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)

Isoelectric focusing (IEF) in horizontal polyacrylamide gels has been used to separate lactate dehydrogenase (LDH) isoenzymes in 97 human permanent hematopoietic cell lines (85 leukemia-lymphoma cell lines and 12 'normal' B-lymphoblastoid cell lines). Maximally 8 LDH bands were seen; the electrophoretically detectable bands 4 and 5 could be separated by IEF into 2 and 3 isoenzymes, respectively. The LDH patterns have been found to vary both in number of isoenzymes and in relative intensity in different cell lines depending upon the stage at which arrest of differentiation occurred. These differences can be used to analyse and distinguish different cell lines. The method should provide a valuable supplement to the enzymatic phenotyping and complete characterization of fresh and cultured leukemias and for the monitoring of phenotypic changes occurring during induction of differentiation.
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PMID:Isoenzyme studies in human leukemia-lymphoma cell lines--IV. Lactate dehydrogenase. 387 28

Neoplastic thymocytes from rat thymic lymphoma-leukemias induced by the rat-adapted Gross leukemia virus (RAGV) were analyzed for a variety of differentiation markers. The neoplasms from individual rats all expressed the antigenic phenotype MP+, W3/13+, Thy-1+, RT-1+, RT-7+, W3/25-. However, approximately two-thirds of the neoplasms were positive for the OX 8 antigen, and one-third were negative. The OX 8- neoplasms only involved the thymus, whereas approximately 40% of the OX 8+ neoplasms involved the spleen as well as the thymus. Virtually all OX 8+ and OX 8- neoplastic cells contained terminal deoxynucleotidyl transferase (TdT), and both OX 8+ and OX 8- lymphomas expressed the lactate dehydrogenase (LDH)-5' isozyme and the primary, but not the secondary, ADA isozyme. This enzymatic phenotype is characteristic of thymocyte precursors, but not thymocytes. Our results therefore indicate that RAGV-induced lymphomas arise from transformed prethymic TdT+ cells which contain the LDH-5' and the primary ADA isozymes. These preleukemic cells presumably migrate to the thymus where they express the RT-7 pan-T-cell antigen and, in some instances, the OX 8 antigen during the development of overt leukemia. The OX 8+ neoplasms, being more differentiated than their OX 8- counterparts, then migrate to peripheral lymphoid tissues.
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PMID:Phenotypic heterogeneity of Gross virus-induced thymic lymphomas in the rat: cellular origins and migratory properties. 387

The hemadsorption-negative plaque test has revealed a new type of viral interference, termed intrinsic interference. Several unrelated types of noncytopathic viruses were shown to induce in infected host cells a state of interference unique in being directed solely against superinfection by Newcastle disease virus (NDV). The NDV-refractory state arises only in those individual cells of a population actually infected by the inducing virus, and presumably results from the action of a protein(s) coded for by the viral genome. Thus, intrinsic interference differs fundamentally from that mediated by an extrinsic protein detectable under conditions favoring resistance to a broad spectrum of viruses and characteristic of interference induced by interferon, the latter being coded for by the cell genome. Intrinsic interference is defined as a viral genome-induced cellular state of resistance to challenge by high multiplicities of NDV, coexistent with a state of susceptibility to a broad spectrum of other viruses, similarly tested at high multiplicities. The capacity to induce intrinsic interference was demonstrated with rubella virus, Sindbis virus (arbovirus, group A), West Nile virus (arbovirus, group B), poliovirus (MEF, type 2), the lactic dehydrogenase virus (Riley's agent), and an unidentified nonhemadsorbing, noncytopathic adventitious virus. A state of intrinsic interference was also observed in the V5 line of mouse cells carrying a murine leukemia virus, probably resulting from some heretofore unsuspected contaminating virus. The molecular basis for intrinsic interference is not known, but it appears to involve a step in the NDV growth cycle beyond that of viral attachment, entry, and eclipse.
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PMID:Intrinsic interference: a new type of viral interference. 431 51

Profound changes in the level of certain dehydrogenase enzymes were observed in lymphoid tissues of rats involved by erythroblastic stem cell leukaemia. In lymphoid tissues free of leukaemic involvement, activity of malate dehydrogenase (MDH) always exceeded that of lactate dehydrogenase (LDH). In those which contained substantial infiltrates of leukaemic cells, activity of LDH was increased while MDH activity was reduced. In leukaemic spleen significant changes were observed in the molecular forms of LDH; the proportion of LDH-5 (muscle-type LDH) was greatly increased while the other molecular forms were reduced. The spleen of rats with leukaemia exhibited a marked increase in the normal level of aerobic and anaerobic glycolysis but the rate of respiration was unchanged.The terminal stages of stem cell leukaemia in the rat are characterized by wide-spread leukaemic infiltration of liver and other tissues. Lymph node involvement, however, was found to be selective. Coeliac lymph nodes greatly exceeded other lymph node groups in their incidence of leukaemic involvement. It is considered that the selective nature of lymph node involvement in stem cell leukaemia derives from topographical considerations.
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PMID:Leukaemia evoked with 7,8,12-trimethylbenz(a)anthracene in rat. 3. Changes in lymphoid tissues. 508 76

