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)

A method employing CD45-gating of blast cells was evaluated for the flow cytometric detection of residual disease in CD19- and myeloid antigen-positive acute leukemia in morphologic remission. In the normal bone marrow, CD45-gating identified at least three populations of immature cells, one of which appeared to retain a minute fraction of CD19- and CD13/33-antigen co-expressing cells. In acute leukemia, CD45 expression separated the blast cell population from the normal marrow cell populations. In the majority of patients with CD19- and myeloid antigen-positive acute leukemia, subpopulations of blast cells with this mixed phenotype were detected during morphologic remission.
Leukemia 1994 Sep
PMID:Flow cytometric detection of residual disease in acute leukemia by assaying blasts co-expressing myeloid and lymphatic antigens. 752 95

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.
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PMID:[Cellular and biological characterization of CD7-positive acute leukemia cells--an investigation of the established cell line, HSM911]. 752 34

We investigated the effect of ubenimex on the growth and differentiation of U937 cells, a histiocytic lymphoma cell line. Ubenimex is a dipeptide ((2S,3R)-3-amino-2-hydroxy-4-phenylbutyryl-L-leucine) and an inhibitor of aminopeptidase B produced by Streptomyces olivoreticuli. Ubenimex inhibited the proliferation of U937 cells in a dose-dependent manner. Ubenimex-treated U937 cells showed condensation of nuclear chromatin, increase of cytoplasmic vacuoles and more intense nonspecific esterase staining compared with untreated U937 cells. Expression of CD13 and CD68 detected by monoclonal antibodies My7 and EBM11, respectively, was enhanced by ubenimex, but the expression of CD4 detected by MT310 was significantly decreased. The effects of ubenimex on U937 cell growth inhibition and enhancement of monocytic cell surface marker expression on U937 cells were reversible when cultivated without ubenimex for more than 6 days. In addition, the bactericidal activity of U937 cells was increased by ubenimex treatment, and was further enhanced by treatment with macrophage colony-stimulating factor (M-CSF). Furthermore, ubenimex augmented the expression of M-CSF receptors by U937 cells and enhanced the tyrosine kinase activity of cellular pp60c-src. These findings indicated that ubenimex inhibited the proliferation of U937 cells and induced morphological, cytochemical and functional differentiation into monocyte/macrophages.
Leukemia 1994 Dec
PMID:Effect of ubenimex on the proliferation and differentiation of U937 human histiocytic lymphoma cells. 752 60

New technology allows highly sensitive flow cytometric detection and quantitative analysis of intracellular antigens in normal and malignant hemopoietic cells. With this technology, the earliest stages of myeloid and lymphoid differentiation can easily and reliably be identified using antibodies directed against (pro-)myeloperoxidase/MPO, CD22 and CD3 antigens, respectively. Particularly for the analysis of undifferentiated acute myeloblastic leukemia (AML) cells, the immunological demonstration of intracellular MPO or its enzymatically inactive proforms is highly relevant, since other myeloid marker molecules such as CD33, CD13, or CDw65 are either not restricted to the granulomonocytic lineage or appear later in differentiation. By combining MPO staining with staining for lactoferrin (LF), undifferentiated cells can be distinguished from the granulomonocytic maturation compartment in bone marrow, since LF is selectively expressed from the myelocyte stage of differentiation onward. The list of informative intracellular antigens to be used in leukemia cell analysis will certainly expand in the near future. One candidate, intracellular CD68, has already been tested by us, and results are presented. Also dealt within this article are surface marker molecules not (as yet) widely used in leukemia cell analysis but with the potential to provide important additional information. Among them are the surface structures CD15, CD15s, CDw65, CD79a (MB-1), CD79b (B29), CD87 (uPA-R), and CD117 (c-kit).
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PMID:Flow cytometric analysis of cell-surface and intracellular antigens in leukemia diagnosis. 753 75

We examined the responsiveness of leukemic cells to colony stimulating factors (CSFs) as determined by 3H-TdR incorporation and surface phenotypes of leukemic blasts. In acute myeloid leukemia (AML), CD13 and/or CD33 positive and HLA-DR negative M1 and M3 cases tended to show high response to G-CSF, GM-CSFs and IL-3, however, all HLA-DR positive M1, M2, M4 and M5 cases were unresponsive to CSFs but showed high autonomous growth. In acute lymphocytic leukemia (ALL), no response was observed to any CSFs but high autonomous growth was found in mixed leukemia cases. Sole T or B lineage cases showed low autonomous growth. These results suggest the varied nature of the proliferative state in leukemia and the existence of a subgroup in M1.
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PMID:Relationship between responsiveness to colony stimulating factors (CSFs) and surface phenotype of leukemic blasts. 870 27

A 70-year-old male was admitted to our hospital because of leukocytosis. The laboratory examination revealed leukocytosis (44,500/microliters) with blasts (99%) in the peripheral blood. Myeloperoxidase staining of the leukemia cells was negative, but the surface phenotype was CD13- and CD33-positive, and negative for all lymphoid antigens. Peroxidase staining using the electron microscope was positive. Thus, the patient was diagnosed as acute myeloblastic leukemia (M0), according to the FAB classification. Although the therapy regimens commonly used for ANLL were effective for some cases with M0, the regimens mainly for ALL were more effective for the others. Thus we cannot determine what is the most effective regimen for M0. Since the patient had many complications, he was treated with low-dose AraC instead of combination chemotherapy. After the beginning of treatment, he became febrile and we added G-CSF to Ara-C. One month later, the patient achieved complete remission without severe infection. After four courses of consolidation therapy, the patient was discharged. He has been maintained in remission for more than 3 years and 8 months with only 5-day oral administration of cytarabine ocfosfate every four weeks.
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PMID:[Continuation of complete remission by oral administration of cytarabine ocfosfate in a patient with M0, who achieved remission by small doses of cytosine arabinoside with G-CSF]. 753 75

