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)

In this paper, we report on a 9-year-old girl with acute nonlymphocytic leukemia (FAB-M5) with a rare chromosome abnormality, t(11;23)(q21;p11). Peripheral blood showed Hb 7.5 g/dl, WBC 3,600 cells/microliters (10% blasts), and platelet count 110 x 10(3) cells/microliters. The bone marrow aspirates showed normal cellularity with 36.7% blasts. On morphological characteristics, micromegakaryocytes were observed, and on chromosome examination the karyotype was shown to be 46,XX,t(11;13)(q21;p11) in all metaphases.
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PMID:11;13 translocation in acute nonlymphocytic leukemia. 151 35

Myelodysplastic features of remission bone marrow were investigated in 46 adults with de novo acute myeloid leukaemia (AML) according to the FAB morphological criteria for myelodysplastic syndromes (MDS). Compared with a group of 18 patients with the common type of acute lymphoblastic leukaemia in remission, micromegakaryocytes (30.4% v. 5.6%, P less than 0.05), multi-separated nuclear megakaryocytes (45.7% v. 0%, P less than 0.01), degranulated neutrophils (39.1% v. 5.6%, P less than 0.05), and neutrophils with hyposegmented nuclei (34.8% v. 0%, P less than 0.01) were significantly more common in the AML patients. In contrast, dyserythropoietic changes had a similar incidence in both groups. When compared with the clinical features at initial diagnosis in AML cases, the dysmegakaryocytic changes in remission marrow were found to be significantly more frequent in patients with monocytic involvement (mainly M4) or trilineage myelodysplasia (T-MDS AML). Disease-free survival was significantly shorter in patients with micromegakaryocytes (P less than 0.05) or neutrophils with hypogsegmented nuclei (P less than 0.05) than in those without these features. Overall survival was also significantly shorter in patients with micromegakaryocytes (P less than 0.05). These findings may help in developing new strategies for the post-remission therapy of AML, and also suggest that myelodysplastic changes in the remission marrow of de novo AML patients may be related to haematopoietic recovery by a preleukaemic clone which eventually leads to early leukaemic relapse. Dysplastic marrow, however, was not necessarily associated with peripheral pancytopenia in the present series, warranting basic research on such putative clonal remissions.
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PMID:Remission with morphological myelodysplasia in de novo acute myeloid leukaemia: implications for early relapse. 152 Jun 22

The case history of a 15 year old boy in whom thrombosis of the internal carotid artery was associated with severe disseminated intravascular thrombosis (DIC) is described. Both peripheral blood smear and bone marrow aspirate revealed acute myelogenous leukemia FAB M-2 type as the cause of the disease. Consumption coagulopathy is common sign of hemostasis disturbances in leukemia. It is frequently observed in acute promyelocytic leukemia, but rarely it may be seen in the other forms of hemoblastosis, too.
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PMID:[Incidence of internal carotid artery thrombosis and disseminated intravascular coagulopathy in the early stages of acute myeloid leukemia]. 154 13

During a 6-year period we received bone marrow (BM) and peripheral blood (PB) samples from 178 patients with acute myeloid leukemia (AML). All patient BM, and occasionally, PB samples were characterized according to FAB criteria, and by immunophenotyping (IP) and cytogenetics (CG). This report summarizes the findings in the 125 patients who were older than 15 years. Their mean and median ages were 39.4 and 37.0 years. There were 8 (6.4%) M1, 27 (21.6%) M2, 15 (12.0%) M3, 49 (39.2%) M4, 14 (11.2%) M5A, 9 (7.2%) M5B and 2 (1.6%) M6. IP showed that HLA-DR was most strongly and frequently expressed by M1 blasts (53.5%, 86%) and least strongly and frequently expressed by M3 blasts (4.5%, 0%). HLA-DR was also relatively strongly expressed by M4, M5A, M5B (21.5%, 43%; 34.9%, 69%; and 19.2%, 56%, respectively). CD11b was uniformly weakly expressed by all FAB subgroups. CD13 was most strongly and frequently expressed by M4 (20%, 43%), and was relatively weakly and infrequently expressed by the other FAB subtypes (9.5%, 9.2%, 16.4%, 8.4%, 16.3%). CD14 was moderately expressed by M4 (15.2%, 25%) and M5B (14.0%, 22%) and M1 (7.0%, 40%). CD33 was most strongly expressed by M3 blasts (26.3% and 61%), and was most weakly expressed by M5B (10.6% and 22%). Fourteen (11.2%) patients had blasts that showed lymphoid antigens (5 T, 5 B, 5 CALLA) in addition to myeloid characteristics. Fifty-four (51.9%) of 104 patients tested had one or more karyotypic abnormalities, the most frequent of which was 8+. Only the t(15:17) was specific, and was seen in M3. Four patients with anomalous IP had trisomy 21, one of whom also had 11q-. We conclude that Saudi Arabian AML shows FAB patterns similar to patients in the West, and that M3 patients have a characteristic IP and cytogenetic pattern. Apart from this the MIC classification failed to reveal characteristic modes.
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PMID:Morphologic immunophenotypic and cytogenetic patterns of adult acute myeloid leukemia in Saudi Arabia. 154 71

