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)

It is difficult to evaluate the protective efficacy of species-specific viruses of humans and expensive companion animals where there is no non-human animal model. This study describes an in vivo model system which allows simultaneous operation of humoral, cell-mediated, interferon-like or other unidentified immunological defence mechanisms. There was evidence of in vivo inactivation of both enveloped and unenveloped DNA and RNA viruses including retrovirus mouse sarcoma virus/mouse leukaemia virus as evaluated by assay of the enzyme reverse transcriptase. This model will allow examination of vaccine efficacy in immunocompetent host animals while avoiding morbidity and/or mortality from virus infection in these animals.
 ...
PMID:In vivo model for evaluation of species-specific virus vaccines. 133 88

The effects of ultraviolet-inactivated feline leukemia virus (UV-FeLV) on the production of alpha and/or beta interferon (IFN) by mononuclear cells stimulated with the Newcastle disease virus (IFN-NDV) was investigated. The production of IFN-NDV and gamma IFN was suppressed by 50% as compared to the control in the presence of 200 ng/ml or 200 micrograms/ml of UV-FeLV, respectively. The presence of UV-FeLV decreased the rate of the production, but the time to reach the plateau of the IFN activity in the culture supernatant was not shortened in both IFNs. It was suggested that the suppressive effects of UV-FeLV against both IFNs were through rather similar mechanisms. The suppressive effects of UV-FeLV on IFN-NDV production was most evident in the cultures to which UV-FeLV was added at the early stages of the culture, and could not be demonstrated when UV-FeLV was added 8 hr after initiation of the culture. These data therefore indicate that non-infectious feline leukemia viral particles can modify the production of feline IFNs by peripheral blood mononuclear cells.
 ...
PMID:Effects of ultraviolet-inactivated feline leukemia virus on the production of alpha/beta interferon by feline peripheral blood mononuclear cells. 133 72

Since 1984 alpha-interferon (alpha IFN) has been the treatment of choice in cases of hairy-cell leukaemia. However, eight years' experience shows that, although a large majority of the patients are improved, they are not cured. Thus, a new type of cytostatic drug, perhaps capable of cure as well, may replace alpha-IFN for the treatment of hairy-cell leukaemia in the future.
 ...
PMID:[Alpha interferon treatment in hairy cell leukemia]. 134 20

The treatment of hairy cell leukemia (HCL) requires continuing update. The role for splenectomy is extremely limited. Alfa-interferon therapy has been available and utilized for five years; there have been few complete remissions. The experience with Pentostatin has resulted in a majority of clinical complete remissions after several months of therapy, but persistence of a small percentage of hairy cells in the bone marrow. The most recent therapeutic agent, 2-chloro-deoxyadenosine (2-CDA) is given for seven days and results in a complete remission in the great majority of patients with no evidence of persistent bone marrow disease. If this trend persists, 2-CDA will become first line therapy for HCL as it may cure the disease.
Leukemia 1992
PMID:The treatment of hairy cell leukemia: an update. 134 62

The role of CD11/CD18 leukocyte adhesion molecules and their ligands in mediating non-major histocompatibility complex (MHC) restricted lymphocyte cytotoxicity is controversial. In order to examine the role of target cell intercellular adhesion molecule-1 (ICAM-1; CD54), a ligand of lymphocyte function-associated antigen (LFA-1) (CD11a/CD18), we exposed the human leukemia cell line, HL-60, to a variety of agents implicated in modulating ICAM-1 expression and/or sensitivity to lymphocyte cytolysis. Exposure of HL-60 cells to retinoic acid (RA), interferon (IFN)-alpha, IFN-beta, and IFN-gamma induced protection from lymphokine-activated killer (LAK) cytolysis. Only RA and IFN-gamma induced ICAM-1 expression. Tumor necrosis factor and vitamin D3, which also induced ICAM-1 expression, increased HL-60 sensitivity to LAK lysis. Granulocyte-macrophage colony-stimulating factor also increased sensitivity to LAK lysis; ICAM-1 was not induced. The state of cellular differentiation and expression of class I and II MHC antigens also did not correlate with sensitivity to LAK cytolysis. Exposure of untreated HL-60 cells and HL-60 cells expressing ICAM-1 to monoclonal antibody (mAb) versus ICAM-1 did not modulate LAK sensitivity. Exposure of LAK cells to mAb versus LFA-1 partially inhibited cytolysis; mAb versus CD18 inhibited cytolysis more completely. HL-60 cells were resistant to natural killer lysis; exposure to the various experimental agents did not alter sensitivity. We conclude that leukemic cell sensitivity to LAK cytolysis can be modulated by a variety of agents. Although our results suggest a role for leukocyte CD11/CD18 adhesion molecules in LAK cytolysis, the poor correlation between ICAM-1 expression and sensitivity to LAK lysis suggest that interactions other than LFA-1/ICAM-1 conjugation may be more central to the processes involved.
 ...
PMID:Modulation of leukemic cell sensitivity to lymphokine-activated killer cytolysis: role of intercellular adhesion molecule-1. 136 53

Recent studies have generated data demonstrating significant clinical activity of alpha-interferon therapy in each of six hematological malignancies, chronic myeloid leukaemia, essential thrombocythemia, polycythemia rubra vera, non-Hodgkin's lymphomas, multiple myelomatosis and hairy cell leukaemia.
 ...
PMID:alpha-Interferon in hematological malignancies. 136 59

