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 set of intraveous injections of 7,8,12-trimethylbenz[a]anthracene consistently elicited leukemia in more than 75% of young adult Long-Evans female rats. There was a profound reduction in the incidence of leukemia in companion groups of rats fed small amounts (1--10 mg) of Sudan III or Sudan IV prior to each injection of the carcinogenic hydrocarbon. Repeated feedings of 1 mg of Sudan III induced cumulative increases in the concentration of menadione reductase (EC 1.6.99.2) in liver, whereas protein concentration was unchanged. A single feeding of 1 mg of Sudan III prevented fatal toxicity in all members of large groups of rats injected with massive doses of 7,12-dimethylbenz[a]anthracene, but 50% of the survivors developed leukemia; unprotected rats succumbed in 1--3 days. Sudan III was not carcinogenic under the experimental conditions.
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PMID:Azo dyes prevent hydrocarbon-induced leukemia in the rat. 10 Jul 87

Acute myelogenous leukemia was induced in outbred Long-Evans rats by iv injections of leukemia cells from a subcutaneous tumor of Shay myelogenous leukemia. In rats with this leukemia the peripheral white blood cell (WBC) counts varied from 2.4 to 700 X 10(9)/liter. No differences were found in the bone marrow of the rats with the high WBC counts and that of rats with low WBC counts. This observation could explain the large variations in the number of circulating leukemia cells caused by differences in cell proliferation or delivery of cells into the circulation. Massive phagocytosis of leukemia cells occurred in animals with low WBC counts (less than 12 X 10(9)/liter) but not in animals with high WBC counts (greater than 150 X 10(9)/liter). This phagocytosis was directed against circulating leukemia cells. The main phagocytes were Kupffer's cells of the liver and macrophages of the spleen parenchyma. In addition, phagocytosis occurred in the spleens and bone marrow by intravascular macrophages, which were derived from extravascular sites. The endothelium of the postcapillary venules of the lymph nodes participated in the phagocytosis of circulating leukemia cells while continuing to be the locus of lymphocytic return from circulation to lymphatic parenchyma. The factors underlying the differences in macrophage activity between the rats with high and low WBC counts were unknown.
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PMID:Destruction of circulating leukemia cells by phagocytosis in rats with myelogenous leukemia. 27 68

Rats frequently develop various tumors, many of them malignant; the majority of tumors in the females develop in the mammary glands. In primary spontaneous tumors and lymphomas virus particles cannot be found on electron microscopic examination; transmission of the tumors by filtered extracts has not been successful. In our colonies of Sprague-Dawley rats the incidence of tumors was 22% in females and 5% in males; in Long-Evans rats the incidence of tumors and 28% in females and 10% in males. In (Sprague-Dawley x Long-Evans) F1 hybrids the incidence of tumors was 67% in females and 32% in males, about twice as high as in the parental strains. Fractionated total-body x-irradiation (150 rads five times at weekly intervals) (1 rad = 0.01 gray) increased the incidence of tumors in Sprague-Dawley rats from 22% to 93% in females and from 5% to 59% in males. In Long-Evans rats, irradiation increased the incidence of tumors from 28% to 63% in females and from 10% to 42% in males. The incidence of malignant tumors was almost twice as high in irradiated Sprague-Dawley and Long-Evans rats as compared with nonirradiated animals of the same strains. Partial shielding during irradiation had no significant effect on the incidence or on the forms of tumors developing in the irradiated animals. In striking contrast to results of experiments carried out on mice, the incidence of leukemia and lymphomas was not increased in the irradiated rats, as compared with control animals.
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PMID:Spontaneous tumors in Sprague-Dawley and Long-Evans rats and in their F1 hybrids: carcinogenic effect of total-body x-irradiation. 29 92

Statistical analysis of 361 cases of primary leukemia induced in outbred Long-Evans and Sprague-Dawley rats by 7,12-dimethylbenz[a]anthracene (DMBA) and 7,8,12-trimethylbenz[a]anthracene (TMBA) showed that the incidence of trisomy of chromosome No. 2 was significantly lower with TMBA (17.8%) than with DMBA (29.3%). This tendency was reproducible in both sexes. Another characteristic chromosome abnormality, long No. 2, was found in 10 cases (2.8%). Quinacrine fluorescence analysis revealed that cells with No. 2 trisomy or either of two types of long No. 2 had total and partial No. 2 trisomy, respectively. Other chromosome members of cells with long No. 2, as well as the chromosomes of cells with typical No. 2 trisomy and "normal diploid" leukemia cells, revealed no band abnormality. The phenotype of No. 2 trisomy, severe anemia of the hosts reported in DMBA-induced leukemias, was also noted in leukemias with TMBA-induced No. 2 trisomy but not in leukemias with long No. 2.
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PMID:Reproducible chromosome changes of polycyclic hydrocarbon-induced rat leukemia: incidence and chromosome banding pattern. 41 46