We report the biological characteristics of leukaemic blasts from two cases of acute leukaemia with an interstitial deletion of the long arm of chromosome 9 (9q-). Case 1 (FAB: M1) showed del(9)(q12q22) as the sole karyotypic anomaly, and case 2 (FAB: M1) presented del(9) (q12q22) in association with trisomy 10. In both cases, leukaemic blasts presented unique cytological features, such as prominent vacuoles on Giemsa staining, or strong localization of myeloperoxidase resembling 'pseudo-Chediak-Higashi' granules. Immunophenotyping of blasts revealed the biphenotypic expression of T-lymphoid/myeloid antigens (CD2, CD7/CD33) in addition to CD34. Neither T-cell receptor beta (TCRB), T-cell receptor gamma (TCRG) nor Ig heavy chain (IGH) genes were clonally rearranged. Furthermore, there was neither rearrangement nor expression of ABL, which is located at 9q34, indicating that the deletion involved bands centrometric to 9q34 did not induce the activation of ABL. DNA synthesis of the blasts was stimulated (stimulation index greater than 2.0) in the presence of interleukin (IL)-3, IL-4, granulocyte colony-stimulating factor or erythropoietin (Epo). IL-3 and IL-4 could also support the in vitro growth of leukaemic blast colonies, and the IL-3- or IL-4-dependent blast colony growth was synergistically enhanced by the addition of IL-6 or Epo. These observations imply that T-lymphoid/myeloid or pluripotent stem cells may be closely involved in the development of 9q- AML.
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PMID:Interstitial 9q deletion in T-lymphoid/myeloid biphenotypic leukaemia. 155 Jul 72

1B2 is an IgM monoclonal antibody binding to glycoconjugates bearing the terminal N-acetyllactosamine structure. It agglutinates human erythrocytes. Various cell lines, peripheral blood leucocytes, normal marrow and blast cells from 179 acute myeloid leukaemia (AML) and 11 acute lymphoblastic leukaemia (ALL) patients were tested for reactivity with 1B2. Myelomonocytic (CFU-GM), erythroid (BFU-E), mixed (CFU-GEMM) and leukaemic (CFU-L) progenitor cells were tested in clonogenic assays. Granulocytes, monocytes, myeloid cell lines and 152 out of 179 AML were positive. All FAB subtypes were equally recognised. Lymphocytes, T-cell and Burkitt's cell lines, and 10 of 11 ALL samples were negative. 1B2 inhibited partially day 7 CFU-GM, whereas it was not toxic for BFU-E, CFU-GEMM and day 14 CFU-GM. Leukaemic clonogenic cells were killed in 33 out of 36 AML (more than 40% growth inhibition). 1B2 identifies the more mature steps of myeloid differentiation. It may be useful in the diagnosis of AML, and is a candidate for remission marrow purging before autologous transplantation.
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PMID:Specific binding of anti-N-acetyllactosamine monoclonal antibody 1B2 to acute myeloid leukaemia cells. 156 87

The standard methods for classifying acute leukaemias now include morphology, cytochemistry and membrane markers. Major advances in immunology, in particular the development of monoclonal antibodies (McAb) with lineage specificity, have provided objective positive criteria for the diagnosis of acute lymphoblastic leukaemia (ALL). The FAB group has recognised the importance of McAb for the classification of some forms of acute myeloid leukaemia (AML), such as megakaryoblastic leukaemia, AML-M7, in which reactivity with McAb against platelet glycoproteins is a requirement for diagnosis. More recently the group has defined a type of myeloblastic leukaemia with minimal differentiation, AML-MO, in which myeloid cytochemistry is negative and the diagnosis is made by the expression of myeloid antigens and negative lymphoid markers in the blast cells. However, new problems have emerged with the wider use of McAb which now need to be addressed: the most important is the precise evaluation criteria for biphenotypic leukaemia for which we have proposed a scoring system in order to recognise the genuine cases which constitute a distinct disease entity. The role of karyotyping in the classification of acute leukaemia is gradually being defined (MIC proposals) and some forms of acute leukaemia can only be diagnosed by chromosome translocations, e.g. Ph+ ALL, resulting from t(9;22) and t(4;11) in infant ALL. Several translocations can also be demonstrated by molecular techniques. Cases with t(8;16) (p11;p13) are characterised by myelomonocytic features, erythrophagocytosis and fibrinolysis and represent a type of AML which can be defined primarily by its cytogenetic abnormality.
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PMID:The classification of acute leukaemia. 157 5

