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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have reviewed the clinical, morphologic, immunophenotypic, and cytogenetic features of 52 patients with erythroleukemia (FAB Cooperative Group; AML-M6) studied by the Cancer and Leukemia Group B (CALGB). The purpose of this study was to correlate morphology with the clinical features, immunophenotypes, and karyotypes of neoplastic cells, and with the response to therapy of patients with AML-M6. Thirty-three patients (63%) were male, median age 59 (range 16-81) years, 47 patients (90%) were white, and 42 patients (81%) had a performance status of < 2. Myelodysplastic changes were observed in at least 1 cell lineage in all cases, and in 2 cell lineages in 45 of 52 (86%) cases. Fifty percent or more of cases studied were positive for CD11b, CD13, CD15, CD33, glycophorin-A, and HLA-DR markers. Fourteen of 27 cases (52%) in whom karyotypic analyses were conducted had cytogenetic abnormalities. Five (19%) were simple (< 3 karyotypic abnormalities), while 9 (33%) were complex (> or = 3 abnormalities). We observed either a complete or partial loss of chromosomes 5, 7, or 12p, or the presence of trisomy 8, in 11 of 27 (41%) patients. Cases of AML-M6 were divided into group 1 (14 patients with bone marrow proerythroblasts and basophilic erythroblasts > 25% of all erythroblasts) and group 2 (38 patients with proerythroblasts and basophilic erythroblasts < or = 25% of all erythroblasts). We observed no significant differences between groups 1 and 2 in regard to sex, age, race, performance status, percentage of blood erythroblasts or myeloblasts, percentage of bone marrow erythroblasts, and periodic acid-Schiff (PAS) or myelodysplasia scores. Six of 6 (100%) patients of group 1, and 7 of 21 (33%) patients of group 2, had normal karyotypes (P = .006). Nine of 13 (69%) patients of group 1 and 15 of 33 (45%) patients of group 2 had a complete remission (CR) (P = .2). Eight of 11 (73%) cytogenetically normal patients achieved CR: 5 of 6 (83%) in group 1, and 3 of 5 (60%) in group 2. Five of 12 (42%) cytogenetically abnormal patients achieved CR. No difference in duration of survival (group 1, median = 4.6 months vs. group 2, median = 10.2 months; P = .93) was observed between the 2 groups. We conclude that AML-M6 is typified by multilineage involvement of hematopoietic cells. The morphology of erythroblasts in patients with AML-M6 may correlate with cytogenetic abnormalities and rate of CR.
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PMID:Morphologic characteristics of erythroleukemia (acute myeloid leukemia; FAB-M6): a CALGB study. 774 Nov 35

Specific chromosomal aberrations and point mutations of the N-ras proto-oncogene are characteristic genetic alterations in acute leukaemias. However, the relationships between these two different genetic changes are unclear. Here we have determined the order of genetic events in a patient with acute myeloid leukaemia characterized by trisomy 8 and a point mutation of N-ras at codon 12 (N12-cys) and codon 61 (N61-his). 30 colonies obtained by in vitro clonogenic assay of leukaemic cells from a patient with AML were individually analysed for the presence of trisomy 8 and each of two different N-ras mutations by fluorescence in situ hybridization (FISH) and the polymerase chain reaction (PCR). Trisomy 8 was detected in 25/26 evaluable colonies. 19/26 colonies contained the N12-cys mutation. The N61-his mutation was not detected in any of the colonies obtained. All the colonies with the N12 cys mutation were also trisomic from chromosome 8, whereas 6/25 colonies with trisomy 8 had no N-ras mutation. These data suggest that trisomy 8 was acquired before N12 cys mutation in the pathogenesis of this leukaemia and that two genetic events can co-operate within a single subclone.
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PMID:Sequential acquisition of trisomy 8 and N-ras mutation in acute myeloid leukaemia demonstrated by analysis of isolated leukaemic colonies. 780 79

