Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LP-BM5 murine leukemia virus (MuLV) induces an immunodeficiency syndrome (MAIDS) in C57BL/6 mice which resembles immunological abnormalities observed in early stages of human AIDS. In our study, MAIDS virus-infected mice were exposed to low doses of ultraviolet radiation (UVR) before and after virus inoculation and compared with MAIDS-infected but not UVR-exposed mice. In all tested parameters (blood IgM levels; mitogenic responses to PHA, ConA, LPS and anti-mu; MLR; antigenic response to SRBC; enlargement and histopathologic changes of the spleen) we observed the same trend: changes due to MAIDS infection were more pronounced in the UVR-exposed group than in the unexposed group. Statistically significant differences between these two groups were seen for mitogenic responses at two different time points after virus inoculation. These results demonstrate that in vivo UVR exposure enhances the immunosuppressive effects of a retroviral infection. UVR exposure may affect the progression of AIDS in a similar manner.
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PMID:In vivo exposure to ultraviolet radiation enhances pathogenic effects of murine leukemia virus, LP-BM5, in murine acquired immunodeficiency syndrome. 133 87

Phosphatidylinositol-specific phospholipase C (PI-PLC) is an enzyme that has the capacity to release glycosyl-phosphatidyl inositol (G-PI)-anchored proteins from the cells surface. Pretreatment of the human T-cell leukemia cell line Molt-4 with PI-PLC resulted in a decrease in the susceptibility to lysis by natural killer (NK) cells. Treatment of the erythroleukemia cell line K562 with PI-PLC had no effect on its NK susceptibility. PI-PLC-treated and untreated Molt-4 bound equally well to lymphocytes in target-binding studies with effector cell preparations enriched for NK cells. Susceptibility to cytolytic granules isolated from rat LGL tumor cells remained the same after treatment of Molt-4 or K562 with PI-PLC. Combined treatment of Molt-4 with PI-PLC and rlFN-alpha or rlFN-gamma resulted in additive reductions of the NK susceptibility, suggesting that PI-PLC and interferons act on different mechanisms to protect cells from NK lysis. When expression of a number of antigens on Molt-4 and K562 was analyzed in flow cytometry, only the expression of CD58 was reduced after PI-PLC treatment. The susceptibility of Con A blasts to MLR derived cytotoxic T-cells was not altered by treatment with phospholipase. These data suggest that PI-PLC treatment reduces the capacity of some target cells to activate NK cells upon contract. The mechanism behind this phenomenon is presently unclear.
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PMID:Phospholipase C treatment of certain human target cells reduces their susceptibility to NK lysis without affecting binding or sensitivity to lytic granules. 170 25

An IgM monoclonal antibody directed against the T-cell E-rosette receptor was obtained by preparing a hybridoma against cells of a human T-cell leukemia line, HPB-ALL. The antibody, named EDN-34B1, reacts exclusively with cells of T-cell lineage, including those of three T-cell leukemia lines. It does not react with cells of B-cell lines, normal B-cells, or monocytes. EDN-34B1 recognizes a single polypeptide of approximately 50,000 molecular weight, is capable of blocking E-rosette formation, and its binding to the target cell can be specifically blocked by monoclonal antibodies 9.6 and OKT-11, both anti-E-receptor antibodies. EDN-34B1 is 100% cytotoxic against normal thymocytes and peripheral T-cells, thus enabling the routine removal of such cells from a mixed lymphocyte population, and kills a higher percentage of normal T-lymphocytes than Ab 9.6, even though immunofluorescence studies have shown that both antibodies bind to the same fraction of PBLs. This phenomenon may be due to the IgM nature of EDN-34B1. Addition of EDN-34B1 and complement to PBLs totally abrogates T-cell functions such as mitogen (PHA) stimulation and response in MLR, while addition of EDN-34B1 alone only affects MLR.
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PMID:An IgM pan-T monoclonal antibody that blocks E-rosette formation. 387 45

