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Query: UMLS:C0023418 (
leukemia
)
93,477
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Antigenic profiles in AML that have generally accepted prognostic significance, and allow treatment stratification, have not yet been defined. In a previous report of Ashman et al., the proto-oncogene c-kit defined by binding of the moab YB5.B8 was expressed on about one third of AML cases, mainly of the undifferentiated FAB-subtypes and associated with poor prognosis and overall survival. In this study, the moab 17F11 also directed against the c-kit structure stained 41/47 AML and 6/8 CML blast specimens, whereas all investigated 40 ALL samples were c-kit negative. c-kit was not restricted to any particular, undifferentiated FAB-subtype, but found in 9/9 AML-M0/M1, 18/19 AML-M2, 0/1 AML-M3, 11/13 AML-M4 and 3/5 AML-M5 subtypes. Immunophenotypical analysis showed no restriction of c-kit expression to immature, CD34+ precursors, but c-kit was also expressed on CD4+ CD34- precursor cells differentiating towards the monocyte lineage. In addition, multi-color labelings revealed an extraordinary heterogeneity of concomitant antigen expression on c-kit+ cells 10/36 c-kit+ CD34+ samples expressing CD56 and 16/36 c-kit+ CD34+ samples being
CD7
positive; two c-kit+ CD34+ specimens carried the B-cell antigen CD19. In correlation to clinical outcome c-kit expression as single parameter was not predictive for poor response to therapy and short survival as previously suggested.
Leukemia
1994 Feb
PMID:AML: immunophenotypic heterogeneity and prognostic significance of c-kit expression. 750 33
A SCID mouse model of human T-ALL has been used to determine the in vivo therapeutic efficacy of two anti-
CD7
-saporin immunotoxins constructed with either a hindered (HB2-SMPT-Sap) or non-hindered (HB2-SPDP-Sap) disulphide bond between antibody and saporin. Groups of 10 SCID mice were injected intravenously (i.v.) with 2 x 10(6) human T-ALL HSB-2 cells followed seven days later by i.v. injection with either a single dose or with 3 doses of HB2-SPDP-Sap or HB2-SMPT-Sap given on alternate days. Control groups received equivalent sham injections of PBS or molar equivalent amounts of unconjugated HB2 antibody+saporin. Animals receiving a single dose of HB2-SMPT-Sap showed better survival than animals receiving a single dose of HB2-SPDP-Sap but the difference was not shown to be significant by log-rank analysis. When given as a triple dose both immunotoxins performed similarly. Comparison of single-dose with triple-dose IT therapy revealed that the therapeutic effect of a triple dose of HB2-SPDP-Sap was significantly better than that of single dose, but this was not the case with HB2-SMPT-Sap. Pharmacokinetic studies of HB2-SPDP-Sap and HB2-SMPT-Sap in normal and HSB-2
leukaemia
bearing SCID mice failed to reveal any difference in clearance rates for these two IT's. We conclude from these studies that there is no therapeutic advantage to be gained from constructing the HB2-Sap IT with a hindered disulphide bond in this particular model of human T-ALL.
...
PMID:Therapy of human T-cell acute lymphoblastic leukaemia in severe combined immunodeficient mice with two different anti-CD7-saporin immunotoxins containing hindered or non-hindered disulphide cross-linkers. 751 86
We report here a
CD7
positive undifferenciated
leukemia
/lymphoma which showed a rapid clinical course. A 27-year-old female was complained of palpitation and edema. She had a mediastinal tumor and pericardial effusion. Lymphoblastic cells were found in the effusion, but in the peripheral blood initially. After admission the blast cells appeared in the peripheral blood, and they were revealed negative for peroxidase and had phenotype of
CD7
and CD33 positive. The patient suffered from cardiac tamponade and died 15 days after admission. The Southern blotting of mediastinal tumor cells disclosed the germline configuration for TCR-beta a chain and the rearrangement of immunoglobulin heavy chain genes.
...
PMID:[CD7 positive undifferenciated leukemia/lymphoma associated with leukemic pericarditis]. 752 May 12
The effects of six recombinant human cytokines: erythropoietin, GM-CSF, G-CSF, interleukin-3, -4 and -6 on the proliferation and differentiation of a human multilineage myeloid leukemia cell line MHH 225, established from the bone marrow of an AML(M7) patient in our laboratory determined by changes in antigen expressions using monoclonal antibodies in APAAP technique were examined in liquid suspension culture. The MHH 225 cells have been growing exponentially without cytokines or conditioned media. About 90 per cent of MHH 225 cells are CD33+ CD34+ CD3-
CD7
- CD19- CD20- TdT- with 57.6 per cent, 28.3 per cent and 7.8 per cent of them being CD41+, glycophorin A+ and CD15+, respectively. After five days of treatment with erythropoietin, GM-CSF, G-CSF or IL-6 no change was observed in MHH 225 cell antigens expression. IL-3 (100 U/ml) induced a moderate increase in only CD13 and alpha naphthyl esterase positive cells from 6.5 +/- 1.9 per cent and 5.7 +/- 2.4 per cent in control cultures to 21.6 +/- 3.0 per cent and 19.1 +/- 2.8 per cent, respectively. On the other hand, 100 U/ml IL-4 significantly increased the number of CD13, CD15 and alpha naphthyl esterase positive cells to 48.9 +/- 5.0 per cent, 47.2 +/- 3.6 per cent and 46.1 +/- 3.0 per cent, p < 0.001, respectively. Also, 100 U/ml IL-4 decreased the number of CD41 positive cells from 57.6 +/- 2.8 per cent to only 25.9 +/- 3.6 per cent and did not change the number of CD33 or glycophorin A positive cells. The present results showed that out of the six myelopoietic growth factors tested, IL-4 was the only one to inhibit selectively the proliferation of CD33+ CD41+ leukemic megakaryoblast cells suggesting that IL-4 may have a lineage regulatory effect in favour of a myeloblastic CD33+ CD13+ CD15+ at the expense of a megakaryoblastic CD33+ CD41+ amplification in human
leukemia
cells and with apparently no effect on leukemic erythroblast cells. The MHH 225 cell line provides a useful tool and freely available model to scientists for studying signal transduction via IL-4 and for studies of 'lineage switch'.
