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)

Forty cases of acute myeloid leukaemia with 41 hypodiploid clones were investigated in a collaborative study. Cases with -5, -7, -X or -Y either alone or in association with an established translocation were excluded. Karyotypes were reviewed in all cases and bone marrow or blood morphology was reviewed in 22 cases. Twenty-six cases were very complex (more than five abnormal chromosomes), 14 cases were complex (two to five abnormal chromosomes) and only one case was simple (one abnormal chromosome). Chromosomes 5, 7, 17 and 18 were involved in a significantly greater number of cases than expected. Only five cases had normal chromosomes 5 and 7. Chromosomes 10, X and Y were involved in significantly fewer cases than expected. Ten cases had ring chromosomes and 18 showed clonal evolution. Patients were aged between 19 and 90, median 61 years. Evidence of myelodysplasia was found on morphological review in 18/22 cases, and on clinical features in a further five cases. There was a high proportion of cases with FAB M6, 'erythroleukaemia' (9/31 cases). Only 4/16 patients treated with cytotoxic therapy achieved remission. Median survival was 2.5 months (35 patients). Survival was slightly better for patients with normal chromosomes 5 and 7, and for those with simpler karyotypes, but this was not statistically significant. This study confirms the association between hypodiploidy, complex karyotype, abnormalities of chromosomes 5 and 7 and a poor prognosis.
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PMID:Complex hypodiploidy in acute myeloid leukaemia: a United Kingdom Cancer Cytogenetics Group study. 863 59

Fourteen patients with hypocellular acute leukemia (HAL) were reviewed. The median age was 72 years, with an equal male-to-female ratio. Severe granulocytopenia with marrow hypocellularity and increased marrow blasts and absence of physical findings were common features. The median peripheral blood blast count was 2%. All except 3 cases of erythroleukemia had marrow blast count that exceeded 30% of all nucleated marrow cells. All cases were classifiable with the FAB criteria. FAB classification revealed a preponderance of the M1 category followed by M2 and M6 types. The majority of blasts were type I and the median myeloperoxidase positivity was 14%. Immunophenotyping of bone marrow cells by flow cytometry in 9 cases showed expression of myeloid antigens (CD13, CD33); 6 cases also expressed CD34 antigen. Significant dysplasia involving erythroid and megakaryocytic lineages was seen in most of the cases. Trilineage dysplasia was observed in 5 cases. Median survival of the entire group was 10.5 months. Eleven patients underwent induction therapy consisting of daunorubicin and cytosine arabinoside +/- 6 thioguanine; 8 patients achieved complete remission (72.6%). Remission duration was 14.5 months. Three patients (27.4%) died secondary to infections during induction therapy. Higher frequencies of trilineage dysplasia and FAB M6 type together with low percentage of peripheral blasts and presence of antecedent hematologic disorders suggest that some of these cases might represent the hypocellular form of acute myeloid leukemia with trilineage dysplasia.
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PMID:Hypocellular acute myeloid leukemia: the Rochester (New York) experience. 865 64

We investigated the effects of extracellular ubiquitin on the colony formation of human hematopoietic progenitor cells (CFU-GM, CFU-E and BFU-E) and a granulocyte-colony stimulating factor (G-CSF)-dependent human myeloblastic leukemic cell line, OCI/AML/1a. Ubiquitin exhibited inhibitory effects on CFU-GM, CFU-E, BFU-E and OCI/AML/1a colony formation. Extracellular ubiquitin also inhibited the growth of KT3 (T lymphoblast), K562 (erythroleukemia) and Daudi (Burkitt's lymphoma) cells, stimulated the growth of HL60 (promyelocytic leukemia) and Jurkat (T-ALL) cells and showed no effect on the growth of U937 cells (monocytic leukemia). These results indicate that another, previously unrecognized function of extracellular ubiquitin is to regulate hematopoiesis.
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PMID:Extracellular ubiquitin regulates the growth of human hematopoietic cells. 867 Feb 63

