg to 810 mg/kg. Administration of 2 X molar cysteine i.v. or i.p. to mafosfamide-treated animals was even more effective against its lethal toxicity (LD50 i.p. 1800 mg/kg and i.v. 1130 mg/kg). Bone marrow toxicity (severe leukocytopenia) was partially abolished by both thiols. Also the therapeutic efficacy of act. CP against L1210 leukemia in DBA2 mice was reduced by 50% in the presence of cysteine and of mesna. Compared with mesna the higher detoxification effect of cysteine is attributed to its longer half-life (t1/2 20 min vs 12 min of mesna) and presumably an accumulation of cysteine in some cell systems (distribution coefficient 1.20 ml/g vs 0.68 ml/g of mesna). Nevertheless, our study clearly demonstrates a distinct systemic deactivation of act. CP by mesna, which might be of clinical relevance.
 ...
PMID:Influence of mesna and cysteine on the systemic toxicity and therapeutic efficacy of activated cyclophosphamide. 310 47

The influence of protein synthesis inhibition by sparsomycin (Sm) on in vivo cisplatin activity has been studied on BALBc X DBA2: F1 mice bearing L1210 leukemia i.p. Sm alone at the dose range from 0.5 to 3.0 mg/kg did not significantly improve animal survival. Sm potentiated cisplatin activity only when given 3 or 6 h prior to cisplatin (P less than 0.001). Sm 0.5-1.5 mg/kg 3 h prior to cisplatin resulted in a significant prolongation of animal survival (P less than 0.001) and 66% cures in each group versus 0% due to cisplatin alone. Sm pretreatment decreased weight loss due to cisplatin suggesting that it probably is able to decrease cisplatin toxicity.
 ...
PMID:In vivo potentiation of cis-diamminedichloroplatinum (II) antitumor activity by pretreatment with sparsomycin. 374 87

The effect of liposome encapsulation of the metabolic activation (phosphorylation) and degradation (deamination) of arabinofuranosylcytosine (Ara-C) in liver and spleen of dogs and mice was investigated. Ara-C in free or liposome-encapsulated form was administered i.v. to dogs and DBA2/CR mice bearing leukemia L1210. At various times after injection the concentration of Ara-C and Ara-C metabolites in the blood, liver and spleen was measured. It was shown that liposome encapsulation results in an increased Ara-C/arabinofuranosyluracil ratio in the liver and spleen of dogs and leukemic mice and that encapsulated Ara-C generates a sustained level of Ara-C triphosphate in the liver and spleen of leukemic mice. These results clearly indicate that 1) encapsulated Ara-C is protected against deamination in the liver, 2) encapsulated Ara-C is slowly released from liposomes in liver and spleen and 3) that liposomes may act as a local depot for Ara-C in these tissues.
 ...
PMID:Distribution and metabolism of lipsome-encapsulated and free 1-beta-D-arabinofuranosylcytosine (Ara-C) in dog and mouse tissues. 709 52


1 2 Next >>