Fourteen cases of dic(9;12)(p11-13;p11-12) in early B-lineage acute lymphoblastic leukemia (ALL) and other hematological malignancies are reported with a review of the literature. Altogether 36 cases were collected for analysis: ALL at diagnosis (31 cases) or in relapse (one case), chronic myeloid leukemia in lymphoid blast crisis (two cases), T-cell lymphoblastic lymphoma (one case) and T-cell non-Hodgkin's lymphoma (one case). We report the first cases of dic(9;12) with a T-cell phenotype. Dic(9;12) occurs predominantly in B-progenitor ALL of childhood and young adults (age range, 1-47 years, median 12 years) but not of infancy. One or more adverse clinical features, age > 10 years, WBC > 100 x 10(9)/l, pre-B immunophenotype, platelets < 100 x 10(9)/l, were found in over 90% of cases. Additional structural chromosomal changes or trisomy 8 were frequently present. Nevertheless with a median follow-up of 5 years, 29/31 cases (94%) remain in first remission conferring an excellent prognosis to this leukemia. Additional cases are being sought to confirm the prognostic value of this cytogenetic aberration in various hematological malignancies.
Leukemia 1995 Jan
PMID:Dicentric (9;12) in acute lymphocytic leukemia and other hematological malignancies: report from a dic(9;12) study group. 784 2

Chronic myelomonocytic leukemia (CMML) is a myelodysplastic syndrome (MDS) subtype, characterized by monocytosis, dysgranulocytosis and a low number of blast cells in the peripheral blood (PB). The clonal nature of MDS has been demonstrated by various techniques: the stem cell involved initially is capable of myeloid and lymphoid differentiation. Fluorescent in situ hybridization (FISH) is a technique which can be utilized without any pretreatment on whole interphase cells. In this study leukocytes of PB Wright-stained smears from four CMML patients with trisomy 8 (three cases) and 9 (one case) have been analyzed by FISH. Utilizing a probe for the centromere of chromosome 8 and for the heterochromatic region of chromosome 9, we observed the cells involved by trisomy. In each of the four cases neutrophils, eosinophils, basophils and monocytes may show trisomy 8 or 9, whereas lymphocytes resulted disomic. The comparison between leukocytes morphology and genotype suggests that the supernumerary chromosome does not influence cellular differentiation and maturation. We conclude that FISH analysis of PB leukocytes of patients with CMML is informative when studying the clonality of the disease. Chromosomal abnormalities seem to involve a hematopoietic cell committed to myeloid but not lymphoid differentiation. Trisomies 8 and 9 seem to confer some proliferative advantage without influencing the morphologic characteristics of leukocytes. Other causes will be investigated to explain dysmorphisms of neutrophils and monocytes typical of this disease.
Leukemia 1995 Jan
PMID:Cytogenetic clonality in chronic myelomonocytic leukemia studied with fluorescence in situ hybridization. 784 4

Acute basophilic leukemia is a relatively uncommon variant of acute nonlymphocytic leukemia accounting for 4-5 percent of cases of acute nonlymphocytic leukemia and less than 2 percent of all hematopoietic malignancies. It is usually characterized by a very rapid clinical course, symptoms of hyperhistaminemia, peptic ulceration, gastrointestinal cerebrovascular bleeding and resistance to therapy. This leukemia is somewhat heterogeneous in term of morphology, immunology and chromosome alterations. No specific marker chromosome has been described but trisomy 8 and monosomy 7 are the most frequent chromosomal abnormalities. The cytochemical reactions in basophilic leukemia are positive results with toluidine blue and Astra blue stains. Peroxidase stain is reported to show positive reactions. Ultrastructural analysis usually reveals immature basophil granules and provides evidence of basophilic differentiation of the blasts.
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PMID:[Acute basophilic leukemia]. 784 33

In Down syndrome, acute megakaryoblastic leukemia (AMKL) occurs frequently during the first 4 years of life and is usually preceded by a period of myelodysplasia (MDS), often associated with chromosomal abnormalities. Archival peripheral blood and/or bone marrow films of six patients with Down syndrome and MDS whose leukemic cells contained monosomy 7 or trisomy 8 were studied to determine whether the abnormal precursors produce mature cells in vivo. Using fluorescence in situ hybridization (FISH) of interphase nuclei with chromosome-specific centromere probes for either chromosome 7 or 8, we were able to determine which cells had one, two, or three signals indicative of one, two, or three no. 7 or 8 chromosomes. In five patients with trisomy 8, 80% to 100% (94.5% +/- 6.2%) of the megakaryoblasts had three signals using a chromosome 8 probe; in one patient with monosomy 7, 96.5% of the megakaryoblasts had one signal using a chromosome 7 probe. In all six patients, the myeloid and lymphoid series did not have evidence of the chromosomal abnormality present in the blasts. In three of five patients with trisomy 8, three signals were observed in 27%, 33%, and 41% of normoblasts, respectively. These data are evidence that the abnormal cell in MDS is a progenitor cell with the potential of forming cells of megakaryocyte and erythroid lineages.
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PMID:Interphase cytogenetic analysis of in vivo differentiation in the myelodysplasia of Down syndrome. 791 46