Adhesion of myeloid leukemia cells to the bone marrow (BM) microenvironment is mediated in part by Beta 1 and Beta 2 integrins. Cells of the erythroleukemia line K562, derived from a patient with chronic myeloid leukemia, bind to BM fibroblasts (BMFs) but the adhesion cannot be accounted for by integrins or other known adhesion proteins including CD44 or members of the Ig or selectin families. Membrane fragments from K562 cells were radioiodinated and allowed to adhere to BMF monolayers. Adherent proteins were solubilized together with the fibroblasts, analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and visualized by autoradiography. Four adherent proteins were consistently observed. Two of these, with reduced molecular weights of 52 kD and 35 to 37 kD, were prominent. Addition of soluble thrombospondin and heparin but not fibronectin inhibited binding of K562 membrane proteins to adherent BMFs and immobilized thrombospondin- and heparin-bound K562 proteins. The 52-kD protein has a multimeric structure nonreduced and has characteristics of a glycoprotein. Its adhesion to fibroblasts is divalent cation and temperature sensitive. The 35- to 37-kD protein, whose function is divalent cation but not temperature sensitive, is phosphoinositol-linked and has characteristics identical to an adherent 35- to 37-kD protein identified on murine progenitor cells. Membrane preparations from two cases of acute myeloid leukemia showed an adherent 35- to 37-kD protein and in one case an adherent 52-kD protein without other adherent bands. A K562 subclone with reduced adherence to BMFs showed reduced amounts of adherent 52-kD and 35- to 37-kD proteins. These proteins may be responsible for the adhesion of malignant and normal hematopoietic progenitor cells to the BM microenvironment.
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PMID:Identification of novel K562 membrane proteins that adhere to bone marrow fibroblasts. 870 84

Differentiation inhibitory factor (nm23 protein) inhibited the induction of differentiation of mouse myeloid leukemia M1 and WEHI-3BD+ and human erythroleukemia HEL, KU812, and K562 cells. Block of differentiation may be associated with the aggressive behavior of leukemia. To examine the role of nm23 in human myeloid leukemia, we investigated the relative levels of nm23-H1, nm23-H2, and c-myc transcripts in 42 patients with acute myelogenous leukemia (AML), and in 5 with chronic myelogenous leukemia at chronic phase by reverse transcriptase polymerase chain reaction. The expression of nm23-H1 and -H2 but not of c-myc in AML was significantly higher than that in normal blood cells. Among AMLs, acute monocytic leukemia (presentation with AML-M5 morphology) was especially associated with elevated nm23-H1 and -H2 mRNA levels. On the other hand, the elevated levels of c-myc expression in AML-M5 were less evident. An analysis of correlation between nm23 expression and clinicopathological parameters showed that resistance to initial chemotherapy is associated with increased nm23-H1 mRNA levels and that a high initial white blood cell count is associated with increased nm23-H2 mRNA levels. Elevated nm23-H1 mRNA levels were associated with significantly reduced the overall survival of AML, especially of AML-M5 patients. The present results indicate that nm23-H1 and -H2 are overexpressed in AML and especially nm23-H1 gene expression predicts the prognosis of AML, especially of AML-M5.
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PMID:Differentiation inhibitory factor nm23 as a new prognostic factor in acute monocytic leukemia. 889 23

Paroxysmal nocturnal haemoglobinuria (PNH) terminating in acute leukaemia (AL) is an infrequent condition. In several cases, flow cytometric analysis of glycosylphosphatidylinositol anchored membrane proteins such as DAF and CD59/MACIF has suggested the leukaemic cells to be derived from the PNH clone, thereby implicating PNH as a potential preleukaemic disease. In the present paper, we review the data for one patient treated in our hospital and 20 cases reported in the literature from 1969 to 1993. The sex ratio is 1 female/2 males, mean age at diagnosis of PNH was 46 years and the mean interval between the diagnoses of PNH and AL was 53 months. AL type was AML M6 in 8 patients, other types of AML in 12 and ALL in one, with a mean survival of 7.1 months following diagnosis of AL. In all cases analyzed, the PNH phenotype of erythrocytes disappeared with progression of AL, whereas reappearance of this phenotype with complete remission of AL was inconstant. PNH would thus appear to be a potential preleukemic disease. When this disorder terminates in AL, the type is often AML M6, although ALL is also possible. The prognosis of AL in PNH is poor as for other secondary leukaemias. Apart from marrow aplasia, leukaemic transformation is another life threatening complication of PNH which may justify allogeneic bone marrow transplantation (allo-BMT) and potential leukaemic transformation can therefore be an additional argument in favour of allo-BMT when pancytopenia develops in PNH patients.
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PMID:Acute leukaemia in paroxysmal nocturnal haemoglobinuria. Case report and review of the literature. 897 94