Chinese hamster ovary (CHO) cells are resistant to infection by all of the major classes of murine retroviruses and are partially resistant to infection by gibbon ape leukemia virus. Treatment of CHO cells with the glycosylation inhibitor tunicamycin rendered these cells susceptible to infection by retroviral vectors with ecotropic, xenotropic, and amphotropic host ranges and increased the titer of gibbon ape leukemia virus pseudotyped vectors 10-fold. Vectors having a polytropic host range did not infect CHO cells in the presence or absence of tunicamycin, showing that the effect of tunicamycin was specific and related to the pseudotype of the vector. We present evidence for three mechanisms of resistance to infection: lack of viral receptors on CHO cells, the presence of nonfunctional receptors which can be made functional by treatment with tunicamycin, and the secretion of a protein factor that blocks retroviral infection of CHO cells. Several criteria indicate that the secreted inhibitor is not an interferon, and secretion of this factor was not detected in several other cell lines that were examined.
 ...
PMID:Tunicamycin treatment of CHO cells abrogates multiple blocks to retrovirus infection, one of which is due to a secreted inhibitor. 137 96

B7 is an activation antigen expressed on activated B cells and gamma-interferon-stimulated monocytes. The B7 antigen is the natural ligand for CD28 on T cells. After engagement of T-cell receptor with antigen in association with major histocompatibility complex class II, a second signal mediated through the binding of B7 to CD28 greatly upregulates the production of multiple lymphokines. We have now mapped the B7 gene to human chromosome 3 using the technique of polymerase chain reaction on a panel of hamster x human somatic cell hybrid DNAs. We have further localized the gene to 3q13.3-3q21 using in situ hybridization on human metaphase chromosomes. Trisomy of chromosome 3 is a recurrent chromosome change seen in various lymphomas and lymphoproliferative diseases, particularly diffuse, mixed, small, and large cell lymphomas, human T-cell lymphotropic virus type I-induced adult T-cell leukemia, and angioimmunoblastic lymphadenopathy. A number of chromosomal defects involving 3q21 have been described in acute myeloid leukemia and also in myelodysplastic and myeloproliferative syndromes. The mapping of B7 may permit further insight into disease states associated with aberrant lymphocyte activation and lymphokine synthesis.
 ...
PMID:The gene for B7, a costimulatory signal for T-cell activation, maps to chromosomal region 3q13.3-3q21. 137 Mar 89

Results concerning a possible link between susceptibility to natural-cell-mediated immune cytolysis and the multi-drug resistance (MDR) phenotype are conflicting. We evaluated in human acute lymphocytic leukemia the relationship between acquired drug resistance and susceptibility to cytolysis mediated by endogenous, interferon-activated, and interleukin-2-activated natural cytotoxic cells. Eight human leukemia drug-resistant/sensitive cell line pairs were evaluated; drug-resistant sub-lines included those selected for primary resistance to adriamycin, etoposide, teniposide, vincristine, and vinblastine. A majority of P-glycoprotein-positive MDR sub-lines displayed slight but statistically significant resistance to endogenous and/or interferon-activated natural-killer(NK)-cell-mediated lysis, as compared with the drug-sensitive parental type. P-glycoprotein-negative sub-lines displayed variable NK susceptibility; within this group, the variants selected for primary etoposide resistance were more susceptible to NK cytolysis than parental cells. Results of cold-target-inhibition experiments suggest that altered NK susceptibility does not arise solely from modulation of NK target recognition and adherence structures. IL2-activated killer (LAK) cells lysed both drug-sensitive and drug-resistant lines. Two MDR lines selected for primary etoposide resistance displayed enhanced LAK susceptibility. In contrast, the 2 variants selected for resistance to adriamycin exhibited partial resistance to LAK-mediated killing, which could be overcome at high effector-to-target ratios. Our results support the development of interleukin-2/LAK immunotherapy for the treatment of leukemias with acquired drug resistance.
 ...
PMID:The relationship between multi-drug resistance and resistance to natural-killer-cell and lymphokine-activated killer-cell lysis in human leukemic cell lines. 137 Apr 37

In nine patients with CLL treated with chlorambucil followed by alpha-2b-interferon (alpha 2b-IFN), T, B and natural killer (NK) cells and NK activity were studied before entering the study, after chlorambucil treatment, and after administration of alpha 2b-IFN. When considered as a whole, basal NK activity was lower in CLL patients than in controls (21.0% +/- 10.9 versus 40.2% +/- 17.4, p less than 0.001); however, when considered individually, four out of nine patients had normal NK activity at diagnosis. Chlorambucil did not increase global NK activity (21.7% +/- 7.1), whereas alpha 2b-IFN did so (44.3% +/- 19.1). After alpha 2b-IFN only one of seven patients studied had low NK activity. Previously increased absolute counts of CD2+, CD4+, CD8+, CD16+, CD57+ lymphocytes were reversed with chlorambucil treatment to normal levels, while after this therapy CD11b+ and CD19+ cells decreased without reaching normal values. During alpha 2b-IFN therapy, an increase up to normal levels in the percentage of CD16+ (2.7% +/- 3.4 versus 7.7% +/- 6.5, p = 0.04) and CD57+ (3.0% +/- 3.0 versus 8.1% +/- 6.2, p = 0.020) lymphocytes was observed whereas the absolute number of CD19+ B-cells further decreased (5.2 x 10(9)/l +/- 2.5 vs 3.8 x 10(9)/l +/- 2.3), albeit not significantly.
Leukemia 1992 Jun
PMID:Recombinant alpha-2b-interferon may restore natural-killer activity in patients with B-chronic lymphocytic leukemia. 137 76


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>