Patients in accelerated phase or blast crisis of chronic myeloid leukemia (CML) frequently develop clonal cytogenetic abnormalities in addition to the Philadelphia chromosome. Using a DNA probe directed to the centromere of chromosome 8, we performed fluorescence in situ hybridization (FISH) on archival Wright-stained blood and bone marrow smears of seven patients with CML and with a known +8 clone by metaphase cytogenetics to determine the distribution of +8 in interphase cells. All slides had been stored at ambient temperature for 12-26 months. The bone marrow aspirate smears of 21 non-leukemic patients served as controls. Trisomy 8 was demonstrated in all myeloid cell lines including the neutrophils, basophils, eosinophils, monocytes, and erythroid precursors, but not in the lymphocytes. The extra chromosome 8 was present in mature segmented granulocytes as well as more immature precursors. The percentage of +8 cells was highest in specimens from patients with CML in myeloid blast crisis (mean 64%), followed by those in accelerated phase (mean 39%). Three specimens from patients in morphologic chronic phase showed the lowest percentage of +8 cells (mean 13%). One patient was studied twice and showed a substantial expansion of +8 cells with progression from accelerated phase to myeloid blast crisis. Compared to metaphase cytogenetics, the proportion of +8 cells detected by FISH was often lower. We conclude that the acquisition of trisomy 8 in CML occurs in a pluripotent myeloid stem cell apparently incapable of expressing mature lymphoid phenotype, and that morphologic progression of disease is generally associated with an expansion of the +8 component.
Leukemia 1994 Oct
PMID:Fluorescence in situ hybridization (FISH) detection of trisomy 8 in myeloid cells in chronic myeloid leukemia (CML): a study of archival blood and bone marrow smears. 793 61

The in situ hybridization technique (ISH), using specific chromosome DNA probes on stained bone marrow or peripheral blood smears, allow us to correlate morphological findings with the cytogenetic abnormalities detected by conventional cytogenetic analysis. We have applied this methodology to study three patients, two of them diagnosed of acute lymphoblastic leukaemia (ALL) and one with a myeloid blast crisis of chronic myeloid leukaemia (BC-CML). Conventional cytogenetic analysis showed, among other chromosomal abnormalities, a trisomy 8 in two cases and a trisomy 7 in one case. ISH demonstrated that cytogenetic clonality was restricted to the lymphoblasts in both cases with ALL. In the BC-CML patient, myeloid blasts as well as mature and semimature granulocytic elements showed three hybridization signals. ISH correlating morphological and cytogenetic findings may be a useful technique for lineage as well as for the follow-up of the haematological patients.
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PMID:[Correlation between cellular and cytogenetic morphology using fluorescence in situ hybridization in the study of malignant hemopathies]. 794 51

Trisomy 8 is a relatively common finding in acute nonlymphoblastic leukemia (ANLL). In childhood acute lymphoblastic leukemia (ALL) it apparently is much more rare. Although Human Gene Mapping 11 included trisomy 8 as a marker for a subgroup of ALL, morphologic and immunologic characteristics of this entity have not been defined. We describe a case of early T-cell ALL (T-ALL) in a pediatric patient in whom this abnormality was the sole chromosome aberration. In situ hybridization with a chromosome 8-specific alpha-satellite DNA probe was performed. Our data are discussed and compared with pertinent literature.
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PMID:Characterization of a new case of trisomy 8 in acute lymphoblastic leukemia. 801 59

Chronic myelocytic leukemia is a particular subtype of leukemia characterized by increased myeloid precursor cells. It has been associated with the presence of the Philadelphia chromosome, described by Nowel and Hungerford in 1960, as a deletion of part of the long arm of a G group chromosome, the 22 chromosome. The present work reports the chromosomal abnormalities observed in 39 patients with chronic myelocytic leukemia, studied at the Genetic Unit, in the Faculty of Medicine of Zulia University, during the period from 1987 to 1991. Sixty per cent of the patients showed different abnormalities, such as 8 trisomy, t (8;22), and in the remaining 15%, no chromosomal changes were detected. The patients with t (9;22) as the only abnormality, had less relapses and longer survival. The clinical course of 50% of the patients with normal karyotype was similar to those with t (9;22) as the only abnormality; the other 50% had an accelerated course with frequent relapses and early death. The present findings confirm that the presence of the Philadelphia chromosome as the only karyotypical abnormality, is indicative of better prognosis, and its association with other chromosomal changes predicts a more accelerated course that will probably require a more aggressive treatment.
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PMID:[Significance of chromosome changes in chronic myeloid leukemia]. 812 10


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