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

The present study describes a comparative study of MLR-S of various stages of fresh and cultured normal or leukemic myeloid, monocytic and erythroid cells. "One-way" MLR was performed, using a slightly modified whole blood method. Fresh leukemic myeloblasts from patients with acute myelocytic leukemia or chronic myelocytic leukemia, in blastic crisis possess a strong MLR-S whereas fresh granulocytes from patients with chronic myelocytic leukemia or from healthy subjects possess no MLR-S. Cultured leukemic myeloblasts from KG-1 or ML-1 cell line possess a very strong or a moderate MLR-S, whereas cultured leukemic promyelocytes from HL-60 cell line possess little or no MLR-S. Fresh leukemic erythroblasts or cultured leukemic erythroblasts from K-562 cell line exert a strong MLR-S whereas fresh erythrocytes exert no MLR-S. Cultured monoblasts from HPL-SK-1 or Murray cell line possess a very strong MLR-S whereas fresh monocytes from healthy subjects or from a patient with chronic monocytic leukemia possess a moderate MLR-S. These observations clearly indicate that there is a good correlation between the MLR-S and the cell differentiation stage. Observations in the present study also support the hypothesis that the MLR-S is a differentiation antigen which is completely lost by the terminal stage of myeloid or erythroid cell maturation or partially lost by the terminal stage of monocytic cell maturation.
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PMID:Expression of MLR-S in human myeloid, monocytic and erythroid cell differentiation. 645 11

A patient with Philadelphia chromosome (Ph1) positive chronic myelogenous leukemia (CML) entered a blast crisis localized to lymph nodes. On light microscopy, by morphology and histochemical staining, the blasts were undifferentiated. In spite of terminal deoxynucleotidyl transferase positivity, some of the lymph node cells expressed a myeloid differentiation antigen, OKM1, and were peroxidase positive by transmission electron microscopy (TEM). However, the majority of cells were peroxidase negative on TEM and expressed OKT-10, a marker found on both primitive myeloid and lymphoid cells. Cultures of lymph node cells stimulated with Epstein-Barr virus or lipopolysaccharide (LPS) revealed the Ph1, indicating B cell involvement in the CML. T cells from cultures stimulated with L4-phytohemagglutinin and T cell growth factor were negative for the Ph1. In unstimulated lymph node cells, the uncomplicated Ph1 could not be demonstrated; instead, a unique complex karyotype involving a masked Ph1 was identified in these and the LPS cultures. This karyotype was not found in bone marrow (BM) metaphase cells. Instead, BM cells showed either the simple Ph1 or the Ph1 with a rearrangement involving chromosomes 13 and 20. The patient had transient responses to three chemotherapy regimens, two of which were designed to treat acute lymphocytic leukemia, but he died 8 months after disease acceleration without BM blast crisis. These findings are compatible with an extramedullary blast crisis originating in a primitive cell with both myeloid and lymphoid characteristics.
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PMID:Unusual karyotypic changes and B cell involvement in a case of lymph node blast crisis of chronic myelogenous leukemia. 661 Apr 45

The presence of the common acute lymphoblastic leukemia antigen (CALLA) on leukemic cells from the great majority of patients with non-T cell acute lymphoblastic leukemia and chronic myelogenous leukemia in blast crisis suggests that CALLA could be differentiation antigen expressed by normal lymphoid and myeloid stem cells. Treatment with a murine monoclonal anti-CALLA antibody and complement lysed CALLA-positive leukemic cells quantitatively, whereas similar treatment of nucleated cells from peripheral blood and bone marrow failed to affect the expression, in semisolid culture, of CFU-G/E, BFU-E, CFU-E, or CFU-C. These data suggest that CALLA is not a normal differentiation antigen of the myeloid bipotent cell or its committed progenitors.
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PMID:Absence of common ALL antigen on normal bipotent myeloid, erythroid, and granulocyte progenitors. 694 21

NCA, a normal colon and granulocyte antigen, which has been found in large amounts in myelocytes and metamyelocytes and in smaller amounts in neutrophil granulocytes, was studied in 50 CML patients in various stages of the disease. Radioimmunoassay was used to demonstrate NCA in serum. Untreated CML patients had a mean level of 732 micrograms NCA/l, poorly controlled patients 421 micrograms/l and well-controlled patients 160 mu/l. These values differ significantly from the mean of healthy persons, which was 71 micrograms NCA/l. The serum NCA levels were related to the number of maturing myeloid cells in blood, and to the clinical course in the chronic phase of CML. In blast crisis low values with a mean of 109 micrograms NCA/l was found. Patients with ANLL had a low mean level, 50 micrograms/l. Low levels of NCA could not be attributed to antibodies to NCA. NCA is a normal myeloid differentiation antigen. Despite this, its occurrence in serum in leukemic patients differs from normal. This probably has to do with the abnormal amount as well as the release of NCA by leukemic maturing myeloid cells.
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PMID:Clinical evaluation of NCA in patients with chronic myelocytic leukemia. 694 77

A monoclonal antibody (anti-B1) specific for a unique B cell surface differentiation antigen was used to characterize the malignant cells from patients with leukemias or lymphomas. All tumor cells from patients with lymphomas or chronic lymphocytic leukemias, bearing either monoclonal kappa lambda light chain, expressed the B1 antigen. In contrast, tumor cells from T cell leukemias and lymphomas or acute myeloblastic leukemia were unreactive. Approximately 50% of acute lymphoblastic leukemias (ALL) of non-T origin and 50% of chronic myelocytic leukemia in blast crisis were also anti-B1 reactive. moreover, 21 of 28 patients with the common ALL antigen (CALLA) positive form of ALL were anti-B1 positive, whereas 0 of 13 patients with CALLA negative ALL were reactive. These observations demonstrate that an antigen present on normal B cells is expressed on the vast majority of B cell lymphomas and on approximately 75% of CALLA positive ALL, suggesting that these tumors may share a common B cell lineage.
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PMID:A unique cell surface antigen identifying lymphoid malignancies of B cell origin. 696 30

CML66 is a newly identified differentiation antigen that is expressed broadly in human leukemia and solid tumors, but its physiological function remains unknown. In the present study, to clarify the feasibility of CML66-targeted cancer immunotherapy, we attempted to identify cytotoxic T lymphocyte (CTL) epitopes derived from CML66. An immunogenic CML66-derived epitope (amino acid residues 76-84; YYIDTLGRI) capable of inducing human leukocyte antigen (HLA)-A*2402-restricted CTL specific for this peptide was identified. CML66-derived peptide-specific CTL efficiently lysed human leukemia cells, but not normal cells, in a HLA-A*2402-restricted fashion. Quantitative real-time polymerase chain reaction revealed that CML66 mRNA is expressed abundantly in primary acute myeloid leukemia cells, acute lymphoid leukemia cells, and chronic myelogenous leukemia cells in advanced phase, and that the expression level of CML66 mRNA in normal cells is low compared with that in leukemia cells. CML66-specific CTL precursors were detected in the peripheral blood of patients with acute leukemia. These data indicate that the CML66-derived epitope identified in the present study is a new target antigen for cellular immunotherapy of human leukemia.
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PMID:Identification of an epitope derived from CML66, a novel tumor-associated antigen expressed broadly in human leukemia, recognized by human leukocyte antigen-A*2402-restricted cytotoxic T lymphocytes. 1842 54


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