Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunologic markers are now available for acute leukemia. These show that most patients now diagnosed as having acute lymphatic leukemia have blast cells which react with antihuman T antisera. In addition, about 20% of patients have blast cells which form E rosettes. These patients tend to be those with high white counts and aggressive disease. Tumor-associated antigens have been identified in acute leukemia. Antisera raised in other species by immunization appear to detect some antigens common to all acute leukemias and other antigens which can distinguish the myeloid from the lymphoid leukemias. The reactivity to leukemia antigens can be related to prognosis. The immune manipulations required to produce cure, however, are not understood. These antigenic markers, by allowing us to detect smaller amounts of tumor than can be detected by morphology alone, may help us to predict relapse and define cure.
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PMID:New looks in leukemia. 23 96

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

The terminal phase of most patients with Ph1-positive chronic granulocytic leukemia (i.e., blast crisis) resembles acute leukemia. The clinical and hematologic features of blast crisis in 73 patients with chronic granulocytic leukemia have been reviewed. Two major morphological subgroups, lymphoblastic and myeloblastic, were identified. The lymphoblastic group in general had more profound thrombocytopenia and a greater number of blasts, while the myeloblastic group had more severa anemia. Extramedullary leukemia was documented in 27 patients. In 12 patients extramedullary leukemia preceded or occurred simultaneously with blast crisis in the bone marrow and peripheral blood. On the basis of this study we present hematologic criteria for the diagnosis of blast crisis and emphasize the importance of extramedullary leukemia in heralding the onset of blast crisis.
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PMID:Characteristics of blast crisis in chronic granulocytic leukemia. 26 37

A case of myelomonocytic leukemia is described in which an increase in primary fibrinolytic activity produced a severe hemorrhagic diathesis. The leukemic cells were demonstrated to be the source of the fibrinolytic activity. Utilizing a fibrin coated slide technique, the intact leukemic cells were shown to release their fibrinolytic activity and to induce local lysis. Intact leukocytes from normal subjects and other patients with acute leukemia of varied cell types were unable to release fibrinolytic activity although in some of the leukemic preparations, increased fibrinolytic activity was demonstrated after in vitro disruption of the cells.
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PMID:Leukocytic fibrinolysis in myelomonocytic leukemia. 26 47

The occurrence of circulating immune complexes was investigated in 467 serum samples from 230 leukemia patients using the [(125)I]Clq-binding test. There was an increased serum [(125)I]Clq-binding activity in 40% of patients with acute myeloid leukemia, 23% with acute lymphatic leukemia, 46% in blastic crisis of chronic myeloid leukemia, 12% with chronic lymphatic leukemia, and 13% with chronic myeloid leukemia. In 48 patients, serum was also tested for soluble immune complexes by the Raji cell radioassay; the correlation between results of the two tests was significant. The Clq-binding material had properties identical with those of immune complexes. It sedimented as 14-28s material on sucrose density gradient. It contained IgG which could be dissociated at acid pH. Its Clq-binding properties could be removed after passage through anti-IgG immuno-absorbant or after a mild reduction-alkylation treatment, but were not sensitive to deoxyribonuclease treatment. Circulating immune complexes were found most commonly during the blastic stage of leukemia.Remission took place in 75.4% of patients with no detectable circulating immune complexes at the onset of acute leukemia, but in only 32.7% of those with detected complexes during this period. Median survival times of the former group of patients were more than 18 mo in acute myeloid leukemia and acute lymphatic leukemia and more than 8(1/2) mo in blastic crisis of chronic myeloid leukemia. The corresponding median survival times in the latter patient group were 64, 135, and 90 days. These findings were unrelated to prognostic features already known.
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PMID:Clinical relevance of circulating immune complexes in human leukemia. Association in acute leukemia of the presence of immune complexes with unfavorable prognosis. 26 30

