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)

L-Asparagine synthetase appears in serum approximately 7 days after the s.c. implantation of 1 X 10(5) cells of Leukemia 5178Y/AR (resistant to L-asparaginase) and increases in activity as the neoplasm grows and metastasizes. The principal source of the enzyme is the primary tumor. After intravranial inoculation of tumor, the rate of leakage of the enzyme is more pronounced than when the subcutaneous, intramuscular, or intraperitoneal routes are used. 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (NSC 79037), a nitro-sourea effective in the palliation of L5178Y/AR, temporarily halts the influx of enzyme into the blood stream, as does surgical excision of the s.c. tumor nodules. Treatment of mice with L-asparaginase within 24 hr of inoculation of the tumor markedly augments both tumor growth and the rate of penetration of L-asparagine synthetase into the circulation. Several other L-asparagine synthetase into the circulation. Several other L-asparaginase-resistant tumors also were found to spill L-asparagine synthetase into the serum, but the correlation between this phenomenon and the specific activity of the enzyme in homogenates of the tumor was imperfect.
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PMID:L-Asparagine synthetase in serum as a marker for neoplasia. 1 81

Cells of a transplantable lymphoid leukemia of mice were tested in vivo and in vitro to see which features of normal lymphoid cells were retained in spite of malignant transformation and lack of growth control. Leukemia cells phagocytosed, adhered to glass, possessed receptors for immunoglobulin, participated in the immune response against SRBC (probably by amplifying a normal response through attachement of antibodies on their surfaces), became recruited into inflammatory reactions elicited by grafting allogeneic of syngeneic skin, and apparently joined graft-versus-host and host-versus-graft reactions, contributing toward damage of hemopoietic target tissues.
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PMID:Participation of leukemia cells in immune responses. 1 44

Aminomalonic acid is a strong in vitro inhibitor of L-asparagine synthetase from Leukemia 5178Y/AR and from mouse pancreas; the agent is formally competitive with L-aspartic acid (Ki = 0.0023 M and 0.0015 M for the tumoral and pancreatic enzymes, respectively). Since aminomalonic acid is unstable and inert in vivo as an inhibitor of L-asparagine synthetase, attempts were made to deliver it to the site of its intended action via precursors: the diamide (2-aminomalonamide), the diester (diethylaminomalonate), and the keto acid (ketomalonic acid). Each of these putative 'pro drugs' was shown to be susceptible to metabolism to aminomalonate by mammalian and bacterial enzymes, in vitro. In vivo, aminomalonamide failed to inhibit tumoral L-asparagine synthetase at any time period up to 24 h after its oral or intraperitoneal administration. The diester and keto acid were similarly inactive. However, with specialized techniques it was possible to demonstrate that the diamide significantly inhibited the amidation and/or incorporation of L-aspartic acid into the L-asparaginyl residues of protein. Chemical manipulations of aminomalonic acid aimed at introducing irreversibly reacting functions are warranted.
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PMID:Aminomalonic acid and its congeners as potential in vivo inhibitors of L-asparagine synthetase. 3 46

In transplantable and in spontaneous lymphoblastic mouse leukemia blood pH, PCO2, TCO2 and BB were examined. Spontaneous Gross-leukemia in AKR mice was found to develop in its final phase respiratory acidosis. Transplantable (TAL) leukemia of AKR mice presents from the onset a tendency toward respiratory acidosis. "L-1210"-leukemia, on the contrary, was shown to alcalise the recipients during the first 8 days after inoculation, later on it can bring about an acidosis. The pH-deviations in "L-1210"-leukemia display a respiratory character in syngeneic DBA/2J recipients, whereas in semiallogeneic recipients the observed changes are metabolic or mixt in nature. This finding strongly argues for the importance of histocompatibility. Intranodally inoculated animals distinctly differ in their parameters in comparison to intravenously and intraperitoneally recipients, hence, an important role of the tissular-milieu which is put first in contact with the leukemic factor must be concluded.
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PMID:[The acid-base equilibrium during mouse lymphoblastic leukemia]. 6 8

Hyperferritinemia in various diseases, mainly hematological, was confirmed by immunological methods. For ferritin detection, anti-human placental ferritin antiserum, anti-human hepatic ferritin antiserum, and anti-human leukemia cell ferritin antiserum were used and the result was compared with each other. Leukemia, malignant lymphoma, multiple myeloma, and aplastic anemia are hematological diseases which showed a positive reaction in this test, among which leukemia showed the highest positivity. Cases of hepatic diseases and non-hematological malignant neoplasms also showed a positive reaction. The positivity was quite low and almost negligible in other diseases and healthy individuals. Anti-human placental ferritin antiserum seemed to be suitable for cancer diagnosis and, antihuman hepatic ferritin antiserum for hepatic diseases. The results of analysis of purified human hepatic and placental ferritins highly suggested the presence of immunological heterogeneities between them. Also, a possibility was pointed out that one of the components of the so-called leukemia-specific antigens might sometimes be the isoferritin of leukemia cells.
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PMID:Immunological heterogeneity in human ferritinemia. 6 5