A CTL line (CTLL-D4) mediating specific cytolytic activity against radiation-induced leukaemia RL male 1 has been established and maintained on a long-term basis without the addition of exogeneous TCGF. This line was originally selected by the limiting dilution of MLTC cells from RL male 1-immune (BALB/c X C57BL/6) F1-nu/+(CB6F1-nu/+) spleen cells (500 cells/well) in the presence of 5% rat TCGF, 2000 rads-irradiated normal CB6F1-nu/+ spleen cells as the feeder cells, and 10,000 rads-irradiated RL male 1 tumour cells as the stimulator. After expansion only with the feeder and tumour cells, CTLL-D4 shows highly specific cytotoxic activity against RL male 1 by in vitro CMC assay, since cells such as RL male 6, RL female 8, RL female 9, P815, MOPC-315 (H-2d), EL-4 (H-2b) and YAC (H-2a) are not killed. Microcytoxicity assay of this line has revealed that CTLL-D4 comprises three subsets of T lymphocytes (100% Thy-1.2+): 15-25% Lyt-1+23-, 60-75% Lyt-1+23+ and 10-15% Lyt-1-23+. The proliferation of this line seems to depend largely upon the syngeneic MLR-like responsiveness of the Lyt-1+23- subsets of CTLL-D4 to the Ia-positive cells in CB6F1-nu/+ splenic feeder cells, and has been restricted to the H-2d-haplotype of the feeder cells. In spite of the vigorous cell proliferation by coculturing with the feeder cells alone, the cytolytic activity of this line begins to decrease after some 7 days of culture in the absence of the stimulator RL male 1 cells which have no capacity to stimulate by themselves. Thus, by long-term culture of CTLL-D4 with the syngeneic feeder cells alone, a new non-cytolytic line (D4f) was established. Mechanisms enabling the long-term maintenance of CTL activity and subset composition have been discussed in terms of cellular cooperation between the subsets of this line.
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PMID:Effector mechanisms of syngeneic anti-tumour responses in mice. I. Establishment and characterization of an exogenous IL-2-independent cytotoxic T-lymphocyte line specific for radiation-induced leukaemia RL male 1. 387 71

The mechanisms of action of, and resistance to, important anticancer agents are briefly described. Their selective toxicity is considerably high, and is chiefly due to the distribution and metabolism in the body. The selective toxicity of some DNA-binding drugs may be attributed to the structural difference of DNA, nucleosome and/or chromatin between neoplastic and normal cells. Some studies of reducing side effects are summarized. In our laboratory, we are studying drug-resistance and metastasis of tumor cells. Since the mechanism of natural resistance of gastric cancer, pulmonary cancer, and other refractory cancers may be related to acquired resistance of leukemia, studies on new agents against drug-resistant tumor cells are important. In our laboratory, we have selected cell sublines of murine T-lymphoblastoma L5178Y for resistance to adriamycin (ADM), aclarubicin (ACR) or bleomycin (BLM), and have observed that the resistance is attributed to decreased influx and increased efflux of the antibiotic, resulting in lowered retention of the drug in the cells. Each resistant subline shows a characteristic cross-resistant pattern, suggesting that membrane alteration involved differs each other. We have also found that glycoprotein-synthesizing activity and alkaline phosphodiesterase activity of plasma membrane are higher in the three resistant sublines than in the parental cell line. We obtained a number of hybridomas producing antibodies to plasma membrane of an ACR-resistant subline of L5178Y cells. Among the syngeneic monoclonal antibodies, one was found by agglutination tests to react with the ACR-resistant cell line, but not significantly with the parental and ADM-, BLM-and MCR-resistant cell lines. Fluorographs of [14C] leucine-labeled ACR-resistant cells demonstrates two protein bands of 230 K and 20 K daltons, which are precipitated by the monoclonal antibody. The former seems to be specific to the ACR-resistant cells. Based on the results so far obtained, the 230 K protein may be related to the drug resistance and may be TATA (tumor-associated transplantation antigen). The results suggest that isolation of drug-resistant neoplastic cells is a novel method of finding TATA.
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PMID:[Mechanism of action and resistance of antineoplastic agents]. 619 71

BALB/c mice treated with total lymphoid irradiation (TLI) develop non-antigen-specific suppressor cells of the adoptive secondary antibody response and of the mixed leukocyte reaction. Suppressors of the adoptive anti-DNP response were eliminated by incubation of spleen cells with anti-Thy-1.2 or anti-thymus-leukemia (TL) antiserum and complement before cell transfer. Thymectomy before TLI prevented the appearance of the latter suppressor cells. On the other hand, suppressors of the MLR were eliminated by incubation of spleen cells with anti-Thy-1.2 but not anti-TL antiserum and complement. Thymectomy before TLI did not prevent their subsequent development. Thus, two subpopulations of suppressor T cells that differ in the expression of the TL surface antigen, dependence on the presence of the thymus, and in regulatory functions develop after TLI. The TL+, thymus-dependent cell suppresses the adoptive antibody response, and the TL-, thymus-independent cell suppresses the MLR.
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PMID:Immunoregulatory changes induced by total lymphoid irradiation. II. Development of thymus-leukemia antigen-positive and -negative suppressor T cells that differ in their regulatory function. 645 53

