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)

The rapid appearance of acute respiratory distress during the course of 25 hyperleukocytic leukemias was associated with the rapid increase of the leukocytosis. The regression of the tachypnea was spectacular when treating hyperleukocytosis by exchange transfusion and chemotherapy. Blood gas studies, although blurred to some extent by in vitro blast consumption of oxygen, showed a hypoxemia with a hypo-or normocapnia. The symptoms seem to be related to the leukostasis by the mechanical obstruction of the pulmonary capillaries. This leukostasis was shown to be responsible for a septal and alveolar oedema. The high frequency of this syndrome during the course of AGL and of acute phase of CGL seems to be linked to the low deformability of the myeloblasts. In CGL at its chronic phase, CLL or even in ALL, the absence of this syndrome could be explained by the greater deformability of the circulating cells. The hyperleukocytic AGL patients which do not have this syndrome are all characterized by a stable or slowly increasing leukocytosis. Thus, this syndrome seems to characterized by hyperleukocytic granulocytic leukemias with a rapid blood leukocyte doubling rate. Treatment in such cases is an emergency.
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PMID:Respiratory distress of hyperleukocytic granulocytic leukemias. 28 51

The phenomenon of premature chromosome condensation (PCC) was used to compare the bone marrow proliferation characteristics of 163 patients with various forms of leukemia prior to the initiation of new therapy. The proliferative potential index (PPI, or fraction of G1 cells in late G1 phase) and the fraction of cells in S phase was determined and compared to the type of disease and the bone marrow blast infiltrate for each patient. Previously untreated patients with acute leukemia exhibited an average PPI value three times that of normal bone marrow (37.5% for acute myeloblastic leukemia [AML], acute monomyeloblastic leukemia [AMML], or acute promyelocytic leukemia [APML] and 42% for acute lymphocytic leukemia [ALL] or acute undifferentiated leukemia [AUL]). Untreated chronic myelogenous leukemia (CML) patients showed intermediate PPI values (25.2%), whereas CML patients with controlled disease exhibited nearly normal PPI values (14.6%). On the other hand, blastic-phase CML patients exhibited PPI values closer to that observed in patients with acute leukemia (35.4%). Seven patients with chronic lymphocytic leukemia (CLL) exhibited even higher PPI values. No correlations were observed between PPI values, fraction of cells in S phase, and marrow blast infiltrate. For untreated acute disease patients, PPI values were prognostic for response only at low and high PPI values. These results suggest that the PCC-determined proliferative potential is a biologic reflection of the degree of malignancy within the bone marrow.
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PMID:Premature chromosome condensation studies in human leukemia. I. Pretreatment characteristics. 29 41

Sixteen chronic myeloid leukaemia (CML) patients in remission were tested with solubilized membrane antigens from CML leukaemic cells, CML blasts, AML blasts and ALL blasts for cellular immunity in vitro by lymphocyte transformation (LT) and leucocyte migration inhibition (LMI) assays. Twelve CML patients in remission were tested with allogeneic PHA-transformed normal lymphoblasts. As controls, peripheral-blood leucocytes from 9 healthy persons were tested with the same antigen preparations. It was seen that 8/16 (50%) CML patients responded to CML antigens by both LT and LMI assays, while 5/16 (31%) patients reacted to CML blasts and 44% (7/16) patients reacted to AML blast antigens. It was interesting to note that 5/11 (45%) CML patients reacted to ALL blast antigens by both assays. One out of 12 patients reacted to PHA-transformed lymphoblasts. None of the healthy controls reacted to leukaemia-associated antigens. The results suggest the sharing of antigens between myeloid leukaemic cells, myeloid blasts and lymphoid blasts.
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PMID:Cellular sensitization in chronic myeloid leukaemia patients to leukaemic blast antigens. 29 50

Despite the incomparability in the reporting of leukemia and lymphoma incidence among populations and the relative rarity of these diseases, real differences in rates are discernible from available data. In general, the incidence of each of the leukemias and lymphomas is lower in Japan than in other Pacific rim populations whose rates are known. Particularly striking is the low incidence of CLL in Japan. Among Japanese in Hawaii, rates of some of these cancers (lymphosarcoma, CML) approach those of whites, whereas rates of other cancers (Hodgkin's disease, multiple myeloma, ALL, CLL, and AML) more closely resemble those of native Japanese. The number of Chinese living in countries served by population-based cancer reporting systems is too small for any firm conclusions to be made about leukemia and lymphoma incidence in this group. The incidence of these diseases in certain other nonwhite Pacific rim residents (i.e., Mexican Americans, blacks, and Maoris) is, by and large, similar to that of whites.
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PMID:Geographical variation in the incidence of the leukemias and lymphomas. 29 90

Permanent human hematopoietic cell lines representing T-cell, B-cell and non T/non B (null-cell) leukemia have been established. Comparative analyses were made for their phenotype characteristics. A number of characteristics common within the 7 T-cell lines studied or distinct from other leukemia-type lines were described. Usefulness, validity and limitation of these findings are discussed in connection to the attempt at classification of ALL, CLL and blastic phase of CML. The great majority of CLL were SmIg+-B-cell leukemia and a single case of T-cell CLL was documented. Except 10% as T-cell ALL and a single case of B-cell ALL, the majority of ALL were found to be the non T/non B ALL. Nevertheless, little evidence was suggested from the present study in favor for a notion that the T-cell ALL and the non T/non B ALL are two distinct diseases.
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PMID:Establishment and characterization of leukemic T-cell lines, B-cell lines, and null-cell line: a progress report on surface antigen study of fresh lymphatic leukemias in man. 30 98

The membrane phenotype of leukaemic cells was analysed during different stages of chronic myeloid leukaemia by a panel of markers. These included antisera against ALL antigen, p23,30 (Ia-like structure) and other T cell, B cell and myeloid markers 'Lymphoid' blast crisis shares the phenotype of common ALL (of non-T, non-B variety). Both leukemias react with anti-ALL serum and have pre-myeloid, pre-B lymphoid and pre-thymocyte characteristics. Their phenotype may reflect the characteristics of the pluripotential stem cell from which they derive. Nevertheless both leukaemias retain their undifferentiated characteristics and lack overt myeloid, B cell and thymocyte differentiation markers. Myeloid blast crisis and AML are negative with anti-ALL serum but some of the poorly differentiated myeloblasts react with anti-p23,30 serum (and negative for SmIg). The anti-p23,30 serum (used in a double marker assay combined with anti-immunoglobulin) detects some (4-11%) intermediate sized agranular p23,30+/SmIg-cells in peripheral blood during the chronic phase of CML as well as in normal foetal bone marrow. These could be myeloid stem cells (from which in CML the myeloid blast crisis arises). The results demonstrate that surface membrane analysis can aid exact diagnosis in different stages of CML.
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PMID:Membrane marker analysis of 'lymphoid' and myeloid blast crisis in PH1 positive (chronic myeloid) leukemia. 30 6

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

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

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

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


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