Short term cultures of bovine leukemic lymphocytes release virus particles with biochemical properties of RNA oncogenic viruses. These particles, tentatively called Bovine Leukemia Virus (BLV) have a high molecular weight-reverse transcriptase complex and a density averaging 1.155 g/ml in sucrose solutions. Molecular hybridizations between BLV-3H cDNA and several viral RNAs show that BLV is not related to Mason-Pfizer Monkey Virus (MPMV) Simian Sarcoma Associated Virus (SSV-1) Feline Leukemia Virus (FeLV) or Avian Myeloblastosis Virus (AMV). Rauscher Leukemia Virus (RLV) exhibits a slight but reproducible relatednesse to BLV. The high preference of BLV reverse transcriptase for Mg++ as the divalent cation suggests that BLV might be an atypical mammalian leukemogenic type C virus. Hybridization studies using BLV 3H cDNA as a probe suggest that the DNA of bovine leukemic cells contains viral sequences that cannot be detected in normal bovine DNA.
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PMID:Bovine leukemia virus: an exogenous RNA oncogenic virus? 6 82

The still increasing amount of carriers and anemics by thalassemia (Th) and other Hb-pathies (approximately 4,000 among approximately 48,000 investigated people) have shown that Campania is the most affected world area by all Hb Lepre conditions. Among 161 people with heterozygous Hb Lepore we have noticed 10 cases associated with (hemo-) blastomata as follows: 2 Chr. Lymphatic Leukemia, 2 Ac. Lymphoblastic Leukemia, 1 Lymphosarcom, 1 Colon Cancer, 1 Uterin Cancer, 1 Plasmocytom, 1 Hodkgin Disease, 1 Ac. Promyelocyte Leukemia (or fatal ac. agranulocytemia?). In the literature we recently found 2 other similar cases. The incidence of such malignancies in our Hb Lepore people reaches 6%. On the contrary in the heterozygous Th. group, among 3,150 carriers, we diagnosed only 20 people with (hemo-) blastomata as follows: 12 Ac. Leukemia (9Lymphoblastic) and 8 Chr. Myeloid Leukemia, with an incidence rate of 0.6% namely a little higher than in normal people. This highly significant discrepancy rate shows an elective predisposition to (haemo-) blastomata from Leporian people.
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PMID:Hb Lepore and (haemo-) blastomata. 6 34

The majority of human lymphocytic and myelocytic leukemia cells express a polymorphic antigen that is found on peripheral blood B-lymphocytes and cultured lymphoblastoid B-cell lines. These B-lymphocyte antigens were detected by 34 human alloantisera that were repeatedly absorbed with pooled platelets to remove all activity against HLA antigens and T-lymphocytes. Absorption studies indicated that a common antigen was present on both B-lymphocytes and positive leukemia cells. Leukemia cells could be subdivided into two groups based on the presence of the B-lymphocyte antigen. Fourteen of 18 acute myelocytic leukemia cells, 10 of 13 acute lymphoblastic leukemia cells, 4 of 6 chronic myelocytic leukemia cells, and 2 of 2 chronic lymphocytic leukemia cells were positive. This group of leukemia cells also reacted with rabbit anti-B-cell sera raised to papain digests of spleen cell membranes. F(ab')2 fragments of the rabbit antsera were shown to specifically block the reactions of the human antisera against B-cells and leukemia cells. These results suggested that the rabbit and human anti-B-cell sera were reacting with identical molecules. This conclusion was supported by immunoprecipitation data.
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PMID:Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. II. Detection by human anti-B-cell alloantisera. 6 14

Leukemia cells from 13 of 27 patients stimulated lymphocytes of their HLA-identical siblings in mixed leukocyte cultures (MLC). Stimulation correlated with high background uptake of tritiated thymidine and high percentages of cells that stained with fluorescein-conjugated polyvalent goat antiserum against human immunoglobulin. Results were similar to those reported with fractionated autologous lymphocyte subpopulations in normal individuals. Investigation of leukemia-specific stimulation in MLC is therefore problematic.
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PMID:Relationship between leukemia antigens and stimulation in mixed leukocyte culture. 6 37

cis-Platinum diamminodichloride has been studied in combination with 2,2'-anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine on an every-4-day schedule in various lines of mouse leukemia. This combination is synergistic in leukemias L1210 and P388 and sublines made resistant to 5-fluorouracil or methotrexate. There is no cross-resistance between cis-platinum diamminodichloride and 2,2'-anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine, but the combination is no more effective against lines of leukemia made resistant to cis-platinum diamminodichloride or to 2,2'-anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine than either single active compound alone. Since these compounds have no cross-resistance, act by quite different mechanisms of action, and have different limiting toxicity, the combination is now being evaluated clinically.
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PMID:Synergistic effects of the combination of cis-platinum diamminodichloride and 2,2'-anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine in transplanted mouse leukemias. 7 Dec 4


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