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)

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

Ferritin has been reported to inhibit the growth of some leukemia cells in serum-supplemented culture. Recently we have found that ferritin stimulates the proliferation of human acute myeloblastic leukemia cells HL-60 and erythroleukemia cells K-562-T1 in serum-free medium. In this study, we examined the effect of ferritin against 14 human leukemia cell lines using human heart ferritin in serum-depleted culture medium. Among 14 cell lines tested, 10 were stimulated to proliferate by ferritin (maximum response at 30-300 ng/ml) with 0-1% fetal calf serum (FCS). The growth of all the cell lines was significantly inhibited by ferritin in the presence of 10% FCS. These results suggest that ferritin has dual functions; it promotes the growth of leukemia cells with low concentrations of FCS, but suppresses their growth with high concentrations of FCS.
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PMID:Growth stimulation of ferritin of human leukemia cells in vitro. 788 78

The epitopes Tn and sialosyl-Tn are expressed on erythrocytes of individuals with a very rare blood group, who often suffer from "Tn syndrome." We surveyed expression of Tn and sialosyl-Tn in normal blood cells, malignant transformed cells, and progenitor stem cells from bone marrow (BM). An anti-Tn antibody, IE3, and an anti-sialosyl-Tn antibody, TKH2, were used in this study. TKH2 reacted with erythroblasts, B cells, and a subset of CD4+ cells; but not with erythrocytes. Erythroblastic cell lines (K562, HEL, and UT7/EPO) and B-cell lines (Daudi, Raji, and B-cell lines transformed by Epstein-Barr virus) showed reactivity to TKH2. Similar results from the reactivity of TKH2 with transformed cells from leukemia patients and lymphoma patients were obtained; TKH2 reacted with blasts from erythroleukemia (M6; for 4 of 4 cases) and with lymphocytes from B-cell chronic lymphocytic leukemia (3 of 3), B-cell lymphoma (5 of 5), and CD4+ adult T-cell leukemia (4 of 4), but did not react with blasts from acute myeloid leukemia (M0 to M5; 0 of 22) or acute lymphoid leukemia (B-lymphoid leukemia, 0 of 11; T-lymphoid leukemia, 0 of 2; undifferentiated leukemia, 0 of 1). IE3 did not react with all of the tested cells. CD2-CD19-TKH2+ normal BM cells (BMC) contained blasts and various maturation stages of erythroblasts. The TKH2+ cells produced a large number of colony-forming unit-erythroid (CFU-E) colonies, whereas they produced a small number of burst-forming unit-erythroid colonies and CFU-granulocyte-macrophage colonies. CD34+ normal BMC did not express Tn and sialosyl-Tn. These findings suggest that sialosyl-Tn expresses in CFU-E to erythroblasts.
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PMID:Expression of sialosyl-Tn in colony-forming unit-erythroid, erythroblasts, B cells, and a subset of CD4+ cells. 790 75

The Raf-1 protein, a cytoplasmic serine/threonine kinase, plays an important role in signal transduction pathways. In order to examine the role of Raf-1 in human myeloid leukemia, we determined raf-1 mRNA expression by Northern blot analysis in blast cell samples from 27 acute myeloid leukemia (AML) cases and peripheral blood mononuclear cells from six healthy donors. A normal raf-1 transcript size was detected in all cases investigated. However, overexpression of raf-1 mRNA was found in 2 of 27 AML cases, both of which were erythroleukemias (AML, FAB M6).
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PMID:Overexpression of the Raf-1 proto-oncogene in human myeloid leukemia. 820 58

Juvenile chronic myelomonocytic leukemia (JCMMoL) is a rare disease with no specific type of chromosome aberration yet delineated. We report a 2-year-old boy who had in his leukemic bone marrow (BM) and peripheral blood (PB) cells the 46,XY,der(15)t(3;15)(q13.1;q26) karyotype. Phytohemagglutinin (PHA)-stimulated lymphocytes of peripheral blood had a normal 46,XY karyotype. The origin of the duplicated part of 3q was proved by fluorescence in situ hybridization (FISH) with the pHSR(sat III 15p) DNA probe and a chromosome 3-specific DNA library (i.e., chromosome painting). The chromosome finding in our case provides further proof of the close relationship between the rearrangement in region 3q13-->3q26 and the pathogenesis of acute myeloid leukemia (AML). Our patient has transformed into erythroleukemia [M6 according to the French-American-British (FAB) classification] during the course of the disease.
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PMID:Partial trisomy of 3q detected by chromosome painting in a case of juvenile chronic myelomonocytic leukemia. 827 54

