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)

High levels of terminal deoxynucleotidyl transferase have been observed in leukocytes of 7 out of 20 patients with chronic myelogenous leukemia in acute blast phase of the disease. These levels are comparable to the levels observed in human and calf thymus gland and cell lines with some T cell characteristics (Molt 4 and 8402). Negligible levels of this activity were observed in chronic myelogenous leukemia not in an acute blast phase of the disease, chronic lymphocytic leukemia, human B cells, mature T cells, and the mixed population of lymphocytes present in normal human blood. The detection of this enzyme in some patients with chronic myelogenous leukemia in acute blast phase of the disease suggests that the blast proliferation may involve primitive stem cells which have more lymphoid than myelogenous characteristics. This enzyme assay may be of use as a biological marker for following patients during treatment and in remission.
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PMID:Terminal deoxynucleotidyl transferase as a biological marker for human leukemia. 1 27

Terminal deoxynucleotidyl transferase (TDT) is an unusual DNA polymerase that does not use template information to synthesize new strands of DNA. It is normally found in high concentration in thymus (50 u/10(8) cells) and in low concentration in bone marrow (less than 5 u/10(8)). We report TDT measurements in the marrow and/or peripheral blood of 51 adult patients, 28 of whom had leukaemia. TDT is present in very high levels (greater than 50 u/10(8) cells) in leukaemic lymphoblasts and in low levels in leukaemic myeloblasts (less than 9 u/10(8) cells). Of two patients who developed lymphosarcoma-cell leukaemia following treatment of poorly differentiated lymphocytic lymphoma, one had high and one low levels of TDT in the leukaemic blast cells. Leukaemic cells from three of seven patients with chronic myeloid leukaemia in blast crisis had TDT levels within the range expected of acute lymphoblastic rather than acute myeloid leukaemia. High TDT in leukaemic cells probably marks them as derivatives of lymphoid progenitor, thymic or pluripotential stem cells. Quantitative assay of TDT may provide information useful in classifying haematological neoplasms.
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PMID:Terminal deoxynucleotidyl transferase measurements in the differential diagnosis of adult leukaemias. 6 84

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

Terminal deoxynucleotidyl transferase (TdT) determinations were carried out on peripheral blood leukocytes or bone marrow cells from 61 adult patients with various types of leukemia. TdT activity was undetectable in the cells of patients with acute myelocytic or acute myelomonocytic leukemia but was present in 12 of 13 patients with acute nonmyelocytic leukemia. None of 3 patients with acute myelocytic transformation of chronic myelocytic leukemia (CML) manifested TdT activity while 4 of 6 patients with lymphoid transformation had such activity. More patients with TdT in their leukemic cells responded to treatment than those without TdT activity. However, our findings suggest that TdT activity may be less useful in management of leukemia than has sometimes been supposed.
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PMID:Terminal transferase in leukemia of adults. 11 12

It was shown by Pincus and Klebanoff that a correlation existed between leukocytic iodination measured in vivo and microbicidal leukocytic activity. We have analyzed the results of this test in relation to time and in the presence of variable quantities of polymorphonuclear leukocytes (PMN). The values observed per time and PMN unit proved to be equivalent in the presence of 2.5 X 105 PMN or 5.0 x 105 PMN per 0.5 ml of incubation medium, measured after 10, 20 and 30 minutes or in the presence of 1.0 x 106 PMN, measured after 10 minutes. That is to say iodination is proportional to leukocyte concentration and incubation time. Increase of either the quantity of cells or the incubation time, beyond the area we defined, reduced iodination per cell and per unit of time. Concerning the patients with an insufficient iodination, we have studied 2 parameters in the presence of 5.0 x 105 PMN: 1) initial iodination measured after 10 and 20 minutes and 2) stability of iodination measured after 60 minutes. These two parameters were equally affected in two cases with myelofi-rosis, 3 patients with acquired refractory anaemia, one with chronic lymphoid leukaemia, one with erythroleukaemia, one with hairy cell leukaemia, one with systemic mastocytosis and almost complete myeloperoxidase dificiency, one with sickle cell disease, two with liver diseases and two with chronic myeloid leukaemia. The iodination at the 60th minute was more affected than at the 10th minute with a patient with myelofibrosis and 4 other patients with acquired refractory anaemias. The significance of these differences is not well understood; however the meaning of the decrease in the iodination of whatever type is that a PMN anomaly exists directly related to the myeloperoxidase H2O2 halogenation system, or to one of the stages of engulfment and/or metabolic events preceeding it and leading to the production of H2O2. This test, with the alterations we introduced, is suggested as a test for detection of functional PMN abnormalities.
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PMID:Quantitative iodination of human blood polymorphonuclear leukocytes. 16 86