An antitumor activity of macromomycin, a polypeptide antitumor antibiotic, was tested in vitro and in vivo. The results obtained were as follows: 1) The cytostatic effect on L1210 cells in culture was identical to that of neocarzinostatin. 2) The effect of MCR on the survival of L1210 or P388 leukemia was as same level as NCS. 3) Effects of MCR were independent from the treatment schedules. 4) MCR was inactive on the survival of Lewis lung carcinoma.
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PMID:[Antitumor activity of macromomycin]. 718 42

We analysed the use of allogeneic bone marrow transplantation (BMT) in the treatment of acute myelogenous leukemia (AML). We evaluated 271 adult patients with newly diagnosed AML treated here between 1983 and 1992; 113 patients (42%) were eligible for BMT because of their age (< 45 years until 1986 and < 50 years later). Of these, HLA typing was performed on 81 patients (72%); 32 patients were not typed (19 had no sibling, 8 had a primary refractory leukemia, 3 died during induction, 1 had important previous toxicity and for one patient there was no recorded reason). Of the 81 typed, 36 patients (44.4%) were found to have an HLA-matched sibling donor and 21 (25%) underwent BMT (8% of the total population); 15 patients did not undergo BMT (6 relapsed before transplantation and did not obtain a second remission, 3 declined the procedure, 1 died during induction, 1 had positive MLR, 1 had positive MLR and HCV hepatitis, 1 was a drug addict with HCV hepatitis, 1 had previous organ toxicity, 1 was psychotic). These data show that only a small fraction of unselected patients with AML can undergo BMT. Such findings make the comparison of BMT with other types of post-remission therapy more complex.
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PMID:Acute myeloid leukemia from diagnosis to bone marrow transplantation: experience from a single centre. 795 Nov 22

We report on 24 patients with leukemia (19 pts), congenital disorders (4 pts) or severe aplastic anemia (1 pt) who received bone marrow transplantation from unrelated volunteer donors in 8 Italian Institutions. All the donor/recipient pairs were serologically HLA-A,B,DR matched; MLR was non reactive in 21 out of 24 cases. Preparative regimens were in accord with standards for diagnosis and disease status and included TBI in 15 patients, busulfan in 8, cyclophosphamide alone in one patient with SAA. GvHD prophylaxis consisted of cyclosporine/methotrexate in the majority of cases; 6 patients received additional immunotherapy with anti-lymphocyte globulin and 1 patient in vivo Campath-1G. The bone marrow was T-cell depleted in 2 cases. Acute GvHD grade II-IV occurred in 87% of patients (gr.III-IV: 57%) and was the main cause of death in 8 cases. Six patients (25%) survive with a median follow-up of 9 months, (16% actuarial survival at 3 years). A trend in favour of a better outcome has been found for age < 20 yrs at BMT (33% vs 22%), intensified GvHD prophylaxis (33% vs 22%) and transplants performed in more recent years (31% vs 18%).
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PMID:Bone marrow transplantation from unrelated donors: the Italian experience. GITMO, AIEOP and IBMDR. 844 60

The functional role of the class Ib thymus-leukemia (TL) Ag expressed within the thymic cortex and intestinal mucosa of the mouse remains unknown. In an approach to elucidate the potential functionality of TL, we developed transgenic mice that ectopically express the H-2T18d gene product on essentially all nucleated cells through the control of a heterologous H-2Kb gene promoter. Transgenic mice demonstrated an increase in the number of CD4+ lymphocytes within the thymus and lymph nodes; these cells displayed an altered T cell receptor repertoire possibly suggesting a role for the ectopically expressed TL protein. The TL protein additionally displayed the characteristics of a bona fide transplantation Ag, because skin grafts from transgenic animals onto MHC- and minor histocompatibility Ag-matched nontransgenic recipient mice resulted in a rapid and vigorous immunologic rejection of the allograft. In MLR studies, transgenic stimulator cells induced the proliferation of responders to a level intermediate between genetically identical and H-2-disparate responder-stimulator combinations. The TL protein was also capable of stimulating cytotoxic T lymphocytes, thereby resulting in specific lysis of TL+ target cells. Further data demonstrated that the TL protein assembles with peptides that are modified at the amino terminus, and that TL retains these molecules at the cell surface. Together, these data suggest that H-2T18d is capable of interacting with T cells via a bound peptide. These data further support the possibility that TL may subserve a specialized function within the immunologic system.
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PMID:Thymus-leukemia antigen interacts with T cells and self-peptides. 855 26


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