To determine the clonal origin and growth requirement of leukemic blast progenitors in erythroleukemia, acute myelogenous leukemia (AML) M6, T cell-depleted mononuclear cells obtained from 5 erythroleukemia patients were cultured in methylcellulose media. Although plating efficiency did not significantly differ from those in the other AML subtypes, the morphology of colonies in erythroleukemia was distinct. Two types of colonies were formed; one was composed of myeloblasts, and the other consisted of erythroblasts and myeloblasts. The "mixed" colony formation was not stimulated by interleukin-3, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor or erythropoietin. Both types of colonies were formed spontaneously in the absence of supplemented growth-stimulatory factor when cultured at high density. The results suggest that leukemic blast progenitors in erythroleukemia originated at the stage of bipotent hematopoietic precursor capable of differentiating into erythroid and myeloid lineages. The formation of mixed colonies composed of erythroblasts and myeloblasts in the absence of erythropoietin or colony-stimulating factor may indicate the deranged hematopoiesis in erythroleukemia.
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PMID:Mixed colony formation composed of erythroblasts and myeloblasts by leukemic blast progenitors in patients with erythroleukemia. 841 64

Chromosome studies were carried out on unstimulated bone marrow cells from a patient with a diagnosis of acute nonlymphocytic leukemia (FAB M6 ANLL). Cytogenetic analysis revealed a mosaic chromosome pattern 46,XX/46,XX,inv(8)(p21q24). This pericentric inversion has not been previously described in ANLL. Because, fragile sites, zinc finger gene loci, and the MYC protooncogene have been localized to band 8q24, a putative role for these sites and genes could be considered.
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PMID:A new pericentric inv(8) in acute nonlymphocytic leukemia. 846 81

A 13-year-old girl presented with swelling in the neck, fever, bleeding of the gums, and hepatosplenomegaly. Bone marrow morphology was suggestive of erythroleukemia (AML-M6). Chromosome analysis of the marrow revealed 48,XX, +21, +21 as the sole clonal abnormality.
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PMID:Tetrasomy 21 as a sole abnormality in erythroleukemia. 853 46

The Coulter VCS is an automated differential counter, which derives a five-part differential count on the basis of differences in cell volume, high frequency conductivity and light scatter. A printed scatterplot relating volume and scatter is readily obtained. Other instruments which use automated cytochemistry can distinguish between AML and ALL, and between AML variants. It was our impression that the Coulter VCS might also be capable of such distinction on the basis of the scatterplot patterns. We therefore collected scatterplots produced by Coulter VCS analysis of peripheral blood from 63 patients presenting with acute leukaemia. The scatterplots were inspected and six basic patterns identified. The scatterplots were inspected and six basic patterns identified. The scatterplots could be reproducibly sorted into pattern-specific groups without knowledge of the diagnosis. Precise leukaemic diagnoses were made routinely by conventional morphology, cytochemistry and immunophenotyping. A comparison was then made with the scatterplot patterns. The 51 cases of AML produced examples of all six patterns. The nine cases of ALL produced only three patterns. These were shared with cases of AML, and two were also shared with the three cases of acute mixed lineage leukaemia. Thus, three of the six patterns were specific for AML, whereas no pattern was specific for ALL or acute mixed lineage acute leukaemia. One pattern was produced only by the three cases of AML M6, and another was produced only by five of the 25 cases of primitive (M0 and M1) AML.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An assessment of the Coulter VCS automated differential counter scatterplots in the recognition of specific acute leukaemia variants. 853 14

A t(3;5)(q25.1;q34) chromosomal translocation associated with myelodysplastic syndrome and acute myeloid leukemia (AML) was found to rearrange part of the nucleophosmin (NPM) gene on chromosome 5 with sequences from a novel gene on chromosome 3. Chimeric transcripts expressed by these cells contain 5' NPM coding sequences fused in-frame to those of the new gene, which we named myelodysplasia/myeloid leukemia factor 1 (MLF1). RNA-based polymerase chain reaction analysis revealed identical NPM-MLF1 mRNA fusions in each of the three t(3;5)-positive cases of AML examined. The predicted MLF1 amino acid sequence lacked homology to previously characterized proteins and did not contain known functional motifs. Normal MLF1 transcripts were expressed in a variety of tissues, most abundantly in testis, ovary, skeletal muscle, heart, kidney and colon. Anti-MLF1 antibodies detected the wild-type 31 kDa protein in K562 and HEL erythroleukemia cell lines, but not in HL-60, U937 or KG-1 myeloid leukemia lines. By contrast, t(3;5)-positive leukemia cells expressed a 54 kDa NPM-MLF1 protein, but not normal MLF1. Immunostaining experiments indicated that MLF1 is normally located in the cytoplasm, whereas NPM-MLF1 is targeted to the nucleus, with highest levels in the nucleolus. The nuclear/nucleolar localization of NPM-MLF1 mirrors that of NPM, indicating that NPM trafficking signals direct MLF1 to an inappropriate cellular compartment in myeloid leukemia cells.
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PMID:The t(3;5)(q25.1;q34) of myelodysplastic syndrome and acute myeloid leukemia produces a novel fusion gene, NPM-MLF1. 857 Feb 4


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