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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cranial computed tomography (CT) was performed on 40 consecutive children with newly diagnosed acute lymphoblastic leukemia (ALL) on admission before any chemotherapy, 5 months after CNS therapy (n = 39) and after 2 to 3 years of therapy (n = 31). Changes related to leukemia were found in only 10% of the patients at the time of diagnosis (4/40). These initial changes, two intracranial hemorrhages, one dural thickening and one contrast enhancement, all disappeared during therapy. The findings which persisted unchanged in the next two CT scans were thought to be normal variations or caused by earlier disorders. CNS therapy consisted of intrathecally and intravenously administered methotrexate in 20 standard risk (SR) patients and cranial irradiation in addition to chemotherapy in 19 intermediate risk (IR) or high risk (HR) patients. Four SR patients developed changes during therapy. Three had enlarged cerebrospinal fluid (CSF) spaces and one developed a focal low density area suggesting disturbances in brain blood circulation and also experienced disturbances in level of consciousness. Of the 19 IR or HR patients, eight developed changes related to the therapy, including four with white matter hypodensity areas, of whom three also had enlarged CSF spaces, and four others who developed enlarged CSF spaces. The medians of the widths of the cortical sulci (P less than .001), insular cisterns (P less than .01), third ventricles (P less than .01), and frontal horns (P less than .05), and also of Evans' ratios (P less than .05) increased significantly after CNS therapy as compared with the findings at diagnosis in the patients who had received cranial irradiation. Most of these changes persisted during the follow-up. We conclude that the clinical value of CT scanning during therapy for ALL is restricted to patients with neurological symptoms or those who have undergone CNS irradiation.
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PMID:Cranial computed tomographic findings in children with newly diagnosed acute lymphoblastic leukemia: a prospective follow-up study during treatment. 160 48

The inhibitory effects of two anionic compounds, Evans blue and aurintricarboxylic acid (ATA), on various kinds of polynucleotide-synthesizing enzymes were examined. Under the assay conditions, optimized for each enzyme species, both these compounds strongly inhibited the activities of the purified human DNA polymerases alpha, beta, gamma, and DNA primase as well as those of DNA polymerase I and RNA polymerase from Escherichia coli and Rauscher leukemia virus reverse transcriptase. ATA was particularly effective in inhibiting retroviral reverse transcriptase and cellular DNA polymerase alpha. Evans blue, which is a structural analogue of suramin, exerted its inhibitory action largely by competing with the template.primer for the same binding site of the enzyme. On the other hand, ATA inhibited most, if not all, of these enzyme activities noncompetitively with respect to either the template.primers or nucleoside 5'-triphosphate substrates. The inhibition constants for ATA were, in general, smaller than those for Evans blue.
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PMID:Differential inhibition of various deoxyribonucleic acid polymerases by Evans blue and aurintricarboxylic acid. 246 Mar 49

The presence and numbers of C-type virus particles in an animal model consisting of mice and rats with either spontaneous or virus-induced leukemia and lymphomas were studied, in order to determine the relation of the appearance of virus particles to viral etiology of such neoplasms. The numbers and distribution of C-type virus particles in organs from 13 mice with spontaneous leukemia and lymphomas were compared with the presence of virus particles in organs of 13 mice with leukemia and lymphomas induced by passage A (Gross) virus inoculation. C-type virus particles were present in organs of all mice with either spontaneous leukemia or leukemia and lymphomas induced by virus inoculation. However, the number of particles observed was significantly higher in those mice in which leukemia was induced by virus inoculation. Virus particles were also observed, but in substantially smaller numbers, in organs of 13 of 25 untreated, healthy mice of the nonleukemic C3H(f) inbred line. In contrast to mice, C-type, or any other virus particles, were not found in organs of 10 Sprague-Dawley, Long-Evans or Sprague-Dawley X Long-Evans F1 hybrid rats with spontaneous leukemia. However, C-type virus particles were consistently present in organs of 11 Sprague-Dawley rats with leukemia induced by rat-adapted passage A (Gross) mouse leukemia inoculation. The virus particles appeared in the organs of the inoculated rats 5 days after i.p., and 11 days after s.c. inoculation. Virus particles were not found in organs of 10 healthy untreated Sprague-Dawley rats. The implications of these observations are discussed.
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PMID:C-type virus particles in spontaneous and virus-induced leukemia and malignant lymphomas in mice and rats. 300 6

The antileukemic potency of the alkyllysophospholipid, 1-octadecyl-2-methoxy-rac-glycero-3-phosphocholine (Et-18-OCH3) and of the retinoid etretinate was examined alone and in combination in 7,12-dimethylbenz-anthracene(DMBA)-induced Long-Evans (LE) rats. Lifelong administration of Et-18-OCH3 at a dose of 20 mg/kg per day slightly but significantly reduced the incidence of leukemias and thereby significantly prolonged the life span of animals. The best effect was seen when treatment started at day 58 of life, i.e. 1 day after the third of 4 DMBA injections (P = 0.0001). Administration of etretinate, however, at a dose of 5 mg/kg did not show any efficacy against leukemia development. The combination of both agents reduced the incidence of mammary neoplasias only (P = 0.04).
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PMID:Protection by the alkyllysophospholipid, 1-octadecyl-2-methoxy-rac-glycero-3-phosphocholine, but not by the retinoid etretinate against leukemia development in DMBA-treated Long-Evans rats. 308 Feb 26

