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)

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

Hematologic changes in panmyelopathia are characterized by a wide-spreading spectrum of symptoms and a rare specifity. Therefore cytological and cytochemical findings do not allow a significant prognosis for the malignant or benign development of panmyelopathia. Cytogenetic experiments showed only the Philadelphia chromosome being of diagnostic value. MEISNER and co-workers, who studied adults with panmyelopathia and proven myelocytic leukemia and 5 children with acute lymphocytic leukemia, found that significant and persistent spontaneous division in unstimulated 24 hr. peripheral blood cultures is an indication of a malignant state. The present work shows that in two of five children with panmyelopathia and with significant spontaneous division chronic myelocytic leukemia developed or was in the very initial state; a third child with spontaneous division is still under control. In contrast to literature only one of 14 children with ALL had significant spontaneous cell division. Therefore the method applied must be checked for its usefulness in ALL and especially for its usefulness in early recognition of a relapse.
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PMID:[Cytogenetic studies as a contribution to the diagnosis of juvenile preleukemia and leukemia recurrence]. 6 24

The majority of human lymphocytic and myelocytic leukemia cells express a polymorphic antigen that is found on peripheral blood B-lymphocytes and cultured lymphoblastoid B-cell lines. These B-lymphocyte antigens were detected by 34 human alloantisera that were repeatedly absorbed with pooled platelets to remove all activity against HLA antigens and T-lymphocytes. Absorption studies indicated that a common antigen was present on both B-lymphocytes and positive leukemia cells. Leukemia cells could be subdivided into two groups based on the presence of the B-lymphocyte antigen. Fourteen of 18 acute myelocytic leukemia cells, 10 of 13 acute lymphoblastic leukemia cells, 4 of 6 chronic myelocytic leukemia cells, and 2 of 2 chronic lymphocytic leukemia cells were positive. This group of leukemia cells also reacted with rabbit anti-B-cell sera raised to papain digests of spleen cell membranes. F(ab')2 fragments of the rabbit antsera were shown to specifically block the reactions of the human antisera against B-cells and leukemia cells. These results suggested that the rabbit and human anti-B-cell sera were reacting with identical molecules. This conclusion was supported by immunoprecipitation data.
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PMID:Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. II. Detection by human anti-B-cell alloantisera. 6 14

A serum against human lymphoblastic leukemia cells was obtained inoculating rabbits. We studied the specificity of the serum before and after particular absorptions in various clinical conditions. The serum was cytotoxic against many cases of acute lymphoblastic leukemia, against continuously cultured Burkitt's lymphoma cells and against chronic myelogenous leukemia in blast crisis. On the contrary, the serum was not cytotoxic against lymphocytes of normal donors, acute lymphoblastic leukemia in remission and other lymphoproliferative disorders.
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PMID:Preparation, purification and in vitro properties of a serum against human lymphoblastic leukemia-associated antigens. 6 31

Two unique cell lines, NALM-1 and BALM-2 derived from lymphoblast-like cells of chronic myelogenous leukemia and rare B cell acute lymphoblastic leukemia patients, respectively, were compared with fresh parent cells from the patients and with a Philadelphia chromosome positive K-562 cell line previously established from a chronic myelogenous leukemia patient in blastic phase. NALM-1 resembled the parent cells in the presence of Philadelphia chromosome, non-T/non-B acute lymphoblastic leukemia specific antigens and lack of T or B cell markers, whereas BALB-2, like the parent cells, had two chromosome markers and bore kappa, delta and mu immunoglobulins. NALM-1 lacked Epstein-Barr virus genome, whereas BALM-2 showed the presence of Epstein-Barr virus genome. K-562 cells lacked all the antigen markers examined. All cells had high DNA polymerase alpha activity and low DNA polymerase gamma activity. NALM-1, like the parent cells and unlike K-562 cells, had high terminal deoxynucleotidyl transferase activity of about 200 mu/mg DNA, whereas BALM-2, like its parent cells, had terminal deoxynucleotidyl transferase activity of 1-2 mu/mg DNA (1 u = 1 nmole Mn++-dGTP/h on dA12-18 initiator). Terminal deoxynucleotidyl transferase was characterized by its chromatographic and sedimentation behavior, thermal sensitivity and specific inhibition by streptolydigin and terminal deoxynucleotidyl transferase antisera. These results indicate that NALM-1 and K-562 may represent different phenotypes of cells in CML blastic crisis. Moreover, NALM-1 and BALM-2 seem to have retained the characteristics of original leukemic cells from which they may have been derived.
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PMID:Terminal deoxynucleotidyl transferase activity and cell surface antigens of two unique cell lines (NALM-1 and BALM-2) of human leukemic origin. 7 Apr 13

