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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

6 cases of AML with a supernumerary chromosome 8 as the only aberration in practically all bone marrow mitoses and 10 cases with a normal chromosome composition of the marrow cells were investigated in order to evaluate the possible influence of trisomy 8 on some clinical and cytokinetic parameters. No significant differences between the groups were found. In our laboratory a supernumerary chromosome 8 is present in 36% of AML cases with chromosomal aberrations.
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PMID:Trisomy 8 in acute myeloid leukaemia: A non-random event. Lack of correlation with prognosis and cytokinetic parameters. 26 94

A patient is shown to have acute granulocytic leukemia, bone marrow mosaicism, and cutaneous fibroblast mosaicism for trisomy 8, an inherited reciprocal translocation involving the short arms of chromosomes 7 and 20, and a family history of cancer. A normal sister who had the same balanced chromosome translocation was evaluated for a preleukemic state; the results were unremarkable. The inherited translocation and postzygotically derived trisomy 8 are thought to represent additive factors contributing to the development of leukemia in the patient.
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PMID:Acute leukemia associated with trisomy 8 mosaicism and a familial translocation 46,XY,t(7;20)(p13;p12). 29 56

Two cases of acute myeloid leukaemia with trisomy 8 in all examined bone marrow cells are reported. The occurrence and the prognostic significance of trisomy C in myeloproliferative disorders are discussed. The published reports of myeloproliferative disorders with chromosomal abnormalities identified by the banding technique are reviewed. It is to be noted that among group C anomalies in the acute myeloid leukaemias, only involvement of chromosome no. 7, 8 and 9 have been reported to far.
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PMID:Trisomy 8 in acute myeloid leukaemia. 105 21

Bone-marrow chromosomes were examined with the G-banding technique in 30 patients with acute myeloid leukemia at the time of diagnosis. In 13 of the 30 patients (43%) only normal diploid bone-marrow cells were found, and no deviations from the normal banding pattern could be detected in these cells. In bone-marrow cells of 17 patients (57%), distinct chromosome abnormalities were found; in 10 of the patients only abnormal cells were observed, whereas in 7 of the patients the abnormal cells coexisted with normal diploid cells without any visible chromosome banding abnormality. The results of the detailed analysis of the karyotypic aberrations demonstrated that when chromosome aberrations occurred they were clearly non-random. All patients except two displayed trisomy 8,9 or 21 or monosomy 7. Analysis of cases of acute leukemia from other laboratories indicated that the same consistent pattern of chromosome involvement prevailed in them.
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PMID:Non-random chromosome changes in acute myeloid leukemia. Chromosome banding examination of 30 cases at diagnosis. 106 19

Two patients with acute myeloblastic leukemia with t(6;9)(p23;q34) translocation and classified as AML-M2 relapsed as acute monocytic leukemia (AML-M5). Trisomy 8 was found associated with t(6;9) at that time in both patients. Such changes in differentiation of leukemic cells have not previously been reported in this subtype of AML and add data favoring the pluripotent nature of the stem cell involved in leukemia with t(6;9).
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PMID:Relapse as acute monoblastic leukemia (AML-M5) of t(6;9) acute myeloblastic leukemia (AML-M2). 143 8

We have performed a retrospective analysis of the clinical, morphologic, and cytogenetic findings in 26 patients diagnosed between January 1969 and September 1991 with acute erythroblastic leukemia de novo (EL or AML-M6). Clonal chromosomal abnormalities were found in 20 (77%) patients (95% confidence interval [CI], 61% to 93%). Loss of all or part of the long arm (q) of chromosomes 5 and/or 7 was observed in 17 (65%) patients (95% CI, 47% to 83%). In addition, the karyotypes were often complex, with multiple abnormalities and subclones. Among the remaining nine patients, six had a normal karyotype and one each had trisomy 8, t(3;3), or t(3;5). The overall frequency of abnormalities of chromosomes 5 and/or 7 observed in our M6 patients is similar to that observed in our patients with therapy-related acute myeloid leukemia (t-AML; 99 of 129 patients, 77%), but substantially higher than that noted in our other patients with AML de novo (French-American-British [FAB] subtypes M1-M5: 52 of 334 patients, 16%). Our M6 patients with abnormalities of chromosomes 5 and/or 7 were older and had a shorter median survival (16 v 77 weeks [P = .005]) than did the M6 patients without these abnormalities. We found no correlation between morphologic features and either cytogenetic abnormalities or clinical outcome. Of note was the finding that the percentage of myeloblasts, which may account for only a small fraction of the total marrow elements when the revised FAB criteria are applied, had no bearing on prognosis. We conclude that acute erythroblastic leukemia, when defined by morphologic criteria, consists of two distinctive subgroups: one group tends to be older, has complex cytogenetic abnormalities, especially of chromosomes 5 and/or 7, and shares biologic and clinical features with t-AML; the other group, with simple or no detectable cytogenetic abnormalities, has a more favorable prognosis when treated with intensive chemotherapy.
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PMID:Clinical, morphologic, and cytogenetic characteristics of 26 patients with acute erythroblastic leukemia. 145 Apr 12