Oncogene activation induced by chromosomal changes is now regarded as one of the most important phenomena during carcinogenesis. We have reported c-abl activation in a rat leukemia cell line K3D, caused by a secondary chromosomal translocation. Another erythroblastic leukemia cell line D5A1, originally derived from a leukemia induced by 7,12-dimethylbenz(a)anthracene (DMBA) in a Long-Evans rat, is characterized by a marker chromosome 1q+, which also probably occurred as a secondary change. In this cell line, the transcription level of Ha-ras related mRNA increased compared with other cell lines. By the in situ hybridization technique, the c-Ha-ras locus was assigned to 1q43 and the breakpoint 1q+. Because the breakpoint was so near the c-Ha-ras locus on the chromosome, the present system may provide a model of activation of the c-Ha-ras gene brought about by chromosomal translocation.
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PMID:Chromosome marker and enhanced expression of c-Ha-ras in a DMBA-induced erythroleukemia cell line (D5A1). 311 19

The influence of 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) and 1-hexadecylmercapto-2-methoxymethyl-rac-propyl-3-phosphocholine (TLP, BM41.440) on methylnitrosourea (MNU)-induced rat mammary carcinomas and of ET-18-OCH3 on 7,12-dimethylbenzanthracene (DMBA)-induced leukemias was investigated. Both agents effectively delayed MNU-induced mammary tumor formation at high, cytotoxic dosages but TLP had no influence at low "immunomodulatory" doses. ET-18-OCH3 also significantly protected against leukemia development in DMBA-treated Long-Evans rats.
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PMID:Modulation of chemical carcinogenesis in rats by alkyl lysophospholipids. 312 47

Sudan III treatment of Long-Evans rats results in increased hepatic monooxygenase activity using ethoxycoumarin and aniline as substrates. Monooxygenase activity towards amino-pyrine and nitrosodimethylamine is not affected. Sudan III treatment results in increased microsomal cytochrome P448 and increased amounts of a protein band which comigrates with purified cytochrome P448 during SDS polyacrylamide gel electrophoresis. The proportions of the different dihydrodiols formed during the incubation of 7,12-dimethylbenz[a]anthracene with microsomes vary between untreated and treated animals. Thus, extracts of microsomes from untreated rats were found to contain materials with chromatographic properties identical to those of the 3,4-dihydrodiol and the 5,6-dihydrodiol when examined on two different h.p.l.c. systems. Extracts of microsomes from Sudan III treated animals were found to contain materials with chromatographic properties identical to those of the 5,6-dihydrodiol and the 8,9-dihydrodiol when similarly examined. These findings suggest that the protective effect of Sudan III against DMBA induced leukaemia is mediated by an alteration in monooxygenase activity.
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PMID:Alterations in the metabolism of 7,12-dimethylbenz[a]anthracene and various xenobiotics by rat hepatic microsomes following Sudan III treatment in vivo. 391 57

Administration of propylnitrosourea p.o. by our protocol induced a high incidence of hematolymphatic neoplasms in all six rat strains studied. Remarkable strain differences in susceptibility to thymic lymphomas were observed. The incidence of thymic lymphomas was high in Fischer 344 (98%) and Wistar/Furth (71%) but low in Sprague-Dawley (29%), ACI/Ms (23%), Donryu (24%), and Long-Evans (10%) strains. Segregation of thymic lymphoma incidence among crosses between highly susceptible Fischer and poorly susceptible Long-Evans rats indicated that the increased susceptibility to thymic lymphomas of Fischer rats was determined by a dominant gene TIs-1 (thymic lymphoma susceptible) and that this gene was linked to the coat color loci, p and c, in Linkage Group I in the order of TIs-1 - c - p. The presence of another independently assorting dominant gene, TIs-2, was also suggested to accelerate the thymic lymphoma-genesis. Expression of the group-specific antigen of murine leukemia virus as well as infectious viruses was not detected in nine propylnitrosourea-induced thymic lymphomas of Fischer rats.
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PMID:Genetically determined susceptibility of Fischer 344 rats to propylnitrosourea-induced thymic lymphomas. 397 15

A series of pulse-doses of 7, 8, 12-trimethylbenz(a)anthracene-induced leukemia rapidly and consistently in very high yield in rats of Long-Evans (L-E) strain. The predominant type was a diffuse hepatic leukemia of erythroblastic stem cells. Progressive hypothermia and a decline in pituitary function are newly recognized signs of advanced leukemia in rat.
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PMID:Hundred day leukemia: preferential induction in rat by pulse-doses of 7,8,12-trimethylbenz(a)anthracene. 541 51

Eight cultured lines with a normal diploid karyotype, no. 2 trisomy, and markers involving chromosome No. 2 were established from three 7,12-dimethylbenz[a]anthracene (DMBA)- and two N-butyl-N-nitrosourea (BNU)-induced erythroblastic leukemias in noninbred Long-Evans rats. Serial in vivo and in vitro passage of these cells frequently evoked karyotype changes in stemline cells. In both lines from DMBA- and BNU-induced leukemias, ordinary and translocation no. 2 trisomy cells appeared and gradually replaced the normal diploid stemline cells. Obvious secondary karyotypic changes were also recognized in the "cloned" leukemia cells. Nucleolar chromosomes such as chromosomes no. 3 and no. 12 were frequently involved in aneuploidy and translocation. One cell line from a BNU-induced leukemia did not change its normal diploid karyotype during 12 months of in vitro passage. The above preferential growth of cells with no. 2 trisomy and the related changes during in vivo and in vitro passage as well as in-colony formation in soft agar suggest that these chromosome changes are somehow associated with the growth behavior of the leukemia cells. No positive correlation was demonstrated between karyotype and dimethyl sulfoxide-induced erythroid differentiation of the leukemia cells.
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PMID:Establishment and chromosome studies of in vitro lines of chemically induced rat erythroblastic leukemia cells. 676 14


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