Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These experiments have investigated cellular mechanisms involved in the generation of cellular immune responses to human acute leukemic blasts. Because normal human lymphocytes are not able to recognize immunologically, in vitro, lymphocytes from MHC identical siblings, the present studies have examined the in vitro proliferative and cytotoxic responses of normal lymphocytes to MHC identical AML and ALL blasts. In those cases where acute leukemic cells were unable to induce a proliferative response by MHC identical lymphocytes, the generation of effective anti-leukemic cytotoxicity required the addition of unrelated stimulating cells to the sensitization culture. In contrast, leukemic blasts that induced a proliferative response by MHC identical lymphocytes were also able to stimulate anti-leukemic cytotoxicity. This could be augmented by the addition of unrelated stimulating cells to the sensitization culture. The specificity of anti-leukemic cell cytotoxicity was demonstrated in all instances by simultaneous testing of putative killer cells on 51Cr leukemic blasts as well as 51Cr-labeled MHC identical phytohemagglutinin blasts or normal lymphocytes. Simultaneous sensitization to MHC identical leukemic blasts and unrelated stimulating lymphocytes did not invariably generate anti-leukemic cytotoxicity even when allogeneic cytotoxicity was observed; the absence of demonstrable suppressor activity in these nonreactive combinations suggested that some individuals may be specifically immunoincompetent, and thereby unable to generate effective anti-leukemic CML.
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PMID:Cell-mediated destruction of human leukemic cells by MHC identical lymphocytes: requirement for a proliferative trigger in vitro. 106 27

In order to investigate the capability of cytokines to induce myeloid leukemia cells from G0 phase to the proliferative stage, blasts from 9 patients with AML and 1 patient with CML-MC were cultured with various cytokines (IL-3, GM-CSF, IL-3 + GM-CSF, G-CSF) for 48 hours or 96 hours in a serum-free culture system. Cells were analyzed by two-color flow cytometry, using PI and the monoclonal antibody Ki-67. The percentage of cells in G0 phase was reduced significantly when the cells were cultured with IL-3 (p < 0.01), GM-CSF (p < 0.01), and IL-3 + GM-CSF (p < 0.01) for 48 hours, as compared with the percentage of cells in G0 phase before culture. Moreover, the percentage of cells in S phase increased significantly when the cells were cultured with IL-3 (p < 0.01), GM-CSF (p < 0.02), and IL-3 + GM-CSF (p < 0.01) for 48 hours, as compared with the percentage of cells in S phase before culture. It is well known that many drugs which are widely used in the treatment of acute leukemia are cytotoxic mainly to proliferating cells, so that if quiescent G0 phase cells can be induced to the proliferative stage, the treatment of acute leukemia would become more effective. The present findings showed that a considerable variation was observed among individual patients in the induction of the G0 component to the proliferative stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Capability of various cytokines to induce quiescent myeloid leukemia cells to the proliferative stage. 128 63

Leukocyte acid phosphatase and its isoenzyme composition was studied in leukemic patients to determine the specificity of different isoenzymes in leukemic leukocytes. It was found that leukocyte acid phosphatase content is significantly increased in ALL, AML, and CML patients, while CLL patients had decreased levels of acid phosphatase. The distribution and intensity of leukocyte ACP isoenzymes vary in respective leukemic condition. Thus isoenzyme 'O' was predominant in AML and CML, while isoenzymes 1, 2 and 3 predominated in ALL. The lack of predominance of isoenzyme 3 was a feature in CLL patients. It was concluded that the isoenzyme patterns, though promising, presented inconclusive picture for diagnosis purpose and further studies on immunochemical characteristics of these isoenzymes are warranted to ascertain their cell specificity.
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PMID:Total leukocyte acid phosphatase and its isoenzymes in patients with leukemia. 129 3

The anti-proliferative effects of selenium were studied both in vivo and in vitro. At a selenium concentration of 0.6 micrograms/ml, cells from patients with ALL-L1, L2 and AML-M1, M3 and M5 were more sensitive than cells from patients with CML. Cells from patients with AML-M2, CLL and leukaemic lymphoma were least sensitive. Normal bone marrow or peripheral blood cells were not sensitive to selenium at this concentration. In the mouse leukaemia models (L797, L615, L7712), the sensitivity of leukaemic cells were: L797 (93% cytotoxicity) greater than L615 (49.7% cytotoxicity) greater than L7712 (4.4% cytotoxicity). Sodium selenite injected i.p. increased the longevity of L797-inoculated mice. Administration of 40 micrograms selenium daily for 7 days resulted in a significant increase in the longevity of mice inoculated with 10(5) L797 cells. However, no remarkable increase of the longevity was observed in either L615- or L7712-inoculated mice after treatment with sodium selenite for 7 days. Treatment of the HL-60 leukaemic cell line with selenium caused a dose- and time-related decrease in DNA, RNA and protein syntheses as measured by [3H]-thymidine, [3H]-uridine and [3H]-leucine uptake respectively. The inhibitory effect of selenium on DNA synthesis was reversed when selenium was removed from the medium, demonstrating that selenium-induced inhibition of DNA synthesis was due to interference with DNA biosynthesis rather than DNA template damage. These results suggest that the anti-leukaemic effect of sodium selenite is associated with inhibition of DNA replication, transcription and translation.
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PMID:The anti-leukaemic effects and the mechanism of sodium selenite. 131 17