Peripheral blood cells from a female patient with Ph1-positive chronic myelogenous leukemia (CML) in blast crisis were serially transplanted in BALB/c nude mice for 16 passages. This in vivo cell line, designated CML-N-1, had Ph1 chromosome abnormality and BCR gene rearrangement. The cells expressed CD11b, CD13, CD33, CD34, CD38, and HLA-DR antigens until the 11th passage and subcutaneous tumors produced by these passages were composed of admixtures of immature and maturing cells that differentiated to basophils when cultured in vitro. From the 12th passage on, the tumors became composed mainly of immature cells expressing CD13, CD34, and HLA-DR, and no longer differentiated to basophils even upon in vitro culture. In contrast to the vigorous proliferation in vivo, CML-N-1 cells from any passage failed to proliferate in vitro under standard liquid culture conditions with or without growth factors, such as granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor, monocyte colony-stimulating factor, interleukin 3, interleukin 6 and stem cell factor. However, a continuously growing cell line, designated CML-C-1, was established by culturing CML-N-1 cells on feeder layers of mouse bone marrow stromal cells. This mouse bone marrow stromal cell-dependent cell line showed immature cell morphology and expressed early myeloid phenotype positive for CD13, CD34, and HLA-DR. These results indicate that mouse bone marrow stromal cells provide a certain growth factor(s) active on human leukemia cells.
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PMID:Direct transplantation of chronic myelogenous leukemia cells into nude mice and establishment of a leukemic stem cell (Ph1+, CD34+) line dependent on mouse bone marrow stromal cells in vitro. 754 Jun 8

A case of 77-year-old female with multiple myeloma (IgG-k) developed acute myelomonocytic leukemia (AMMoL) following a myelodysplastic stage after chemotherapy with melphalancyclophosphamide combinations for 6 years. The leukemic blast cells expressed both myeloid antigens (CD11b, CD13, CD14, CD15, CD33 and CD34) and T/B lymphoid antigens (CD2, CD4, CD22 and PCA1). Cytogenetic analysis revealed a chromosome deletion -7. Analysis of immunoglobulin genes showed the heavy chain genes in germ line configuration. These findings indicate that the AMMoL was a therapy-related stem cell leukemia and was a clonal origin genetically different from multiple myeloma irrespective of plasma cell phenotype.
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PMID:Acute myelomonocytic leukemia in a patient with multiple myeloma: evidence for different clonal origin. 754 40

The rare t(2;14)(p13;q32) was previously described in the three pediatric patients with acute lymphatic leukemia. In these cases this abnormality was found at diagnosis, manifested the sole chromosomal abnormality, and was associated with a favorable prognosis. We here describe three cases of leukemia where such translocations were found at relapse, were associated in two of the cases with additional known characteristic chromosomal aberration, and were associated with a grave prognosis. Interestingly enough, the malignant cells of all three patients shared the same surface antigens: CD34, HLA DR, CD10, CD20, and the myeloid marker CD13. The leukemic clone exhibiting t(2;14) probably evolved from a t(1;19)6q- pre-B acute lymphatic leukemia in one of the cases, and from a chronic phase Ph1 chromosome in another. The significance of the translocation and the coexistence of CD10 and CD13 on the same cell are discussed.
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PMID:Translocation (2;14)(p13;q32) in CD10+ ;CD13+ acute lymphatic leukemia. 755 84

This study assesses the value of immunologic and ultrastructural methods in disclosing the lineage commitment of cells from acute leukemias (ALs). Two hundred and fifty-one ALs were characterized morphologically, cytochemically, and immunologically. Myeloperoxidase (MPO) positivity in > 3% of blasts was regarded as evidence of the myeloid origin of leukemic cells, cytoplasmic CD22 (cCD22) expression was taken as an indication for B-lineage acute lymphoblastic leukemia (ALL), and CD3+ (membrane or cytoplasmic) cases were classified as T-ALL. Diagnosis of minimally differentiated acute myeloid leukemia (AML-M0) was made when blast cells had undifferentiated features by light microscopy, reacted with at least one of the antibodies to myeloid-specific antigens (CD13, CD33, MPO), and lacked CD19, cCD22, and c/mCD3. Megakaryoblastic differentiation was demonstrated by the expression of CD41 and/or CD61. Following these criteria, 209 cases were classified as acute myeloid leukemia (AML) and 39 as ALL. Expression of lymphoid antigens was detected in 45% of AML cases and 30% of ALLs showed myeloid antigens. One case was regarded as a true biphenotypic leukemia because of the combined expression of MPO and CD33 for the myeloid lineage, and cCD3, CD2, and CD5 for the T-cell lineage. Two cases lacked signs of myeloid or lymphoid differentiation and were studied by electron microscopy methods. One displayed platelet peroxidase (PPO) activity and was classified as a megakaryoblastic variant, one other reacted with anti-CD33 and was considered AML-M0. We conclude that light microscopy and standard immunologic methods can accurately demonstrate the lineage orientation in greater than 99% of ALs. Integration with ultrastructural analysis can define the cell nature of virtually all cases of AL.
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PMID:Lineage identification of acute leukemias: relevance of immunologic and ultrastructural techniques. 755 58


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