...
PMID:Interleukin-4 inhibits proliferation of human leukemic megakaryoblast cell line MHH 225. 752 Aug 82
A novel human
CD7
-positive
leukemia
cell line (HSM911) derived from the peripheral blood of a patient with acute myelogenous leukemia (AML) was studied for its cellular and biological characterization. Proliferation assay using a variety of cytokines demonstrated that the HSM911 cells proliferate in response to recombinant granulocyte-macrophage-colony stimulating factor (rGM-CSF), recombinant Interleukin-3 (rIL-3) and recombinant stem cell factor (rSCF), but do not in response to recombinant granulocyte-colony stimulating factor (rG-CSF), natural macrophage-colony stimulating factor (M-CSF), rIL-1, rIL-2, rIL-4, rIL-5, rIL-6 or recombinant erythropoietin (rEpo). Polyclonal anti-GM-CSF antibody and polyclonal anti-IL-3 antibody blocked the proliferation of HSM911 stimulated with rGM-CSF and rIL-3, respectively. HSM911 maintained in the presence of rGM-CSF expressed the
CD7
, CD13, CD33, CD34, CD41a, HLA-DR, VLA1-VLA5, CD11a, CD54, CD44 and LAM1. These findings suggest that HSM911 might be of multipotent progenitor cell origin. GM-CSF receptors and rIL-3 receptors expressed on this cell line were simultaneously suppressed by rGM-CSF or rIL-3, whereas only IL-3 receptors were down-modulated by rSCF. Treatment with 12-o-tetradecanoyl-phorbol-13-acetate (TPA) induced the differentiation of HSM911 cells into macrophage-like cells but not erythroblasts, megakaryocytes or lymphocytes. Interferon-gamma and transforming growth factor-beta (TGF-beta) suppressed the proliferation of HSM911 cells in a dose dependent manner. HSM911 was relatively resistant against anti-cancer drugs compared with fresh AML cells and other leukemic cell line. HSM911 is a useful tool for analyzing
CD7
-positive acute myelogenous leukemia.
...
PMID:[Cellular and biological characterization of CD7-positive acute leukemia cells--an investigation of the established cell line, HSM911]. 752 34
CTLs bearing certain T-cell receptor V beta-regions are directed by the bacterial superantigen Staphylococcus enterotoxin A (SEA) to lyse MHC class II-positive cells. In order to extend superantigen-dependent cytotoxicity to MHC class II-negative carcinoma cells, covalent conjugates of superantigen and mAbs against surface markers of these cells have been used. We now describe a novel strategy which allows rapid selection of mAb suitable for superantigen targeting against MHC class II-negative tumor cells. A recombinant fusion protein of protein A and SEA binding to the mAbs
CD7
or CD38 was able to mediate T cell-dependent lysis of MHC class II-negative Molt-4 and CCRF-CEM acute lymphatic leukemia cell lines. Lysis was dose dependent and correlated with E:T cell ratio. In contrast, SEA alone did not induce any significant lysis. In order to decrease the MHC class II affinity of the protein A-SEA complex, a point mutation was introduced into SEA (protein A-SEA mu9). The mutated fusion protein had similar potency as protein A-SEA against Molt-4 cells but was 100-fold less active against MHC class II-positive cells. Considering the efficiency and specificity of the mutated SEA protein interacting with mAb in targeting T lymphocytes against MHC class II-negative
leukemia
cells while only marginally affecting normal MHC class II-positive cells, we suggest the development of SEA-mAb fusion proteins as a potential adjuvant therapy of leukemias.
...
