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)

Leukemic cells from all human chronic granulocytic leukemia (CGL) and some acute myelomonocytic leukemia (AMML) donors are lysed by rabbit antisera to a purified glycoprotein of Friend murine leukemia virus (FLV gp71) in a microcytotoxicity assay. These antisera are not cytotoxic to cells from patients with acute myelocytic leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), or to peripheral blood lymphocytes from normal donors. A goat antiserum to gradient purified FLV in addition to reacting with cells from CGL and AMML donors also reacted with cells from AML patients and some ALL donors. However, this antiserum failed to react with cells from CLL patients. Peripheral blood and bone marrow leukocytes prepared from leukemic patients in clinical remission failed to react with antisera to FLV and FLV gp71. Absorption experiments demonstrated that the antigen on CGL cells which is reacting with the antiserum to FLV gp71 is also present on normal human platelets and neutrophils. Similar absorption studies showed that the antigen on AML cells detected by the FLV antiserum is not present on normal leukocytes and platelets and appears to be related to the major internal p30 antigens of mammalian RNA tumor viruses. Another antigenic relationship between oncornaviruses and membrane antigens of human leukemia cells was shown by the ability of FLV antigens to absorb the cytotoxic reactivity of nonhuman primate antisera detecting human leukemia-associated antigens. FLV and FLV gp71 antigens were able to absorb all cytotoxic activity of monkey and chimpanzee antisera to human myeloid leukemia antigens when these antisera were tested with CGL cells. These two approaches to an analysis of cross-reactivity indicate that the antigenic determinant(s) detected by the cytotoxic reactions of the FLV gp71 antiserum with human CGL cells is different from the determinant on FLV gp71 which is responsible for the inhibition of the reactivity of simian antisera with CGL cells. Since the goat and rabbit antisera to FLV and FLV gp71 are able to distinguish AML from CGL cells by direct cytotoxicity testing and absorption, they may be valuable reagents for the serological diagnosis of myeloid leukemia. In addition, since peripheral blood cells from AML and CGL patients in clinical remission were seronegative, the antisera may be valuable as management aids. The data in this report indicates that whatever the mechanism of leukemogenesis is in man, cells from CGL and AML patients possess certain membrane antigens which cross-react with FLV structural components such as p30 and gp71.
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PMID:Relationships between membrane antigens of human leukemic cells and oncogenic RNA virus structural components. 5 69

Peripheral leucocytes from 16 patients with chronic myeloid leukaemia (CML) were examined for the presence of oncornavirus p30 antigens by indirect cytoplasmic immunofluorescence. The leucocytes of 12 patients who could be kept in balance by chemotherapy proved to be negative or contained the p30 antigen of mammalian endogenous oncornaviruses as the only viral antigen. In the leucocytes of four patients being in blastoid crisis, an antigen related to the p30 antigen of mammalian leukaemia-sarcoma viruses was detected. In five of six patients decrease in sensitivity to chemotherapy, or blastoid crisis, was preceded by expression of leukaemia-sarcoma virus p30 antigen(s). Leucocytes from 15 CML patients kept in balance by chemotherapy and those from seven being in blastoid crisis, were examined by indirect membrane immunofluorescence for the presence of antigen(s) related to the gp70 antigen of the simian and murine leukaemia-sarcoma virus. All tests proved to be negative.
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PMID:Expression of oncornavirus antigens in peripheral leucocytes of patients with chronic myeloid leukaemia. 29 Jan 30

We studied a patient with a Philadelphia chromosome-positive chronic myeloid leukemia, who died in relapse after multiple transfusions and grafting with bone marrow from his monozygotic twin brother (referred to as "donor" in this paper). We present data indicating that this patient may have had a retro-virus infection that this virus is related to the group of exogenous primate type C retroviruses. Antibodies to simian sarcoma virus (SSV) M.W. 30,000 protein (p30) but not endogenous feline virus RD-114 could be found in patient but not donor serum. Patient but not donor cells were able to actively synthesize a p30 protein that could be precipitated with patient serum and rabbit anti-SSV p30 but not with donor serum or rabbit anti-RD 114 p30. Patient p30 resembles SSV p30 but not RD-114 p30 in peptide mapping by limited proteolysis and subsequent slab gel electrophoresis. Patient but not donor cells were able to actively synthesize a M.W. 78,000 protein that could be precipitated with goat anti-SSV. An enzyme with properties of reverse transcriptase was increased 30-fold ion patient cells when compared with donor and other control cells. Related to the presence of widespread infectious agents may be the finding that, in the course of the patient's disease, donor serum showed increasing amounts of possibly immunoregulatory (Cancer Research, submitted for publication) antibodies, reactive with autologous and, more effectively, with patient-derived cell membrane M. W. 80,000 protein (a possible idiotypic receptor structure) and M.W. 94,000 protein (a T-cell alloantigen).
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PMID:Synthesis of a viral protein with molecular weight of 30,000 (p30) by leukemic cells and antibodies cross-reacting with Simian sarcoma virus p30 in serum of a chronic myeloid leukemia patient. 617 17