Scored at 24 hours, the LD-50 of a solution of beta-propiolactone administered intravenously to young rats was 225 +/- 55 mg/kg. Twenty-four hours after a single intravenous injection (100 mg/kg = 1.4 m mole/kg) of beta-propiolactone into male and female rats of both the Long-Evans and Sprague-Dawley strains, the incidence of breaks found in the chromosomes of metaphase marrow cells was low (8.8 percent vs. 5.0 percent in controls). The s5 chromosomes were preferentially damaged. A 200 mg/kg dose increased the incidence modestly to 11.3 percent. In comparison, a single intravenous dose of benzo(a)pyrene (40 mg/kg = 0.16 m mole/kg) produced a break incidence of 19 percent. In long-term experiments multiple (five) intravenous injections (100 mg/kg each) of beta-propiolactone given in a 6 week period elicited only two neoplasms (a chloro-leukemia and a mammary fibroadenoma) among 37 animals during the following 12-13 months. In contrast, four injections of benzo(a)pyrene (40 mg/kg) produced a 14-times greater mammary tumor incidence in the Sprague-Dawley female rat than did beta-propiolactone. Marrow cell chromosome examination indicated no significant chromosomal changes due to the earlier beta-propiolactone treatment except for one animal with a consistent 43-chromosome karyotype resulting from S1 trisomy; no neoplasm was evident in that animal. Earlier treatment with benzo(a)pyrene produced a persistent and significant elevation in break incidence. Both the carcinogenic and clastogenic effects of intravenous beta-propiolactone are low in rats and are not comparable in magnitude to those produced by benzo(a)pyrene.
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PMID:Comparison of the clastogenic and carcinogenic effects of intravenous beta-propiolactone and benzo(a)pyrene in rats. 52 52

Cytogenetic studies were done on 34 primary leukemias induced by N-nitroso-N-butylurea (NBU) in outbred Long-Evans rats. The results revealed leukemia cells with No. 2 trisomy and long No. 2 chromosome, which characterized the leukemias induced by polycyclic hydrocarbon carcinogens such as 7,12-dimethylbenz[a]anthracene and 7,8,12-trimethylbenz[a]-anthracene. These findings suggest a common mode of action of different carcinogenic chemicals at the chromosome level, although the lower incidence of these chromosome changes and of erythroblastic leukemias with NBU suggests subtle difference in their actions.
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PMID:Involvement of chromosome No. 2 in chromosome changes in primary leukemia induced in rats by N-nitroso-N-butylurea. 65 Jul 3

Hypophysectomy of rats bearing 7,12-dimethylbenzanthracene-induced leukemia has been reported to result in a prompt and persistent regression of the leukemia. The purpose of this study was to determine whether or not marked alterations in prolactin secretion would influence this neoplastic process. To determine this, immature male and female Long-Evans rats were divided into three groups: Group 1, controls; Group 2, pituitary grafted (hyperprolactinemia); and Group 3, 2-bromo-alpha-ergocryptine-treated (hypoprolactinemia). Two weeks after the initial treatment and at 2-week intervals thereafter (6 total), each rat was given a single intragastric intubation of 7,12-dimethylbenzanthracene (10 mg/rat). Two months after the initial carcinogen treatment and at 2- to 3-week intervals thereafter, all rats had liver biopsies for the identification of leukemia. Results clearly show that despite nearly 10-fold difference in mean serum prolactin levels in the three groups of female rats and nearly a 20-fold difference in the level of this hormone in male rats, no significant differences in the magnitude of this leukemogenic process could be detected. Thus, striking changes in prolactin secretion do not appear to influence significantly this leukemogenic process.
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PMID:Influence of prolactin on carcinogen-induced leukemogenesis in Long-Evans rats. 81 55

