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)

The eldest brother in a sibship of five children died of acute myelogenous leukemia at 10 years of age. The second and third eldest brothers died of hypoplastic anemia at ages five and nine years, respectively. A surviving 6 year old brother, the proband of the study, has abnormalities that suggest a preleukemic state: mild pancytopenia, platelet dysfunction, immunodeficiency, and bone marrow hypoplasia with approximately 18 per cent blast forms. His 17 year old sister has a mild normochromic normocytic anemia. Cytogenetic studies revealed C-group monosomy in the bone marrows of the proband and the third brother (45, XY, -C); band studies demonstrated that a No. 8 chromosome was missing in the proband (45, XY, -8). At least four of the siblings and their father had cerebellar ataxia, and evidence of a small cerebellum at autopsy examination or by computerized axial tomography. The disorder in this family has major features of two autosomal recessive preleukemic diseases, ataxia-telangiectasia and Fanconi's anemia. However, these and other inherited conditions were excluded by clinical or laboratory criteria, and no environmental causes of the familial disorder were found. The constellation of abnormalities in the family may constitute a new genetic syndrome.
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PMID:A family with acute leukemia, hypoplastic anemia and cerebellar ataxia: association with bone marrow C-monosomy. 28 89

Alternate expressions of the blood group A and H antigens on red cells are described in a patient with acute myelocytic leukemia. The patient's red cells showed mixed field agglutination with anti-A and anti-H sera and lectins, and no agglutination with anti-B serum. The agglutinability of the A red cells with Dolichos biflorus lectin was between A1 and A2 (A intermediate). Inagglutinable red cells were separated with anti-A agglutinin, and the proportion was about 80% of total cells. The agglutinating activity with Ulex europaeus anti-H of red cells, which were inagglutinable with anti-A, was 16 times weaker than that of group O cells. The weaker reaction with Ricinus communis lectin and the stronger reaction with Psathyrella velutina lectin on the inagglutinable cells with anti-A than those on the group O cells suggest that fucosyl alpha (1-2) and galactosyl beta (1-4) residues at the nonreducing end of carbohydrate chains of H antigens on the red cells were diminished, and N-acetylglucosaminyl beta (1-3) residues were sequentially exposed. His saliva contained A and H substances in normal amounts of a secretor. Serum alpha-N-acetylgalactosaminyltransferase activity which converts O red cells to A red cells was the same as those in sera from A1 individuals. These results suggest that the synthesis of H precursors is partially blocked in this patient's red cells.
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PMID:Altered expression of blood group A and H antigens on red cells from an acute leukemic patient. 130 92

Prognosis of second marrow transplantation after leukemia relapse is usually gloomy. We report a patient with AML who was successfully treated by the second marrow transplant following high dose busulfan, etoposide, and Ara-C for the testicular relapse after the first marrow transplantation. A 24-year-old man was diagnosed as having acute myeloid leukemia (AML) in September, 1988. In December of 1989 when he was in early relapse after his 2nd remission, he received the first allogeneic BMT from his HLA identical brother after high dose busulfan and cyclophosphamide conditioning. His posttransplant course was uneventful and graft versus host disease was not observed. Three months after BMT, he noticed swelling on right testicle. Leukemic cell infiltration was confirmed by aspiration cytology. The testicular relapse was followed by marrow relapse. After successful remission induction chemotherapy, he received 17.5 Gy testicular irradiation and second marrow transplantation using high dose busulfan, etoposide, and Ara-C conditioning. Although his posttransplant period was complicated by severe mucositis, high fever and bronchopneumonia, hematologic recovery was obtained by 3 weeks after the second transplant. He is now continuing in complete remission 18 months after the second BMT. This case report suggests that the combination of high dose busulfan, etoposide, and Ara-C could be a choice as a conditioning regimen for resistant AML relapsing after BMT.
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PMID:[Second marrow transplantation following high dose busulfan, etoposide, and Ara-C after testicular relapse in a patient with AML]. 157 38

A 59-year-old man was admitted because of generalized lymphadenopathy with fever and vomiting. His peripheral blood showed leukocytosis with a WBC of 93,500/microliters, and the bone marrow picture revealed a predominance of blast cells. The blasts were negative for peroxidase, alpha-naphthyl butyrate esterase and PAS, and had the phenotype of CD 7, 13 and 33 positive. A diagnosis of AML M0 was made, based on the criteria of the NCI-sponsored workshop in 1988. His initial status had been compromised by acute renal failure which necessitated hemodialysis. He responded partially to chemotherapy consisting of daunorubicin, cytarabine and prednisolone. However leukemia recurred and the patient suffered from various episodes of infection and died six months after admission. The Southern blotting showed the germ line configuration for TCR-beta chain and immunoglobulin heavy chain genes. No messenger RNA was detected for myeloperoxidase, c-myc and c-jun, while c-fms, c-fos and c-myb were expressed on Northern blotting. It is intriguing to detect c-fms and c-fos expression in these poorly differentiated leukemic cells.
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PMID:[A case report of AML M0:CD7, 33 (+) AML M0 case initially presented with cervical lymphadenopathy]. 160 10

For some years, there has been an increasing success in transplanting PBSC instead of autologous bone marrow in patients suffering from leukemic diseases. In healthy cytapheresis donors, we achieved peripheral blood mononuclear cell (PBM) recoveries of 74%, using a discontinuous flow separation technique (Haemonetics V50, Lymphosurge). At the moment, we have collected PBSC from 4 patients (3 AML, 1 ALL) in 28 cytapheresis procedures ranging from 12.9% to 80.1% (mean: 40.1%), whereas stem cell recoveries, defined by CFU-GM, were significantly better (mean: 66%). At present, one of these patients has been transplanted with PBSC alone, receiving 2.11 x 10(8) PBM/kg with 2.8 x 10(4) CFU-GM/kg. His posttransplantation cytopenia was shorter compared to other patients undergoing autologous bone marrow transplantation. The period of disease-free survival is now more than eight months while he is completely reintegrated into social and working life.
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PMID:[Stem cell concentrates in autologous transplantation]. 170 29

