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)

An early sign of erythroblastic leukemia in rat was nodule formation in the spleen. Hyperplastic foci of stem cells, indistinguishable histologically from leukemic stem cells, were found in the red pulp whereas the malpighian corpuscles were uninvolved. Anemia is a normal phenomenon in immature rats and the spleen of the prepubertal rat possesses considerable hemopoietic potential. Pulse-doses of 7, 8, 12-trimethylbenz(a)anthracene prevented the physiologic hematological development of maturing rats and was associated with subsequent development of leukemic stem cells in the red pulp of the spleen. Significant enzyme changes were observed in leukemic spleens. Compared with the spleens of normal littermates, the concentration of lactate dehydrogenase rose while that of malate dehydrogenase fell; the content of alkaline phosphatase rose whereas acid phosphatase fell. Increased alkaline phosphatase activity in leukemic spleen was attributed to nonleukemic foci of myelopoiesis.
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PMID:Leukemia evoked with 7,8,12-trimethylbenz(a)anthracene in rat. I. Changes in spleen and thymus. 528 70

The incidence of chromosome aberrations in rat bone marrow, examined 6 hr after the administration of 7,12-dimethylbenz(a)anthracene, was significantly enhanced by induction of anemia 0-48 hr before the carcinogen treatment and was suppressed by induction of polycythemia. The suppressive influence of polycythemia was reversed by sheep erythropoietin injected shortly before or after the carcinogen injection; this suppressive effect was proportional to the dose of erythropoietin used. These data suggest that erythropoietin is essential to make bone-marrow cells susceptible to chromosome aberrations with 7,12-dimethylbenz(a)anthracene. The incidence of carcinogen-induced leukemia was also increased by anemia and suppressed by polycythemia induction.
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PMID:Role of erythropoietin in 7,12-dimethylbenz(a)anthracene induction of acute chromosome aberration and leukemia in the rat. 528 53

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

Lymphoid leukemia induced by 7,12-dimethylbenz(alpha)anthracene (DMBA) in rats and maintained by serial intraperitoneal transplantations in newborn rats was subjected to immunological and enzymological characterization. The Thy-1 antigen positivity rendered evidence for the T cell origin of the leukemia studied. Expression of cell surface complement binding receptors and patterns of cytoplasmic acid phosphatase and nonspecific acid alpha-naphthyl acetate esterase enzymes drew the attention to the dominance of lymphoblasts and prolymphocytes.
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PMID:Rat lymphoid leukemia of T cell type induced by 7,12-dimethylbenz(alpha)anthracene. Immunological and enzymological characterization. 612 12

G-banding analysis was carried out on T-cell leukemias induced in various Robertsonian mice by 7,12 dimethylbenz(a)anthracene (DMBA), N-methyl-N-nitrosourea (MNU), or Moloney virus. Trisomy 15 was the only regularly seen chromosome aberration whether chromosome No. 15 was involved in a centric fusion or not. Translocated No. 15 chromosomes were not preferentially duplicated. These results show that it is not the translocated state of chromosome No. 15 but the genetic content that is of importance in leukemia development.
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PMID:Robertsonian translocation studies on the significance of trisomy 15 in murine T-cell leukemia. 640 48

In the experimental rat leukemia system, induced by repeated 7,12-dimethylbenz(a)anthracene (DMBA) pulses, the sensitivity of the spleen colony-forming hematopoietic stem cells (CFU-s) to the cytocidal action of a challenging DMBA injection (35 mg/kg body weight) varied with the number of pulses already applied and the organ source of CFU-s (femoral bone marrow or spleen). Assessment of the fraction of DNA-synthesizing CFU-s with the [3H]thymidine suicide technique at the time of DMBA challenge and comparison with the 20-hr CFU-s reduction values by DMBA in vivo showed an inverse correlation (p less than 0.001). It was deduced, therefore, that S-phase CFU-s are relatively resistant to DMBA cytocide. Since initiation by chemical carcinogens has been shown to be relatively S-phase specific, S-phase-resistant cytocide would lead to a selection of initiated cells and, in the case of repeated applications, to a selection of cells with multiple successive initiation hits. Preferential differentiation and organ site of leukemia, as well as evolution in sequential morphological steps, fit this assumption.
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PMID:S-phase resistance of rat hematopoietic stem cells to 7,12-dimethylbenz(a)anthracene cytocide and its implications for leukemia development. 643 May 52

In mice, there is a correlation between genetically regulated levels of inducible aryl hydrocarbon hydroxylase (AHH) activity and the risk of polycyclic hydrocarbon-induced leukemia or solid tumors. Recent clinical studies suggest a relationship between high AHH activity and lung cancer associated with cigarette smoking (Kouri, R.E., McKinney, C.E., Slomiany, D.J., Snodgrass, D.R., Wray, N.P., and McLemore, T.L. Cancer Res. 42: 5030-5037, 1982). To determine whether there is a similar genetic relationship in humans between inducible AHH and the occurrence of pediatric cancers, we examined AHH activity in mitogen-stimulated benzo(a)anthracene-treated lymphocyte cultures from primary relatives of children with leukemia or solid tumors. Control families (parents and siblings with no history of cancer) comprised friends or neighbors of the proband families. By comparing variance among family members with variance among nonrelated individuals, we conclude that a small, but real, genetic component is detectable. Adjusting for age, smoking history, and the length of time during which the lymphocytes had been cryopreserved, however, we find no difference among 77 leukemia, 71 solid tumor, and 100 control family members with regard to median units (+/- median S.E.) of maximally induced AHH activity per unit of reduced nicotinamide adenine dinucleotide-cytochrome c reductase activity: 0.31 +/- 0.03; 0.28 +/- 0.03; and 0.28 +/- 0.03, respectively. Thus, benzo(a)anthracene-induced AHH activity in cultured mitogen-activated lymphocytes in our study population does not appear to be associated with the risk of occurrence of childhood leukemia or solid tumors.
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PMID:Aryl hydrocarbon hydroxylase inducibility among primary relatives of children with leukemia or solid tumors. 669 48

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

9,10-Anthracenedicarboxaldehyde bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone] (bisantrene, VI-1) showed anticancer activity in mice vs. both leukemias and solid tumors. Increases in life span vs. the following neoplasms were: P-388 leukemia, 137%; B-16 melanoma, 122%; Lieberman plasma cell tumor, greater than 85%; colon tumor 26, 150%; Ridgway osteogenic sarcoma, 85%. There were significant numbers of long-term survivors. Both DNA and RNA synthesis were strongly inhibited. The drug was resistant to biodegradation and was bound strongly to tissues; in monkeys the half-life for disappearance from serum was 6 days. Related hydrazones were synthesized, and structure-activity relationships are discussed. Two routes to ring-substituted anthracene-9,10-dicarboxaldehyde intermediates were developed.
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PMID:Antitumor agents. 2. Bisguanylhydrazones of anthracene-9,10-dicarboxaldehydes. 680 75

The experimental induction of leukemias of two sorts by two powerful chemical carcinogens was investigated in rats of a single strain. In Sprague-Dawley rats a series of intravenous injections of N-nitroso-N-methylurea selectively elicited myelogenous leukemia in high yields, whereas erythroleukemia was not evoked. Conversely, a set of intravenous injections of 7,8,12-trimethylbenz[a]anthracene specifically elicited erythro-leukemia in high incidence in the rats, whereas myelogenous leukemia was not produced.
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PMID:Specific induction of erythroleukemia and myelogenous leukemia in Sprague-Dawley rats. 681 59


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