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)

Fifty-six untreated patients with acute leukemia (38 acute myelogenous leukemia, 16 acute lymphoblastic leukemia, and 2 blast crisis of chronic granulocytic leukemia) were randomized on admission to one of three groups--one to receive oral anticandidal prophylaxis through the period of remission induction chemotherapy with nystatin, another to receive natamycin, and the third to receive no anticandidal prophylaxis. Neither of the first two groups show any advantage over the last and it is concluded that provided gut sterilization regimes are not employed, prophylactic oral anticandidal treatment is of no value in these patients and should be reserved until there is clinical evidence of infection.
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PMID:Oral anticandidal prophylaxis in patients undergoing chemotherapy for acut- leukemia. 31 10

Combined immunologic assays for TdT enzyme and membrane markers show that TdT+ cells in nonleukemic human bone marrow carry ALL-associated and Ia-like antigens but no thymocyte markers or surface Ig. These cells could be precursors involved in acute lymphoblastic leukemia of the "common" or non-T, non-B type and in lymphoid blast crisis of Ph' positive chronic myeloid leukemia. A few TdT+, Ia+ cells express cytoplasmic IgM, indicating that some pre-B cells may be TdT positive.
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PMID:Terminal transferase-positive human bone marrow cells exhibit the antigenic phenotype of common acute lymphoblastic leukemia. 31 63

The following rare Ph1-positive chromosome constitutions, based on the cytogenetic findings in three cases with acute leukemia, are presented. 1) A hypodiploid karyotype, primarily 43, -X, -7, -8,9p+ and a Ph1, in a patient with acute lymphoblastic leukemia (ALL) in relapse, followed by a complete remission and a normal chromosomal picture and then by the appearance of cells with a 46,XX,Ph1 karyotype. The Ph1 was due to a standard translocation between chromosomes no. 9 and no. 22. 2) The first demonstration of an unusual Ph1-translocation between chromosomes no. 19 and no. 22 in a condition other than chronic myelocytic leukemia (CML), i.e., acute myeloblastic leukemia (AML). 3) The presence of a Ph1 in acute erythroleukemia (EL) due to a translocation between chromosomes no. 4 and no. 22, this apparently being the first description of such a translocation in any disease. The cytogenetic findings, particularly those in the Ph1-positive case of ALL, were evaluated in relation to the cytologic and immunologic features, clinical courses and implications, and the interrelationship between the three conditions (AML, blastic phase of CML and ALL), which have to be considered in cases of Ph1-positive acute leukemia.
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PMID:Chromosomes and causation of human cancer and leukemia. XXV. Significance of the Ph1 (including unusual translocations) in various acute leukemias. 33 21

Subclassification of leukemias in childhood by cytochemical methods or blast size is arbitrary to some extent. The increased knowledge of physiological development of hematopoetic cells allows to classify these diseases according to the degree of differentiation of the cells involved. Immunological cell-membrane structures are used as for markers differentiation. In this way, 4 types of lymphoblastic leukemias and 5 types of myeloid leukemias can be diagnosed. This classification can help to answer clinical and theoretically important questions. In ALL and during the blast crisis of CML, new groups with increased risk are defined, important for the choise of initial therapy, and evaluation of therapeutic trials. The immunological markers can help to detect already small numbers of blasts at the beginning of a hematological relapse. Transformations of the blast type during the course of the disease can be explained. Experiments in animals indicate that an immunological classification of leukemias correlates with differences in pathogenesis and etiology.
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PMID:[Immunological diagnosis of leukemias in childhood (author's transl)]. 34 55

Neoplastic cells from 253 patients with leukemia and 46 patients with malignant lymphoma were studied for the presence of terminal deoxynucleotidyl transferase (TdT) by biochemical and fluorescent antibody technics. TdT was detected in circulating blast cells from 73 of 77 patients with acute lymphoblastic leukemia, 24 of 72 patients with chronic myelogenous leukemia examined during the blastic phase of the disorder and in cell suspensions of lymph nodes from nine of nine patients with diffuse lymphoblastic lymphoma. Blast cells from six of 10 patients with acute undifferentiated leukemia were TdT positive, but the enzyme was found in only two of 55 patients with acute myeloblastic leukemia. TdT was not detected in other lymphocytic or granulocytic leukemias or in other types of malignant lymphomas. The fluorescent antibody assay for TdT permits rapid and specific identification of the enzyme in single cells. The TdT assay is clinically useful in confirming the diagnosis of acute lymphoblastic leukemia, evaluating patients with blastic chronic myelogenous leukemia, and distinguishing patients with lymphoblastic lymphoma, whose natural history includes rapid extranodal dissemination, from patients with other poorly differentiated malignant lymphomas.
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PMID:Terminal deoxynucleotidyl transferase in the diagnosis of leukemia and malignant lymphoma. 34 33

A proportion of patients with blast crisis of CML have blast cells identical to those found in common non-T, non-B all, and whilst this disease is often referred to as lymphoid blast crisis (LBC), evidence is presented that it may in fact arise from a prelymphoid, pre-myeloid (pluripotential) stem cell. Recently developed membrane and enzyme markers (anti-ALL antiserum, TdT assay) have provided convenient diagnostic tests for the detection of LBC. The clinical and haematological features of LBC are reviewed: patients with LBC show a higher response rate to therapy with vincristine and prednisolone, and their survival may be significantly prolonged. The frequent occurrence of meningeal leukaemia suggests the need for prophylactic CNS therapy in LBC patients achieving remission.
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PMID:Lymphoblastic transformation of Ph1-positive chronic myeloid leukaemia: therapeutic implications and relevance to haemopoietic stem cell theory. 36 48