Generally, malignant hematologic disorders have been believed to be of monoclonal origin. However, cytogenetically unrelated clones have been reported in some disorders including one case of acute leukemia (AL), one of acute lymphoblastic leukemia (ALL), one of acute myeloblastic leukemia (AMMoL), and five of myelodysplastic syndromes (MDS). The most frequent chromosome abnormality was trisomy 8 (75%), followed by trisomy 21 (37.5%, including tetrasomy 21) and trisomy 11 (25%). Two patients showed both trisomy 8 and 11, one also had trisomy 21 (triclonal). One patient showed two cytogenetically distinctive clones in which one was 47,XY,+8, related to myeloid cells, and the other had a del(6q) and del(9p), suggesting lymphoid cells. One patient we report and 5 from the literature had two unrelated clones with trisomy 8 and deletion of the long arm of chromosome 5 (5q-); all had MDS. Review of our records showed that 11 patients with both trisomy 8 and 5q- in the same abnormal karyotype (not biclonal) had AL, i.e., 10 of acute nonlymphocytic leukemia (ANNL) and one of chronic myelogenous leukemia (CML) in blastic crisis. These findings suggest that cytogenetically unrelated clones may indicate hematopoietic biclonality.
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PMID:Cytogenetic biclonality in malignant hematologic disorders. 152 Dec 30

In this work we present the results of cytogenetic analysis of the malignant cells in 27 children with acute nonlymphocytic leukemia (ANLL). The aim of our investigations was to determine the frequency and types of chromosome aberrations in our population of children with ANLL. Successful cytogenetic analysis was carried out in 24 (89%) patients. Aberrant karyotypes of malignant cells were established in 58% of the cases. The most frequent chromosomal abnormality was t(8;21), identified in 5 (20.8%) patients, i.e., 4 of 10 M2-ANLL. Aberration frequency of chromosome 11 was 16.6% and was identified in 3 of 8 M5-ANLL. Trisomy 8 and monosomy 7 were identified in one patient each with M3 and M2-ANLL, respectively. del(13), a rare chromosome aberration in hemoblastoses, was found in a child with M1,t(8;21) and the loss of chromosome Y. Translocation t(1;11;21) with a break in regions 1q23, 11q23, and 21q22, is unusual and was identified in a boy with M2-ANLL; it can be considered as a variant form of the t(8;21).
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PMID:Cytogenetic analysis in children with acute nonlymphocytic leukemia. 155 Oct 80

Trisomy 8 is a common anomaly in bone marrow (BM) cells of patients with myeloproliferative disorders (MPD), myelodysplastic syndromes (MDS), or acute nonlymphocytic leukemia (ANLL). We studied the efficacy of fluorescence in situ hybridization (FISH) detection of trisomy 8 in patients with MPD, MDS, or ANLL using directly labeled fluorescent alpha-satellite and whole chromosome paint (WCP) DNA probes specific for chromosome 8. Using FISH, we analyzed interphase nuclei and metaphase spreads from randomized series of BM specimens from normal individuals and patients with varying proportions of trisomy 8 as determined by conventional cytogenetic analysis. The BM of all normal donors contained less than or equal to 2.0% nuclei with 3 interphase FISH signals and less than or equal to 1 metaphase with 3 WCP FISH signals. Ninety-five percent and 98% of BM specimens with at least two metaphase cells with trisomy 8 by cytogenetic analysis contained greater than 2.0% nuclei with 3 interphase FISH and greater than 2 metaphases with 3 WCP FISH signals, respectively. Thirteen patients had 1 in 20 or 1 in 30 metaphase cells with trisomy 8 by conventional cytogenetic studies. Of these patients, four had greater than 2.0% nuclei with 3 interphase FISH signals. The BM of all four patients contained positive metaphase FISH results. We then studied the usefulness of FISH analysis to detect occult trisomy 8 by analyzing BM nuclei from 144 patients who had MPD, MDS, or ANLL and either 20 normal metaphase cells or an abnormal karyotype without trisomy 8. Seven patients had greater than 2.0% nuclei with 3 interphase FISH signals (range, 2.10% to 3.40%) and six patients had 2 or more cells with trisomy 8 upon metaphase FISH or extensive conventional cytogenetic analysis. Our results show that interphase and metaphase FISH analyses are useful methods to detect trisomy 8 cells in BM specimens, especially for specimens with normal or uncertain conventional cytogenetic results.
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PMID:Fluorescence in situ hybridization: a sensitive method for trisomy 8 detection in bone marrow specimens. 159 71

Fifty percent of patients with the myelodysplastic syndrome, frequently following treatment by radiation or chemotherapy, have prognostically unfavorable deletions of the long arms of chromosomes 5 and 7, or trisomy 8, as have the 25% of patients with acute myeloblastic leukemia where remissions last 6-12 months, and where relapse cannot be prevented. In contrast, patients with prognostically favorable cytogenetics (translocation 15; 17 or 8; 21 or inversion 16) maintenance chemotherapy may prevent relapses. Of chronic myelocytic leukemia patients, 85% can achieve hematological remission with interferon alpha, and 40% a partial cytogenetic remission, which probably delays relapse.
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PMID:Prevention of chemotherapy-induced leukemia and of leukemia relapses. 172 55


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