A patient with acute myelomonocytic leukemia (M4 in FAB classification) refractory to various kinds of intensive chemotherapy was intravenously administered low doses (7 or 14 mg/m2) of aclacinomycin-A (ACM-A) daily. This increased mature neutrophils and monocytes and decreased leukemia cells in the peripheral blood. Pelger Huet-like nuclear anomaly, observed in the neutrophils, suggested the leukemic nature of these cells. The in vivo findings were clearly correlated with the in vitro results in which ACM-A could induce myelomonocytic differentiation of the leukemia cells. During the course of the treatment, the patient achieved and maintained good general condition for more than nine months after the initiation of the treatment. In clinical trials, nine patients, five with acute myeloid leukemia (AML) and four with myelodysplastic syndrome (MDS), were treated with low doses of ACM-A. Five patients, three AML and two MDS, responded to the treatment. The results suggest that low doses of ACM-A may induce in vivo differentiation of leukemia cells, and may be a potential therapeutic strategy in the treatment of AML or MDS that is refractory to conventional chemotherapy.
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PMID:Possible differentiation treatment with aclacinomycin A in acute myelomonocytic leukemia refractory to conventional chemotherapy. 158 May 53

A 57-year-old female presented with general fatigue. She had neither lymphadenopathy nor hepatosplenomegaly. Laboratory data revealed anemia and leukopenia (1,500/microliters) with a differential count of 4.5% leukemic cells. The myelogram revealed 34.4% leukemic cells, of which diameter ranged from 20 to 28 microns. The diagnosis was acute myelogenous leukemia (FAB: M2) with myelodysplasia. Cytogenetic analysis revealed that the leukemic cells had chromosome abnormalities involving both diploidy and tetraploidy with structural rearrangement. Structural rearrangement included del(5) (q22q33), del(15) (q22q24), and t(3; 12) (q25;p13). Small dose aclacinomycin-A treatment was effective in reducing the number of leukemic cells in bone marrow, and both anemia and leukocytopenia were improved.
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PMID:[Acute myelogenous leukemia transformed from myelodysplastic syndrome with tetraploid chromosome constitution]. 160 14

Myelodysplastic syndromes originate from a pluripotent stem cell. This view, previously suggested by G-6-PD and cytogenetic investigations, has been established unequivocally by X-chromosome inactivation analysis based on DNA polymorphisms and by studies of mutated oncogenes. Two genomic alterations associated with MDS have been analyzed in more detail. Activation of the RAS oncogenes, preferentially N-RAS, is demonstrated in approximately 35% of MDS patients. Mutations in the FMS gene, encoding the CSF-1 receptor, are found in 16% of cases. Interestingly, RAS and FMS mutations are predominantly observed in disorders of myelomonoctic differentiation, i.e., the CMML subtype in MDS and the AML FAB type M4. Moreover, homozygous deletion of the FMS gene may be an important event in the genesis of the MDS variant 5q- syndrome. Preliminary data indicate that defects in tumor-suppressor genes, namely p53, may also contribute to the development of MDS. Different lines of evidence suggest that clinical preleukemia is preceded by a phase in which genetic alterations accumulate without any hematologic change. Cases in point are the detection of RAS and FMS mutations in healthy individuals who had been treated in the past with cytotoxic therapy for lymphoma, the frequent observation of clonal remission in AML patients, or the identification of oncogene mutations in healthy individuals without even a history of malignancy or chemotherapy. Possibly, either germline mutations of oncogenes or tumor-suppressor genes and the process of genomic imprinting may constitute additional factors that predispose hematopoietic stem cells to malignant transformation. Limited as they are, the currently available data suggest that accumulation of genomic lesions, rather than their precise order of development with respect to one another, characterize the multistep process of leukemogenesis in which MDS already represent more advanced stages. The prognostic significance of oncogene mutations in MDS patients is controversially discussed. This issue awaits prospective analyses taking into account the influence of treatment modalities. However, the clinical relevance of molecularly defined parameters has already been established for their use as clonal markers in determining the mode of action and efficiency of different therapeutic approaches.
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PMID:Molecular genetic aspects of myelodysplastic syndromes. 161 6


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