We analyzed the rearrangement of T-cell receptor (TcR) delta chain gene in 196 cases of hematological malignancies. This rearranged band (s) was observed in 15% of the total cases investigated. All T-ALL patients and cell lines, except for P30/Okubo, had a new band (s) or deletion of J delta 1 gene locus, indicating the gamma delta T-cell type or the alpha beta T-cell type. In the other T-cell malignancies, the delta rearranged band (s) was recognized in 5% of T-cell lymphomas, 20% of AILD but not in ATL, Hodgkin's disease, T-CLL. Inappropriate delta rearrangement was frequently recognized in 63% of B-ALL and 50% of CML-BC but none or few (5% less) in B-CLL, B-lymphoma and AML. Southern blotting, using J delta 1 and V delta gene probes or Pst I enzyme digestion, indicated that the inappropriate delta rearranged band in B-ALL and CML-BC is V delta 2D or DD without a J delta locus. The rearranged band (s) involved J delta locus, was mostly recognized in 5/6 cases of CD7 (+) stem cell leukemia. Therefore, the TcR delta gene is useful in evaluating clonality for the most immature T-cell neoplasms, not showing rearrangement of the other TcR genes. Moreover, this delta gene may be a useful tool for distinguishing T-lineage from the other lineages, using the characteristic rearrangement pattern (V delta 2D as a inappropriate pattern, or (D) DJ and V (D) DJ as the T-lineage pattern (s)).
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PMID:[Analysis of T-cell receptor delta chain gene in hematological malignancies]. 132 69

The objective of this study was to develop a simplified method for the simultaneous analysis of cellular karyotype and phenotype which would permit the identification of cell origin. We studied 6 patients with AML, 3 with CML (one of which was in blastic transformation) and one ALL. We used a method in which the suspension of bone marrow cells was incubated in TC 199 medium with colchicine and with hypotonic solution formed from glycerol, NaCl, KCl, CaCl2, MgCl2 and sucrose. The slides were prepared from this cell suspension by cytospin and stained for peroxidase, PAS, esterases and iron. The karyotype was studied by direct method and culture. It was possible to relate the cytogenetic marker with cytochemistry characteristics in the same cell in 3 cases, showing the feasibility of cytochemistry techniques in cytogenetical preparations. The best preparations were found through peroxidase. The presence of iron granules allowed identification of erythroblastic lineage in the combined staining. Mitosis with a marker chromosome of leukemic clone in an AML cell with negative peroxidase probably showed a proliferation of more primitive precursor not sufficiently differentiated to show markers.
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PMID:Simplified method for the analysis of cellular karyotype and phenotype in leukemias. 134 Oct 1

The expression of C-myc proto-oncogene were studied at the levels of protein in bone marrow cells obtained from patients with AML and CML. It was found that the expression of C-myc in florid AML and during blast phase of CML were much higher than that in remission of AML and in chronic phase of CML. In 7 cases of AML diagnosed for the first time, 2 cases with high C-myc expression had no remission after 3-6 months, while 5 with rare C-myc expression had remission after 3-6 months. This results suggest that the expression of C-myc proto-oncogene are possibly sensitive indicator of the prognosis of leukemia.
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PMID:[The expression of C-myc oncogene in leukemia and its relationship to clinical symptoms]. 139 24

Circulating immune complexes (ClC) were estimated in 78 patients of leukaemias and lymphomas by Clq deviation ELISA and PEG assay. In all leukaemias a significant elevation in ClC was seen at the time of first presentation. While in ALL a decrease occurred on therapy as partial or complete remission was achieved, no such fall was seen in AML or CML-BC when treated. ClC levels were much higher in non-Hodgkins lymphoma than in Hodgkins disease and showed a direct correlation with B symptoms and activity of the disease. The ClC levels were highest in null-ALL followed by those in common ALL and T-ALL. The mean duration of remission in patients of ALL without elevation in ClC was much longer than in those with ClC.
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PMID:Circulating immune complexes in leukaemias and lymphomas. 139 53

The human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origin and spread of human leukemia. 143 86

10 patients between the ages of 5 and 40 yrs with myeloid leukemia (4 acute, 6 chronic) in early (5 cases) or intermediate stage of the disease were given Cyclophosphamide and Busulfan (6 cases) or Cyclophosphamide, Busulfan and VP-16 (4 cases with CML) and bone marrow transplants from HLA-matched donors (in 9 cases from siblings and in one case from HLA phenotypically matched father). There was one transplant related death and 3 relapses in CML cases. In cases which relapsed GvHD was not observed. Altogether acute GvH and chronic GvHD was seen in 2 and 4 cases, respectively. All grafted cases with AML survive in continuous remission lasting more than 2 years (median 30.5 month).
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PMID:[Allogeneic bone marrow transplantation in myeloid leukemia: chemical conditioning, clinical course and results]. 148 72


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