PMID:Antibody-targeted superantigens induce lysis of major histocompatibility complex class II-negative T-cell leukemia lines. 753 May 98
In mast cells, antigen-mediated aggregation of the high-affinity receptor for immunoglobulin E, Fc epsilon RI, stimulates tyrosine phosphorylation and activation of multiple signaling pathways leading to the release of several classes of mediators of the allergic response. Early events induced upon cross-linking of Fc epsilon RI include tyrosine phosphorylation of Fc epsilon RI subunits and activation of the tyrosine kinase p72syk (Syk), which binds to tyrosine-phosphorylated Fc epsilon RI. Clustering of Syk, as a result of its interaction with aggregated Fc epsilon RI, may play a role in activating one or more of the signaling pathways leading to mediator release. To test this possibility, Syk was introduced into a model mast cell line (rat basophilic
leukemia
cells) as part of a chimeric transmembrane protein containing the extracellular and transmembrane domains of CD16 and
CD7
, respectively. Clustering of the Syk chimera, using antibodies against CD16, was found to be sufficient to stimulate early and late events normally induced by clustering of Fc epsilon RI. Specifically, aggregation of Syk induced degranulation, leukotriene synthesis, and expression of cytokine genes. Induction of mediator release was dependent on the kinase activity of Syk. Consistent with this finding, clustering of Syk also induced the tyrosine phosphorylation of a profile of proteins, including phospholipase C-gamma 1 and mitogen-activated protein kinase, similar to that induced upon clustering of Fc epsilon RI. These results strongly suggest that Syk is an early and critical mediator of multiple signaling pathways that emanate from the Fc epsilon RI receptor and give rise to the allergic response.
...
PMID:Clustering of Syk is sufficient to induce tyrosine phosphorylation and release of allergic mediators from rat basophilic leukemia cells. 753 80
A 66-year-old male patient was admitted with dyspnea; physical examination revealed petechiae and systemic lymphadenopathy. Laboratory findings showed
leukemia
. The blasts in the peripheral blood were negative for cytochemical myeloperoxidase, and had condensed nuclear chromatin with a nucleolus. The histological diagnosis of the biopsied neck lymph node was lymphoblastic lymphoma. The
leukemia
cells expressed CD2, CD6,
CD7
, CD13low, CD56, beta chain of IL-2 receptorlow (IL-2R beta), and HLA-DR antigens, but not other pan-T (CD5, CD3, CD4, and CD8); pan-B (CD10, CD19, CD20, and CD24); natural killer (NK) (CD16, CD57); or myeloid (CD33) antigens. Electronmicroscopy revealed convoluted nuclei with conspicuous nucleoli and peripherally condensed heterochromatin. Membrane-bound granules containing an electron dense matrix were observed in the cytoplasm, indicating the NK cell nature of the neoplastic cells. While terminal deoxynucleotidyl transferase (TdT) and cytoplasmic CD3 were not detected by immunofluorescence on fixed smears, Northern blot analysis revealed the gene expression of CD3 epsilon, CD3 zeta, and TdT. Gene rearrangement analysis revealed that the beta, gamma, and delta chains of T-cell receptor (TCR) and immunoglobulin heavy chain (IgH) were of germline genotype. While the overall interpretation of the phenotype and genotype was difficult, the derivation of an immature stage of NK lineage was strongly suggested, based predominantly on the electronmicroscopic features. Despite initially successful chemotherapy, the patient died 14 months after initial presentation.
...
PMID:Novel leukemic lymphoma with probable derivation from immature stage of natural killer (NK) lineage in an aged patient. 753 82
Antigen CD34 and other markers of cell membrane were investigated in cells from 43 patients with primary acute nonlymphoblastic
leukemia
(ANLL) by immunofluorescence test. The blast cells of 13 patients (30.2%) expressed antigen CD34. The patients with positive CD34 were no significantly different from the remaining 30 patients with negative CD34 with respect to age, serum lactate dehydrogenase (LDH), hemoglobin, white blood cell count, platelet count and the proportion of blast cells in blood and bone marrow, but their blasts were more likely to express HLA-DR, CD38,
CD7
and lack of CD15 antigen. These patients had FAB M1 or M5a morphologic characteristics and lower complete remission (CR) rate. This result demonstrated that CD34 positive ANLL is poorly differentiated.
...
PMID:[Clinical and immunophenotyping features of CD34-positive acute nonlymphoblastic leukemia]. 754 28
We report here a case of hypoplastic
leukemia
with T cell markers in whom complete remission was obtained with granulocyte-colony-stimulating factor (G-CSF) alone. A 23-year-old male was diagnosed with hypoplastic
leukemia
: Hb 2.6 g/dl, platelet count 29.0 x 10(9)/l after transfusion, WBC 2.9 x 10(9)/l, hypocellular bone marrow with 70.7% blasts. He was given G-CSF 300 micrograms/day by intravenous drip infusion without antileukemic agents for severe pneumonia. After the administration of G-CSF for 15 days, hematological examination and bone marrow findings had improved to normal, and complete remission was obtained. However, the patient relapsed 45 days after discontinuation of G-CSF. The characteristics of the relapsed
leukemia
cells were similar to those on admission: negative for myeloperoxidase and positive for T cell markers (CD2 and
CD7
). The possibilities for the differentiation of leukemic cells and the recovery of normal hematopoiesis with G-CSF are discussed.
...
PMID:Complete remission in a patient with hypoplastic acute lymphoblastic leukemia induced by granulocyte-colony-stimulating factor. 754 23
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