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

Inoculation of Ehrlich ascites carcinoma cells (EAC) into the peritoneal cavities of outbred ddY mice induced interferon (IFN) in the circulation. The maximum titer (1,280 U) was obtained at 24 hr after inoculation. This induced IFN had the characteristics of type I IFN, i.e., stability at pH2 and lability at 56 C. An increase in natural killer cell (NK) activity was also observed for the first 3 days after inoculation. In addition, plasma lactate dehydrogenase (LDH) activity was elevated in these mice. Inoculation of ascitic fluid or serum of EAC-bearing mice into normal mice increased plasma LDH activity six- to sevenfold over normal levels and elevated activities persisted throughout the life of the mice. These results suggest that the LDH-elevating agent was responsible for IFN induction and for enhancing NK activity. Because lactate dehydrogenase-elevating virus (LDV) can be eliminated from tumor cells by passage in vitro, we attempted to grow EAC in tissue culture for several months and re-examined whether the inoculation of such cells could elevate plasma LDH activity induce IFN and enhance NK activity. The results showed that inoculation of the passaged cells had no effect on these activities in normal mice. Therefore, we concluded that the IFN inducer was LDV which contaminated the EAC and then enhanced the NK activity. N-tropic murine leukemia virus also contaminated EAC, but this virus was not responsible because cultured cells of EAC still shed this virus.
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PMID:Lactate dehydrogenase-elevating agent is responsible for interferon induction and enhancement of natural killer cell activity by inoculation of Ehrlich ascites carcinoma cells into mice. 616 92

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly, but flared up after several years. Skin lesions appeared in the form of erythema, papules, or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was 0%-2%. The serum lactate dehydrogenase (LDH) value was within normal range and was not associated with hypercalcemia; lymphadenopathy, hepatosplenomegaly, and bone marrow infiltration were very slight. In most cases, hypergammaglobulinemia was seen, and in one case, monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their anti-ATLA antibodies were positive; none had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness and died of cryptococcus meningitis. Based on clinical and pathologic differences, we believe that these cases should be distinguished from typical ATL cases for the purposes of prognosis and treatment.
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PMID:A proposal for smoldering adult T-cell leukemia: a clinicopathologic study of five cases. 622 22

Five cases of adult leukemia with L3 morphology in bone marrow were studied for the presence of immunologic, metabolic, and enzymatic markers. Among the five patients, there were four males and female. Median age was 66 with a range of 16-80 yr. Median survival was only 5 mo. Serum lactate dehydrogenase (LDH) levels, 3H-thymidine labeling indices, and DNA/RNA content of the L3 lymphoblasts were markedly elevated. B-cell markers were found in three cases, two exhibiting surface membrane IgM-lambda, and one IgG-K. Terminal deoxynucleotidyl transferase (TdT) enzymatic activity was consistently low in this group. In one case, the L3 lymphoblasts displayed only surface Fc receptors demonstrated by the binding of aggregated IgG. TdT activity was found to be significantly increased. In another instance, the lymphoblasts formed spontaneous rosettes with sheep erythrocytes and exhibited paranuclear staining with acid phosphatase. TdT activity was found to be low. Although most of the L3 leukemias are neoplasias of B lymphocytes, other lineages may also express this morphology.
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PMID:Heterogeneity of cell lineages in L3 leukemias. 624 17

Intraperitoneal injection of neuropathogenic strains of lactic dehydrogenase virus (LDV) causes a histologically distinctive fatal paralytic disease characterized by an inflammatory destruction of motor neurones in the brain stem and cord in C58 mice aged over 9 months. To elicit the disease in the naturally susceptible C58 strain requires an age-associated or X-ray induced loss of immunological competence, LDV infection and genetic susceptibility. Genetic studies of the common inbred mouse strains showed that susceptibility to the disease was not linked to the major histocompatibility complex but correlated with the FV-1n allele, susceptibility to spontaneous leukaemia, and infection by neuropathogenic strains of LDV. These observations suggested that neuropathogenic strains of LDV elicit the disease only in those strains of mice that carry multiple copies of N-tropic C-type retroviruses in their genomes and that are permissive for retrovirus replication. Presumably the expression of these viral genomes (high titres of virus in tissues correlating with age) is the important factor. Here we present genetic evidence to support this hypothesis and briefly discuss the possible implications.
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PMID:Co-infection by lactic dehydrogenase virus and C-type retrovirus elicits neurological disease. 625 63

During the course of serial passage of 50 human xenografts in the athymic mouse over a period of 5 years we have observed two cases of induction of sarcomas in the murine stromal tissue associated with the human xenografts. Both times the growth of the murine sarcomas overtook that of the human xenograft. This change was monitored by analysis of the lactate dehydrogenase isozyme profile and histology of each passage of the human xenografts in the athymic mice. The two murine sarcomas were subsequently established in tissue culture. The sarcoma cell lines were found to be malignant by morphological and growth characteristics and were tumorigenic. They contained large amounts of murine leukemia virus when assayed for reverse transcriptase activity by infection of mouse SC-1 cells and BALB/c and NIH Swiss fibroblasts with filtered supernates, and some type C virus particles were observed by electron microscopy in tumor tissues. However, we were unable to demonstrate the presence of murine sarcoma virus by in vitro transformation of fibroblasts or sarcoma formation in vivo will cell free filtrates. Preliminary biochemical data indicate that the sarcomas are extremely high in plasma membrane ATP phosphohydrolase.
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PMID:Induction of sarcomas in athymic mice. 628 53


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