A cytotoxic common ALL antiserum (CALLA) specific for leukemic cells of most patients with non-T-cel- acute lymphoblastic leukemia (ALL) and of some patients with chronic myelogenous leukemia (CML) in blast crisis has been reproducibly prepared using cell lines for absorption. CALLA reacts with leukemic cells of 110 of 134 patients (82%) with non-T-cell ALL; 1 of 71 (1%) patients with acute myelogenous leukemia (AML); 2 of 7 patients (29%) with chronic myelogenous leukemia in blast crisis; 7 of 92 patients (8%) with other hematologic malignancies; and with the leukemic cell lines Laz 221 and NALM-1. It does not react with the normal hematopoietic cells, B- or T-cell lines, or cells from 26 patients with T-cell ALL that were tested. CALLA reactivity and periodic acid Schiff (PAS) staining correlate poorly, with CALLA reacting with cells from 86% (64 of 74) of patients with PAS-positive and 76% (29 of 38) of those with PAS-negative non-T-cell ALL. In these patients, CALLA reacts with cells from 89% of those under age 12 (78 of 88); 74% of those aged 12--20 (20 of 27); and 58% of those over 20 (11 of 19). Using only CALLA and antisera specific for Ia-like and T-cell antigens, we can now distinguish most cases of ALL from AML and other hematologic malignancies.
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PMID:Leukemia-associated antigens in ALL. 38 10

Autologous marrow infusion has been attempted in three patients with chronic myeloid leukemia (two in blast crisis, one with severe myelofibrosis and pancytopenia) and one patient with acute lymphatic leukemia. One patient with blast crisis of CML expired prior to marrow infusion. One patient with myelofibrotic phase of CML is alive seven months post marrow infusion. The other two patients expired 6 and 16 days post marrow infusion. Bone-marrow repopulation is feasible in the face of severe myelofibrosis.
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PMID:Autologous bone-marrow and peripheral blood buffy coat cell infusion in the treatment of chronic myeloid and acute leukemia. 40 Jun 95

Thirteen leukemic patients with disease refractory to conventional chemotherapy were treated with 1.0 to 7.5 g/m2 of Cytosine Arabinoside (Ara-C) over 29 drug cycles. Drug infusions were spaced at 12-hour intervals; a maximum of four doses was administered over 36 hours. After single dose tolerance had been established, three or four dose cycles were given at 2- to 30-day intervals. There were three partial remissions (PR) and one complete remission (CR) in a treatment group of four patients with AML, five with ALL, two with lymphoma converted to leukemic phase, one CML in blast crisis, and one promyelocytic leukemia. Five of the patients were septic and considered terminally ill at the time of treatment. All other patients had evidence of drug responsiveness. The nadir of the white count occurred from 3 to 12 days after treatment, with subsequent recovery of the peripheral granulocyte count between days 12 and 28. Toxicity included nausea and vomiting (GI symptoms) in twelve patients, central nervous system (CNS) disturbances in eight patients, one episode of inappropriate antidiuretic hormone syndromes (SIADH), one of hyperuricemia, and fever in eleven patients. There was no evidence of hepatic or renal dysfunction. These high doses of Ara-C appear useful for treatment of patients with refractory leukemia. Hospitalization is brief and toxicity acceptable.
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PMID:High dose cytosine arabinoside (HDARAC) in refractory acute leukemia. 49 9

The present study was undertaken to obtain more precise information about the purine biosynthetic pathway in human blood cells. 5'phosphoribosyl-l-pyrophosphate (PP-ribose-P) amidotransferase was found in cell-free extracts from all leukemic cells and normal lymphocytes and therefore these cells could synthesize the first intermediate of the purine-de-novo-synthesis. Normal leucocytes, erythrocytes and bone marrow cells lack this enzyme system and have an absolute requirement for externally supplied purines via salvage pathway. Leukemic blast cells show different enzyme activities independent of their cell count. Kinetic studies with the crude enzymes showed sigmoidal substrate velocity curves for PP-ribose-P, whereas glutamine shows hyperbolic kinetics. The leukemic cell enzymes from all four donor types (ALL, CLL, AML and CML) are rapidly saturated with low concentrations of PP-ribose-P and less inhibited by the physiological feedback inhibitor, adenosine 5'monophosphate. The crude enzymes of normal spleen lymphocytes and leukemic cells were further purified (10 to 15-fold) and substrate velocity curves for PP-ribose-P and glutamine show now hyperbolic kinetics and double reciprocal plots were linear with and apparent Km for PP-ribose-P of 0.14 mM and for glutamine 2.0 mM. In the presence of different concentrations of AMP, the PP-ribose-P substrate velocity plot changed from a hyperbolic to a sigmoidal curve; no difference in the degree of the inhibition between both partially purified enzymes (normal spleen lymphocytes and leukemic cells from all four donor types) could now be observed.
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PMID:Purine nucleotide synthesis in normal and leukemic blood cells. 64 99


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