Two rare de novo cases are presented of pediatric erythroleukemia (EL), AML-M6 in a four-month-old (patient A) and four-year-old (patient B) African-Americans who presented to the Medical College of Georgia from 1989 to 1995. The clinical, morphologic, immunophenotypic and cytogenetic features of both patients are reviewed. The purpose of this study is to correlate the bone marrow morphology with the immunophenotypes and the karyotypes of the neoplastic cells. The patients were both female, presented with flu-like symptoms, and were noted to have hepatosplenomegaly on physical examination. The peripheral blood examination was significant for anemia (Hb 54 (A), 84(B)g/L), and thrombocytopenia (86 (A), 70(B) x 10(9)/L). The bone marrow contained 75 percent (A) and 76.8 percent (B) erythroblasts and showed myelodysplastic changes in the erythroid cell line. Cytochemical analysis was performed, and greater than 10 erythroblasts per 100 cells were periodic acid-Schiff positive. Immunophenotypes of the pretreatment bone marrow showed glycophorin-A, CD71, and CD11b positivity. The karyotypes of both patients contained complex (> 3 per clone) cytogenetic abnormalities. Our data suggest that the initial presentation and course of disease are different in adults and children. However, once the adult form reaches the acute leukemia stage, the laboratory findings are similar to those at initial presentation in pediatric EL.
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PMID:Erythroleukemia of childhood and infancy: a report of two cases. 909 14

Werner's syndrome is a rare clinical entity and approximately 150 cases have been reported in the medical literature. Werner's syndrome, inherited by autosomal recessive transmission, is characterized primarily by a short stature, premature greying and balding, trophic ulceration of the legs, diabetes mellitus and hypogonadism. These features combine to present a picture of adult progeria. In this brief report we describe a 51-year-old Bedouin male with Werner's syndrome, diagnosed as erythroleukemia (AML-6), and presenting as acute pancytopenia. The patient died two months after diagnosis. This is a rare case of erythroleukemia in a patient with Werner's syndrome. We survey current knowledge of the cytogenetic pathogenesis of Werner's syndrome and erythroleukemia, and attempt to explain the possible link between these two rare syndromes.
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PMID:A patient with Werner's syndrome and erythroleukemia: just coincidence? 917 19

A case of Di Guglielmo's syndrome passed through the three stages of chronic erythromyelosis, erythroleukemia and acute myeloid leukemia (AML). According to the FAB classification the subsequent stages of this syndrome were refractory anemia (RA), RA with excess of blasts (RAEB), AML-M6, AML-M2 and undifferentiated AML-MO as the end-stage disease. Light- and electronmicroscopice findings on peripheral blood and bone marrow slides showed a pronounced trilineage myelodysplastic syndrome (MDS) during the RA, RAEB, AML-M6 and M2 phases of the disease, i.e. dysplastic erythropoiesis with PAS-positive erythroblasts, agranular and hypogranular neutrophils and dysplastic megakaryocytes. It is concluded that this case of Di Guglielmo's syndrome with chronic erythromyelosis, erythroleukemia and AML appears to be a continuum of trilineage MDS, AML-M6 and M2 with dyserythropoiesis which evolved into AML-M0.
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PMID:The natural history of trilinear myelodysplastic syndrome and erythroleukemia. 929 60

The receptor for human interleukin-9 (hIL-9) might be a target for selective immunotherapy. It is expressed on a variety of malignant cells, including Hodgkin's lymphoma, non-Hodgkin lymphoma and acute myeloid leukemia (AML). We therefore constructed a new chimeric toxin by fusing hIL-9-cDNA to modified Pseudomonas aeruginosa exotoxin A (ETA'). The binding properties of the new recombinant protein, rhIL-9-ETA', were assessed on different cell lines expressing the hIL-9 receptor. The antitumor potency of rhIL-9-ETA' was evaluated against the Hodgkin-derived cell lines L540Cy, KM-H2 and L1236, the Burkitt lymphoma cell line Daudi, the erythroleukemia cell line K562, and the mastocytoma cell line P815-hIL9R, transfected with hIL-9 receptor cDNA. Recombinant hIL-9-ETA' exhibited potent specific cytotoxic effects against P815-hIL9R, K562 and L1236 cells, inhibiting protein synthesis by 50% (IC50) at concentrations of 0.05, 0.58 and 3 micrograms/ml respectively. The cytotoxic effect was abrogated after addition of polyclonal antibodies against the human IL-9. rhIL-9-ETA' might be of potential use against hIL-9R-expressing malignancies.
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PMID:A deletion mutant of Pseudomonas exotoxin-A fused to recombinant human interleukin-9 (rhIL-9-ETA') shows specific cytotoxicity against IL-9-receptor-expressing cell lines. 938 98


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