A human serum (obtained from a multiparous and multiple-transfused patient with chronic myelogenous leukemia) and a rabbit antiserum (obtained by immunization with papain extracts from a B-lymphoblastoid cell line) showed reactivity against antigenic specificities (different from HLA) expressed on peripheral blood B-lymphocytes, unmarked lymphocytes, and monocytes. These antigenic determinants were expressed on myeloblasts and lymphoblasts from patients with acute leukemia (during the active phase of their disease) and on B-lymphoblastoid cell lines and lymphocytes from patients with chronic lymphocytic leukemia. Purified peripheral blood T-lymphocytes, mitogen (phytohemagglutinin)-activated T-lymphocytes, and lymphoblasts (with T-cell characteristics) obtained from patients with acute lymphoblastic leukemia or established lymphoblastoid cell lines lacked these antigenic specificities. Absorption experiments indicate that the antigen(s) detected on normal mononuclear cell populations, leukemia cells, and B-lymphoblastoid cell lines were either identical or highly cross-reactive.
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PMID:Recognition by human and rabbit sera of common antigens to leukemia blast cells, peripheral blood B-lymphocytes, and monocytes. 7 Nov 97

A child presented with "acute leukemia" in which the blast cells resembled lymphoblasts and had negative cytochemical staining (PAS, Sudan black, and myeloperoxidase). Remission was induced and typical adult-type chronic myelogenous leukemia (CML) followed. Cytogenetic studies initially and during remission and subsequent "acute leukemia" relapses revealed the presence of the Philadelphia chromosome abnormality. Terminal transferase assay performed on peripheral blood blast cells was markedly elevated and soft agar culture growth parameters were typical of acute lymphoblastic leukemia T and B cell marker studies revealed no markers. This case report with supportive laboratory studies suggests that a cell line with lymphoid characteristics may predominate during acute leukemic transformation. This type of subclassification of leukemia may be of importance in therapeutic planning.
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PMID:Lymphoblastic conversion in chronic myelogenous leukemia. 7 81

Rabbit or goat antisera directed to ALL, CLL, AML and CML cells were investigated in cytotoxicity tests with different leukaemia and normal cells as targets. After absorptions with erythrocytes and spleen cells from allogeneic donors the antisera killed only leukaemia cells. There was no reaction with remission leukocytes or blood leukocytes from normal donors. Anti-ALL-Sera reacted in 35 out of 49 tests with ALL cells from 13 patients. Apparently the ALL antisera which were directed to the T cell subtype of ALL preferentially affected ALL cells of this subtype. Cross reactions with cells from CLL, AML and CML were not found. Anti-CLL-sera reacted in 10 out of 12 tests with CLL cells from 4 donors, and in 4 out of 20 tests with ALL cells from 7 donors and also with the cells of a CML patient. AML cells from two patients were not killed. Antisera against AML and CML showed extensive cross reactions with cells of myelocytic and lymphocytic leukaemias. Absorption tests demonstrated the presence of two antibody specificities in AML antisera, one of which being directed to a common antigen of AML and ALL cells and another against an antigen of myelocytic leukaemia cells.
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PMID:Specificities of heterologous antisera against human leukaemia cells. 1. Reactions against leukaemia cells. 8 65

Hydroperoxidase-positive Phi bodies and rods are much more prominent and prevalent than rods visualized with a Romanovsky-type stain (Auer rods) in immature leukocytes of patients with active acute myelogenous leukemia (AML). They are readily observed with the light microscope in peripheral blood or marrow films of AML patients stained to show their peroxidatic activity. In many of these patients, Auer rods, which apparently constitute only a small subpopulation of the hydroperoxidase-positive Phi bodies and rods, were detected with difficulty, if at all. The hydroperoxidase-positive Phi bodies and rods were observed in 92% of 36 patients with active disease. They were never observed in leukocytes of patients with other hematopoietic disorders or of normal individuals. Thus, they facilitated the distinction of AML from acute lymphocytic leukemia and chronic granulocytic leukemia in blast crisis. They were absent in full clinical remission after chemotherapy and were greatly diminished in partial remission. They were present in disease relapse and reappeared in five patients who had been in full remission. These results suggest that these hydroperoxidase-positive enlarged particles are pathognomonic of AML and that monitoring them with the light microscope may aid in guiding its clinical management.
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PMID:Facilitated light microscopic cytochemical diagnosis of acute myelogenous leukemia. 8 86

Antisera against human acute myelocytic leukaemias were tested in complement-dependent in-vitro cytotocity tests against leukaemia cells and normal cells as targets. After absorption with erythrocytes and spleen cells from allogeneous donors the antisera reacted with leukaemia cells, but not with leukocytes from bone marrow and the peripheral blood of children in remission, lymphocytes from healthy donors, enriched B-lymphocytes, enriched T-lymphocytes, PHA-induced blasts and cord blood lymphocytes. Extensive cross reactions were obtained in the tests against leukaemia cells. The antisera reacted not only with AML cells, but also with ALL, CLL, and CML cells. It was possible to remove the cross-reactivity with ALL cells through absorption with ALL cells or with fetal tissue, and to remove the cross reactivity with CLL cells through absorption with CLL. A complete absorption of the anti-AML sera was possible with AML and CML cells. After absorption with fetal tissue and CLL cells the antisera showed exclusively specificity for myelocytic leukaemias. Thus, AML cells contain three leukaemia-associated membrane antigen components: an antigen of fetal origin, a "CLL-specific" antigen, and an antigen that occurs on myelocytic leukaemias.
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PMID:Human leukaemia-associated antigens expressed by acute myelocytic leukaemia cells and their detection by heterologous antisera. 8 82


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