Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 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

The natural killer activity of isolated mononuclear cell populations of acute myelocytic leukemia (AML) patients in remission and relapse was compared with that of mononuclear cells obtained from normal subjects. The target cells consisted of 51Cr-labeled blast cells of the K-562 cell line, which was originally obtained from a patient with chronic myelocytic leukemia in blast crisis. The natural killer activity of lymphocytes from AML patients in remission was similar to or higher than that of normal subjects. A marked depression in this function was associated with relapse, as well as with heavy combined chemotherapy. It is concluded that natural killer activity assessed in vitro is an accurate indicator of the clinical stage of AML patients.
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PMID:Natural killer activity in patients with acute myelocytic leukemia. 31 67

Of particular interest in the study of cell membrane markers of leukemic cells were cytotoxic and immunofluorescent results obtained in comparing Ia alloantigen and complement receptor (CR) expression on normal leukocytic and leukemic cell types. Using discontinuous Ficoll gradients, Ia alloantigens were found on varying numbers of leukemic myelo- and lymphoblasts, and on the early stages of normal melocytes. Ia alloantigens, however, were not detectable on mature polymorphonuclear cells. This establishes human Ia alloantigens as cell surface differentiation markers. The appearance of complement receptors was observed later than that of Ia alloantigens. CR1 (EAC1-4b) showed up later in the differentiation than CR2 (EAC1-3d). Thus, an immunological discrimination between AML blasts and CML blast crisis blasts appears to be possible: AML blasts are mostly Ia-positive but CR-negative, whilst CML blast crisis cells are only 20-30% Ia-positive and carry complement receptors in at least equal amounts. The AML blast cell would appear as the less-differentiated cell type when compared to the CML blast crisis cells. The picture, however, remains complex since in CML blast crisis at least three different types of blast cells can be identified: an Ia-positive and an Ia-negative myeloid blast as well as an Ia-positive lymphoid blast. The quantitative composition of these three elements within the myeloid differentiation profile can vary somewhat from patient to patient. Furthermore, these studies revealed a disturbed differentiation of leukemic cell types.
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PMID:Classification of leukemic cells by Ia alloantigens and complement receptors. Surface probes for cell differentiation. 37 3

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

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

Acute myelofibrosis is an uncommon fulminant disorder characterized by pancytopenia, premature myeloid elements in the peripheral blood, and bone marrow fibrosis. We report the case of a 59-year-old man who had acute myelofibrosis and peripheral myeloblastosis clinically suggesting the diagnosis of acute granulocytic leukemia. The disease was unresponsive to cytotoxic drugs or androgens and the patient died five months later. The association of bone marrow fibrosis with large numbers of myeloblasts in the peripheral blood has rarely been reported and suggests a spectrum of morphological changes in acute myeloproliferative disorders, analogous to the merging of chronic myeloproliferative disorders into one another and into leukemic blast crisis.
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PMID:Acute myelofibrosis with peripheral myeloblastosis: an acute myeloproliferative disorder. 58 48

Fourteen cases of philadelphia chromosome (Ph1) positive chronic myeloid leukaemia in blast transformation have been investigated using cell surface markers. Morphologically eight cases were lymphoid and the remainder myeloid in appearance. All cases were negative with surface markers for thymocytes and T and B lymphocytes. Five of the lymphoid cases reacted with an antiserum specific for acute lymphoid leukaemia )ALL) of non-T non-B type and were also weakly reactive with a lymphocyte reactive antiserum. A sixth patient, whose blast cells were anti-ALL negative (ALL-) at presentation, subsequently developed central nervous system leukaemia with anti-ALL positive (ALL+) blast cells in the CSF. In all cases the leukaemic blast cells showed greatly diminished expression of cholera toxin receptors when compared to granulocytic cells from the chronic phase of CML. This parallels weak or negligible expression of the cholera toxin receptor in ALL and AML. These results suggest that the blastic phase of CML may involve different cellular derivatives of a pluripotential stem cell in which the primary malignant/genetic changes reside. The blast crisis of CML can therefore be heterogeneous with respect to cellular expression and in a significant proportion of patients involves a cell which is by membrane markers and morphological criteria indistinguishable from that seen in the common form of ALL. In these cases the Philadelphia chromosome may be the only distinguishing cellular characteristic.
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PMID:Blast crisis of chronic myeloid leukaemia (CML). II. Cell surface marker analysis of "lymphoid" and myeloid cases. 78 72

The possibility that oxymetholone might induce or enhance leukemia after androgen therapy for aplastic anemia prompted us to study the direct action of oxymetholone on the DNA synthesis of AML cells in vitro. The peripheral blasts of 10 patients, 8 with AML and 2 with CML in blast crisis have been studied. The DNA synthesis of the leukemic cells with and without oxymetholone was measured by the 3H-methyl-thymidine incorporation determined by liquid scintillation. The results have been shown a wide variation of DNA synthesis from patient to patient with a range from 2,000 to 40,000 cpm but no significant difference between test and control cultures. We may conclude that oxymetholone does not increase directly the proliferation capacity of the peripheral AML cells cultured in vitro.
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PMID:Oxymetholone effect of acute myeloblastic leukemia cells in vitro. 82 Dec 91

Cell membrane antigens associated with the blast phase of human acute leukemia are separable from inhibitory proteins and from histocompatibility antigens also present in the membranes. Since these antigens are not detectable in remission or normal white blood cells, they provide a useful marker for identification of cells undergoing carcinomatous changes. Blast antigens from acute lymphatic leukemia (ALL) are also present on early human fetal thymus cells; antigens from both sources produce cell-mediated immune (CMI) responses and are structurally similar. Blast antigens from acute myelocytic leukemia (AML) are not associated with fetal antigens and do not cross react with ALL antigens. ALL cells possess a larger quantity of CMI inhibitory protein than AML cells. The isolation, purification and idenfication of these blast antigens is a step toward their use in studying cultured and cloned subpopulations of cells thought to be associated with pre-leukemia.
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PMID:Cell membrane antigens associated with human adult acute leukemia. 100 2

Remission induction was assessed by clinical and cell-culture criteria for 65 patients with acute myelogenous leukemia (AML), 11 patients with chronic myelogenous leukemia (CML) in blast crisis and 19 patients with acute lymphoblastic leukemia (ALL). Cyclophosphamide, cytosine arabinoside and vincristine (CAV) therapy resulted in complete remission in 23 of 50 previously untreated patients with AML and in 3 of the 11 patients with CML. Fourteen patients with ALL responded to vincristine-prednisone induction therapy and two to induction therapy with CAV. The median duration of survival of the responding patients was 2.2 years, compared with 4 months for the patients who did not respond to treatment. Granulopoietic colony formation, assessed by assay of colony-forming units dependent on colony-stimulating activity in culture (CFU-C), was abnormal in 37 of 42 bone marrow aspirates from patients with AML before treatement. CFU-C concentration increased when leukocyte-conditioned medium (LCM) was added to the cultures; 13 cultures had normal or elevated CFU-C concentration with LCM. Marrow cells of patients with ALL or CML in blast crisis demonstrated a similar pattern. Serial studies of marrow CFU-C concentration of 31 patients with AML demonstrated a change to a normal pattern with successful remission induction. Results of this study suggest that administration of purified LCM to leukemic patients might increase granulocyte production from potential but unstimulated granulopoietic precursors. This therapy would lessen the probability of death from infection during remission induction.
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PMID:Acute leukemia in adults: assessment of remission induction with combination chemotherapy by clinical and cell-culture criteria. 105 7


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