The activities of acid phosphatases (AP) were measured in leukocytes from patients with chronic myelocytic leukemia (CML), macrophages, granulocytes, in the fractionated mononuclear cells of patients with CML and with hairy-cell-leukemia (HCL) and in the cells from patients with acute leukemia (AL). The lowest activities were found in lymphocytes of normal subjects and of patients with chronic lymphatic leukemia (CLL) and in thrombocytes. Isoenzyme (IsE) 1 was characteristic for thymocytes, IsE 2 for granulocytes, IsE 3 for pathologic blast-cells, lymphocytes and thrombocytes, IsE 4 for macrophages, IsE 5 with components a and b for the mononuclear fraction of patients with HCL. In addition IsE 5 was detected in lymphocytes, macrophages and CLL-cells. In 4 patients with HCL the relative percentage of IsE-5-fraction was slightly greater than the percentage of tartrate resistant cells. In two patients with questionable HCL well marked IsE-5-fractions were recognized but no tartrate resistant cells. In one patient with HCL a relatively high percentage of tartrate resistant hairy-cells and in comparison an inadaquate low IsE-5-fraction was found. These different relations were explained with the more sensitive method of gelelectrophoresis and different affinity of substrates to AP.
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PMID:[Isoenzymes of acid phosphatase in blood cells of normal subjects and patients with leukemia (author's transl)]. 26 45

A 6-year-old boy with Fanconi anemia, developed acute myelomonocytic leukemia with marker chromosomes from an interchange in the malignant clone in the bone marrow. The possible aetiological role of therapy, the morphological characteristics and chromosome aberrations of the bone marrow cell line are discussed in relation to previous reported cases of Fanconi anemia in which acute leukemia has supervened.
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PMID:Fanconi anemia leading to acute myelomonocytic leukemia: cytogenetic studies. 26 49

The sera of 21 adult patients with acute leukemia were studied for the presence of antibody reacting with surface antigens of autologous leukemia cells. Sequential serum samples were obtained from patients and were tested on cryopreserved leukemia cells in immune adherence assays. Three patients showed autologous serum reactivity and the serum of one of them was analyzed in detail. This antibody reacted with autologous acute lymphocytic leukemia cells but not with autologous cells obtained from peripheral blood, bone marrow, or spleen during clinical remission. In absorption tests, the antigen could not be detected on normal autologous or allogeneic blood lymphocytes, lymphoblastoid lines of T- or B-cell origin, or cells infected with simian sarcoma virus, baboon C-type virus, or Mason-Pfizer virus. Leukemia cells from two other patients with acute lymphocytic leukemia and one patient with acute nonlymphocytic leukemia absorbed specific reactivity. These studies indicate that certain acute leukemia cells express a common antigen that elicits a humoral immune response in the autologous host.
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PMID:Detection of antibody to autologous human leukemia cells by immune adherence assays. 27 Jul 2

The authors reviewed 181 patients who received local radiation therapy for the prevention or control of extramedullary disease resulting from acute leukemia. 126 had acute lymphocytic leukemia and 55 had acute granulocytic leukemia. They were treated over a 18-year period of time with different forms of chemotherapy. Most had not received prophylactic CNS radiation therapy. Patients were evaluated for local control until death or hematologic relapse intervened. More than 80% of patients with clinical ALL meningeal leukemia had a successful response to doses over 1000 rads. This same response was not apparent in AML. More than 80% of clinical non-CNS extra medullary leukemia was controlled with doses of 600 rads or greater. Only one patient with extra-medullary relapse is still alive. The authors feel that lower preventative doses of radiation to the CNS are compatible with similar control rates, based on their own data and other suggestive data.
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PMID:The management of extramedullary disease in acute leukemia with therapeutic radiations. 27 30

Acute leukemia in 93 children was cytochemically classified into three groups: 1. the PAS-Typ (acute undifferenciated leukemia) paramyeloblastic leukemia, 2. the AML, and 3. the Acid Phosphatase Typ (SP-Typ). Therapy for the first group differed from that for AML. The acid-Phosphatase-Typ was found in only a few cases, where the acid Phosphatase is good to see in the paranuclear region of the cell. These cases have a bad prognosis. It is proposed to publish even single cases of the acid Phosphatasetype leukemia in order to find the optimal therapy.
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PMID:[Correlation of the cytochemical classification of acute leukemia in children with the course of their disease (author's transl)]. 27 64


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