A fifty-year old patient was treated for acute lymphoblastic leukemia. One month after a complete remission, a syndrome suggesting chronic myeloid leukemia led the authors to study the marrow karyotype which revealed the existence of a Philadelphia chromosome. A second lymphoblastic attack occurred rapidly and a second complete remission was easily obtained. A few weeks later, occurred lymphoblastic meningitis. A new cytogenetic study then showed duplication of the Philadelphia chromosome. One may imagine that the initial attack represented acute lymphoid transformation of chronic myloid leukemia. The theoretical and practical significance of this case is discussed.
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PMID:[Inagural lymphoblatic transformation in chronic myeloid leukemia. Clinical and cytogenetic study of one case]. 20 44

Two children presented with Ph1-positive leukemia, confirmed by Giemsa banding as 22q-. One child showed an initial presentation characteristic of acute lymphoblastic leukemia, followed by development of chronic myelocytic leukemia 2 yr later. A second child presented in blast crisis. Both patients showed blast cells possessing both lymphoid and myeloid characteristics, as demonstrated by histochemical, biochemical, or surface receptor properties of each cell series. The evidence provided supports the assumption of mixed lymphoid-myeloid properties of blast cells in chronic myelocytic leukemia in children. Detailed study of the leukemic cells may aid in the understanding of complex stem cell relationships and suggest more effective therapeutic approaches.
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PMID:Ph1-positive childhood leukemias: spectrum of lymphoid-myeloid expressions. 26 77

Forty cases of chronic myeloid leukemia (CML) were studied and subgroups of cases with similar chromosomal abnormalities in terminal stage were defined. Certain correlations were observed between the type of chromosomal changes, and clinical and morphologic manifestations of the disease: (1) It seems that, in cases without any karyotype changes other than translocation (9;22), the terminal stage is longer and milder than in cases with additional chromosomal abnormalities; (2) cases with marker i(17q) are clinically and morphologically rather uniform and are characterized by distinct signs of myeloid differentiation of blast cells, absent in other cases; (3) in cases with various atypical chromosomal abnormalities, the course of the terminal stage is the most rapid and grave. The blast cells differ from myeloblasts and resemble lymphoid elements.
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PMID:Chromosome abnormalities and clinical and morphologic manifestations of chronic myeloid leukemia. 27 70

Vindesine is a derivative of vinblastine and of vincristine. A high proportion of remissions were obtained in acute lymphoid leukaemia (6 complete and 1 incomplete remissions in 15 patients), in blastic crisis of chronic myeloid leukaemia, and a few responses have been registered in lymphosarcoma and Hodgkin's disease. Permanent 48 h i.v. infusion may include a remission where i.v. pusch of the same dose has failed. The most remarkable characteristic of vindesine is the absence of cross-resistance with vincristine as documented in acute lymphoid leukaemia.
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PMID:[Leukaemias and lymphomas treatment by vindesine. Result of a phase II trial in terms of remission induction (author's transl)]. 27 88

A 10-year-old boy, who had been in an uninterrupted remission of acute lymphocytic leukemia (ALL) for six years, developed polycythemia vera (PV). One and a half months after detection of PV, he was found to have active leukemia. Both the polycythemia and leukemia receded with anti-leukemia therapy. Three possible explanations for the development of PV in a child with ALL are discussed: 1) PV was a part of his original ALL and recurred whtn patient relapsed. The PV phase was detected only during relapse because the patient was under close observation. 2) PV was a second neoplasm independent of ALL. 3) PV was part of a second leukemia which was different from the original leukemia; this new ALL was derived from a pluripotential cell line involving both erythroid and lymphoid elements. A precedent for this explanation has been observed in chronic myelogenous leukemia.
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PMID:Polycythemia vera in a child with acute lymphocytic leukemia. 28 32


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