The anti-leukemic antibiotics, anthracyclines, are most effective agents in the treatment of acute leukemia. However, they have severe cardiac toxicities, which ordinarily shows dose-dependency, but sometimes produce acute cardiomyopathy. We experienced Torsade-de-pointes arrhythmia during the treatment of acute myelocytic leukemia (AML); The patient was a 28 year old woman and had an AML-M1. After the short course administration of daunorubicin (total 90 mg/m2) and aclarubicin (total 219 mg/m2), she suffered from an attack of Torsade-de-pointes ventricular tachycardia and passed away, since any treatment against ventricular arrhythmia was not effective. Autopsy studies revealed degeneration and atrophy of cardiac muscle in the area around His's bundle, which suggested an anthracycline-induced cardiac toxicity.
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PMID:[Torsade de pointes ventricular tachycardia in a patient with acute myelocytic leukemia]. 194 37

The changes of expression of oncogenes in the mononuclear cells of MDS case was studied during his clinical course, in series. His bone marrow was considered to maintain its function partly in initial stage, since both peripheral blood and bone marrow responded to clinical episodes. However, his hematopoietic function was gradually impaired with the disease evolution to AML. We examined the expression of four oncogenes in the mononuclear cells of his three clinical stages, early RAEB-t, RAEB-t and AML, to study the cause of transformation from MDS to AML. Early RAEB-t cells expressed all oncogenes studied other than c-myb, while only c-myc was weakly observed in RAEB-t. AML cells expressed c-myc, c-jun and c-myb, except for c-fms. The expression of c-fms and c-jun of early RAEB-t was considered to reflect the monocytosis induced by infections, and the expressions of c-myb and c-myc of AML cells were regarded as one of malignant signs of tumor transformation. These findings suggest that the evolutional transformation of MDS to AML was affected by the altered expression of oncogenes.
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PMID:[Altered expression of protooncogenes during clinical course in an AML case transformed from MDS]. 194 45

A 29 year-old-man who had been diagnosed as having myelodysplastic syndrome (MDS) in August 1985 was re-admitted to our hospital because of fever and palpitation. His peripheral blood showed severe pancytopenia and bone marrow findings remained to be compatible with MDS (refractory anemia), but karyotype of bone marrow cells revealed 7 monosomy in 17 of 20 metaphases examined. Other laboratory findings revealed decreased serum haptoglobin, positive urine hemosiderin and the normal resistance of red cell membrane. In addition, both Ham test and sugar water test were negative. The titer of cold agglutinin was low, Donath-Landsteiner antibody was not detected. These findings suggested the association of autoimmune hemolytic anemia (AIHA), although both direct and indirect Coombs' test were negative. After administration of 50mg of prednisolone daily, the frequency of red cell transfusion was markedly decreased and transfused red cell life span was prolonged from 10.4 days to 27 days. Afterward, his hematological status rapidly transformed into that of acute nonlymphocytic leukemia about 13 months after admission and he died of gastrointestinal bleeding and cerebral bleeding. Cases of MDS with immunological disorder have been reported. This is, however, the first case of MDS associated with Coombs negative AIHA.
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PMID:[Coombs negative autoimmune hemolytic anemia in a patient with myelodysplastic syndrome]. 202 40

Two cases of childhood acute nonlymphocytic leukemia (ANLL) with 21 trisomy as a sole cytogenetic change are reported. The first case was a 4-year-old boy with FAB-M5a. 47, XY, +21 was found in 7 of 12 metaphases at diagnosis and in all 15 metaphases examined at relapse 4 years and 3 months later. The second case was a 14-year-old boy with FAB-M1, all 20 cells examined showed 21 trisomy at diagnosis. His peripheral blood in remission revealed normal male karyotype. Although 21 trisomy is relatively common in ANLL of children, 21 trisomy as a sole anomaly is extremely rare, and to our knowledge, only 2 cases (19 included adult cases) have previously been reported.
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PMID:[Acute nonlymphocytic leukemias with 21 trisomy as a sole anomaly]. 215 Apr 18

The acute leukemias have been considered to represent a clonal expansion of a malignant transformed hematopoietic progenitor cell with adherence to either the myeloid or lymphoid lineage--"lineage fidelity." Lineage fidelity has been challenged by the demonstration of lineage switching or mixed-lineage leukemias. We describe a 7 year old male who presented with undifferentiated acute leukemia and nasopharyngeal and cervical masses. His blasts had the morphologic appearance of myeloblasts (FAB M1) and were positive solely for the myeloid antigen CD15. He entered a complete remission (CR) with acute nonlymphocytic leukemia therapy. At first relapse he had evidence of mixed-lineage leukemia with B-cell lymphoid and myeloid phenotypes. He again relapsed from a second CR with Burkitt-cell leukemia. Cytogenetic findings showed a consistent 14q+, 17p+ abnormality in the blasts and nasopharyngeal mass. The t(8;14) associated with Burkitt's lymphoma was found in the mass tissue only following passage in the nude mouse. Our patient demonstrates that limitations still exist in our ability to classify acute leukemia. That leukemic transformation occurred in a multipotential progenitor cell leading to undifferentiated leukemia at diagnosis and/or that chemotherapy can influence the genetic programs of leukemic cells leading to the evidence of mixed-lineage leukemia and lineage switching is supported.
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PMID:Undifferentiated acute leukemia and lineage infidelity (difficulties in classification and management). 229 88


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