The erythroblastic leukemia produced in Long-Evans rats by the administration of 7, 8, 12 trimethylbenz (a) anthracene has been used as a model of the most immature form of the erythrocyte series. In conjunction with studies of the maturation of several other membrane functions, the permeability of this cell to water and to certain definitive non-electrolytes was measured with osmotic methods. The hydraulic conductivity, L-p was 6.2 micro (minute)-1, (atm)-1 at 25 degrees C, quite high and characteristic of mature erythrocytes, but different from values of 0.65 for immature myeloid cells. The effect of temperature provided an energy of activation of 4.4 kCal/mole, also typical of mature mammalian erythrocytes but again different from 13 to 18 kCal/mole for immature myeloid cells. Urea was compared to thiourea. The permeability coefficient for urea was 76.7 micra (minute)-1 plus or minus 13.8 (S. E.); the value for thiourea was 1.55 micra (minute)-1 plus or minus 0.18 (S. E.). Phloretin at 0.25 mM inhibited urea permeability by 90% with 50% inhibition occurring at 0.05 mM. Inhibition was reversible. Permeability to the glycols was also compatible with mature erythrocytes. We infer from these findings that the structure which underlies these basic, passive membrane functions is laid down early and persists after loss of nucleus and subsequent maturation.
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PMID:Maturation of membrane function: the permeability of the rat erythroblastic leukemic cell to water and to non-electrolytes. 105 96

The membrane changes which occur during cellular maturation of erythroid cells have been investigated. The transport of alpha-aminoisobutyric acid, alanine, and N-methylated-alpha-aminoisobutyric acid have been studied in the erythroblastic leukemic cell, the reticulocyte, and the erythrocyte of the Long-Evans rat. The dependence of amino acid transport on extracellular sodium concentration was investigated. Erythrocytes were found to transport these amino acids only by Na-independent systems. The steady state distribution ratio was less than 1. Reticulocytes were found to transport alpha-aminoisobutyric acid and alanine by Na-dependent systems, but only small amounts of N-methylated-alpha-aminoisobutyric acid. Small amounts of these amino acids were transported by Na-independent systems. The steady state distribution ratio was greater than one for Na-dependent transport. The erythroblastic leukemia cell, a model immature erythroid cell, showed marked Na-dependence (greater than 90%) for alpha-aminoisobutyric acid and alanine transport, and greater than 80% for the Na-dependent transport of N-methyl-alpha-aminoisobutyric acid. The steady state distribution ratio for the Na-dependent transport was greater than 4. In the erythroblastic leukemic cell, at least three Na-dependent systems are present: one includes alanine and alpha-aminoisobutyric acid, but excludes N-methyl-alpha-aminoisobutyric acid; one is for alpha-aminoisobutyric acid, alanine and also N-methyl-alpha-aminoisobutyric acid; and one is for N-methyl-alpha-aminoisobutyric acid alone. In the reticulocyte, the number of Na-dependent systems are reduced to two: one for alpha-aminoisobutyric acid and alanine; one for N-methyl-alpha-aminoisobutyric acid. In the erythrocytes, no Na-dependent transport was found. Therefore, maturation of the blast cell to the mature erythrocyte is characterized by a systematic loss in the specificity and number of transport system for amino acids.
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PMID:Maturation of membrane function: transport of amino acid by rat erythroid cells. 124 Jan 4

Four classes of murine leukemia virus (MuLV) which display distinct cellular tropisms and bind to different retrovirus receptors to initiate virus infection have been described. In the present study, we describe a rapid, sensitive immunofluorescence assay useful for characterizing the initial binding of MuLV to cells. By using the rat monoclonal antibody 83A25 (L. H. Evans, R. P. Morrison, F. G. Malik, J. Portis, and W. J. Britt, J. Virol. 64:6176-6183, 1990), which recognizes an epitope of the envelope gp70 molecule common to the different classes of MuLV, it is possible to analyse the binding of ecotropic, amphotropic, or xenotropic MuLV by using only a single combination of primary and secondary antibodies. The MuLV binding detected by this assay is envelope receptor specific and matches the susceptibility to infection determined for cells from a variety of species. The binding of amphotropic MuLV to NIH 3T3 cells was shown to be rapid, saturable, and temperature dependent. Chinese hamster ovary (CHO-K1) cells normally lack the ability to bind ecotropic virus and are not infectible by ecotropic vectors. Expression of the cloned ecotropic retrovirus receptor gene (Rec) in CHO-K1 cells confers high levels of ecotropic virus-specific binding and confers susceptibility to infection. Characterization of MuLV binding to primary cells may provide insight into the infectibility of cells by retroviruses and aid in the selection of appropriate vectors for gene transfer experiments.
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PMID:Detection of receptor-specific murine leukemia virus binding to cells by immunofluorescence analysis. 131 32


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