Peripheral leucocytes from patients with chronic myeloid leukemia were examined for the presence of oncornavirus p30 antigens by indirect cytoplasmic immunofluorescence. The leucocytes of patients who could be kept in balance by chemotherapy proved to be negative or contained the p30 antigen of baboon endogenous oncornavirus. In the leucocytes of patients being in blastoid crisis, an antigen related to the p30 antigen of simian sarcoma virus was detected. In five of six patients decrease in sensitivity to chemotherapy, or blastoid crisis, was preceded by expression of leukaemia-sarcoma virus p30 antigen(s). Plasma samples of patients with acute myeloid leukemia (AML) and potentially preleukemic hematological disorders were studied for the presence of anti-HL 23 virus antibodies by indirect membrane immunofluorescence. In patients with untreated AML, antibodies could be detected when the peripheral leucocyte count was low. After treatment of AML with cytostatic drugs the presence of high titer antibodies was connected with long lasting remission. Of twelve patients with potentially preleukemic disorders, five proved to be positive for the presence of HL 23-specific antibodies. In half a year period development of overt leukemic disease could be observed in four patients, who proved to be antibody negative in the preleukemic phase.
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PMID:Studies on antigens of C-type primate viruses and antibodies to them at patients with myeloid leukemia and potentially preleukemic hematological disorders. 626 16

A large series of leukaemias (1,512 cases) and leukaemic cell lines (40) have been tested for selective expression of a monomorphic HLR-DR determinant using a monoclonal antibody (DA2). Relatively mature myeloid leukaemias (APML, CGL) and erythroid leukemias are DR-, in contrast to most (72% leukaemias of myeloid precursors (e.g. AML) which are DR+. Non-T ALL are DR+ but T (thymic) ALL are invariably DR-. In contrast to the latter, some leukaemias with mature T cell phenotypes are DR+. Leukaemias or lymphomas of B cells and B cell precursors (e.g. pre-BALL) are invariably DR+, whereas myeloma or plasma cell leukaemias are DR-. This pattern of selective expression appears to closely parallel that seen in normal haemopoietic differentiation. Biochemical features of HLA-DR structures on leukaemic cells have been compared with the known features of B cell derived DR molecules and in one case ALL compared with an autologous (EBV transformed) B cell line. Most leukemic cells showed the same general alpha and beta two chain structure. However, B cell line and most chronic leukaemias showed the presence of an extra band of molecular weight 30,000 daltons (p30) with an intermediate electrophoretic mobility on SDS-PAGE between that of the alpha and beta DR chains. In acute leukaemias and leukaemic cell lines (i.e. immature cells) p30 was not seen unless short labelling times were used. Two dimensional NEPHGE/SDS-PAGE under appropriate labelling conditions showed that the pattern of spots obtained from an ALL line (Nalm-6) and its autologous EBV transformed partner (B85) were similar though not identical. Pulse chase labelling of Nalm-6 and B85 showed that the turnover rate of p30 relative to DR alpha and beta chains, differed in the two lines.
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PMID:Characterization of HLA-DR antigens on leukaemic cells. 695 50

The monoclonal antibody 013, which detects the cell surface glycoprotein p30/32mic2 (CD99) is a characteristic, if nonspecific, marker for peripheral neuroepithelioma and Ewing's sarcoma. 013 was first produced against a human thymus leukemia antigen and has also been found in immature terminal deoxynucleotidyl transferase (TdT)-positive T cells and in a small group of hematopoietic precursor cells in the bone marrow. 013 is reactive in lymphoblastic lymphomas and acute leukemias, as well as in a variety of other hematologic malignancies. Because the distribution of 013 positivity in hematopoietic proliferations is similar to that of TdT, we hypothesized that 013 might correlate with TdT positivity. We studied 67 lymphoblastic lymphomas and acute lymphoblastic leukemias, 6 chronic myelogenous leukemias in blast crisis, a variety of acute myeloid leukemias, 5 granulocytic sarcomas, and a spectrum of 94 diffuse lymphomas other than lymphoblastic type. With the use of heat-induced epitope retrieval and automated immunostaining, we compared the results obtained with 013 and TdT, a well-established marker of lymphoblastic lymphomas and acute lymphoblastic leukemias that can also be successfully demonstrated in tissue sections by use of a similar technique. In our study, all of the 013-positive cases were also TdT positive. 013 reacted with 44 (71%) of 62 of the TdT-positive lymphoblastic lymphomas and acute lymphoblastic leukemias cases studied. We also found 013 to be positive in one case of TdT-positive acute myeloid leukemia, in two cases of chronic myelogenous leukemia in blast crisis, and in three TdT-positive granulocytic sarcomas. 013 was negative in all of the other high-grade malignant lymphomas and in TdT-negative leukemias. With use of our technique, 013 positivity appears to be restricted to hematologic proliferations that demonstrate TdT positivity. 013 may be a helpful additional marker in the diagnosis of TdT-positive leukemias and lymphomas in conventionally processed tissue sections.
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PMID:013 (CD99) positivity in hematologic proliferations correlates with TdT positivity. 911 Feb 87