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

The case of a patient with a t(8;16)(p11;p13) chromosomal abnormality and acute myelomonocytic leukemia is described. Review of cases with this translocation showed that 11 of 13 patients had acute monocytic or myelomonocytic leukemia with a high frequency of extramedullary disease and phagocytosis of normal blood cells by the malignant cells. While these patients are not clinically distinct from others with acute monocytic leukemia, the characteristic features of this subset of patients will certainly evolve.
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PMID:Translocation (8;16)(p11;p13) in patients with acute monocytic leukemias. An evolving syndrome? 306 Feb 48

We report a case of acute nonlymphoblastic leukemia (M5) with a rare cytogenetic abnormality involving chromosomes 8 and 16, t(8;16)(p11;p13). The leukemic blasts were determined to be monocytic by cytochemical and immunochemical studies. Morphological changes of the leukemic cells in response to phorbol myristate acetate further supported their identification as monocytic in nature. This chromosomal abnormality has apparently been reported only thrice in the literature. Translocation (8;16)(p11;p13), though rare, may be of primary importance in the process of leukemogenesis in some cases of histiocytic/monocytic malignancies.
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PMID:Acute monoblastic leukemia with a single chromosomal rearrangement involving breakpoints on chromosomes 8 and 16, 46, XX, t(8;16)(p11;p13). 311 1

A 29-yr old woman developed urticaria pigmentosa which subsequently progressed through systemic mastocytosis to Philadelphia chromosome negative (Ph neg) chronic myelogenous leukemia (CML) with t(8;17). Further cytogenetic evolution occurred at the time of transformation to the aggressive phase of the disease. Unlike Ph-positive CML, chromosome number 9 was not involved, nor was the breakpoint cluster region located at band 22q11. This clearly separates this case from other Ph-negative CML patients who do have involvement of 9q34 or the breakpoint cluster region. Since this is the first case of its type to be reported with cytogenetic abnormalities, the clinical relevance of the unique chromosomal rearrangement t(8;17)(p11;q25) in the setting of systemic mastocytosis is unclear. Additional cases need to be reported to determine if this genetic rearrangement is a nonrandom marker of leukemia evolving in a setting of malignant mast cell disease.
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PMID:Mast cell disease followed by leukemia with clonal evolution. 311 98

The leukemic cell karyotype was studied in 103 children with acute lymphoblastic leukemia. An abnormal chromosome pattern was revealed in 81 of 98 patients studied before treatment (82.6%) and in the five children studied in relapse. Aside from specific chromosomal abnormalities defined by the Third International Workshop on Chromosomes in Leukemia, other nonrandom rearrangements were observed, particularly del(14)(q11-13), del(12)(p11-12), and t(1;19)(q22-23;p13), often associated with partial trisomy for 1q. Patients with del(14) had tumorous lymph-nodes or other extramedullary tumors. The course of the disease in these children was rapid. Patients with markers such as Ph, 6q-,14q+, and with a t(4;11) had a low incidence of complete remission and short survival. The most favorable course of the disease was observed in the group of children with over 50 chromosomes in the leukemic cells.
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PMID:Nonrandom chromosomal abnormalities in acute lymphoblastic leukemia of childhood. 316 59

A report is given of three new cases of acute monocytic leukemia, FAB M5a, with a t(8;16)(p11;p13). Two cases showed a marked erythrophagocytosis, including one with phagocytosis of normoblasts and granulocytes. Phagocytosis was absent in the third case. The t(8;16) was the only abnormality in two cases, whereas one case showed clonal evolution with partial trisomy 1q and a deletion of part of the short arms of chromosomes 1 and 3. Treatment results and survival were poor in all cases. A complete remission was achieved in two patients, which lasted only for 3 and 6 months, respectively. In one of these cases a central nervous system relapse occurred. Survival was short, lasting between 1 and 9 months. One patient succumbed to interstitial pneumonitis, a complication of allogeneic bone marrow transplantation without evidence for relapsing leukemia.
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PMID:Translocation t(8;16) in acute monocytic leukemia. 316

The adhesion receptors Mac-1, LFA-1, and p150,95 are cell surface alpha/beta heterodimers that play a key role in leukocyte adhesion processes. The genes for Mac-1, LFA-1, and p150,95 alpha subunits have been located to chromosome 16 by means of Southern blot analysis using a series of somatic cell hybrids. Chromosomal in situ hybridization has demonstrated that the genes for the three alpha subunits map to the short arm of chromosome 16, between bands p11 and p13.1, defining a cluster of genes involved in leukocyte adhesion. The gene encoding the LFA-1/Mac-1/p150,95 beta subunit, and defective in leukocyte adhesion deficiency, has been located on chromosome 21, band q22. The leukocyte adhesion receptor alpha and beta subunits are mapped to chromosomal regions that have been shown to be involved in cytogenetic rearrangements in certain patients with acute myelomonocytic leukemia and the blast phase of chronic myelogenous leukemia, respectively.
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PMID:Chromosomal location of the genes encoding the leukocyte adhesion receptors LFA-1, Mac-1 and p150,95. Identification of a gene cluster involved in cell adhesion. 328 62

A cell line with immature blast cell morphology was isolated from HL-60 promyelocytic leukemia cell cultures and designated HL-T. This new cell type is biphenotypic, expressing terminal transferase (TdT) together with myelomonocytoid immunologic features. TdT enzymatic activity, undetectable in HL-60, was determined to be 140 to 180 units/10(8) HL-T cells by the dGTP-assay, approximately 20% of the activity found in lymphoblastoid cell lines. HL-T predominantly synthesize the known 58-kDa TdT-protein plus a minor 54/56-kDa doublet. The 58-kDa steady state form is nonglycosylated and is phosphorylated. Precursor antigens S3.13 and MY-10, absent on HL-60, are expressed by HL-T; however, the cells are negative for HLA-Dr. Southern blot analysis by hybridization with immunoglobulin heavy chain (JH) and T cell-receptor chain gene (T beta) probes shows JH to be in the germ-line configuration in both cell lines and the T beta gene to be in germ-line in HL-60 but to be rearranged in HL-T. Truncation of the gene encoding the granulocyte-macrophage-colony-stimulating factor (GM-CSF), as found in HL-60, is not observed in HL-T. HL-T are resistant to differentiation-induction by retinoic acid and 1,25-dihydroxyvitamin D3. Cytogenetically HL-T share with HL-60 a deletion of the short arm of chromosome 9 at breakpoint p13, an aberration frequently found in patients with T cell leukemia. In addition, HL-T display t(8;9)(p11;p24) and trisomy 20. Tetraploidy is observed in 80% of HL-T metaphases with aberrations identical to those in the diploid karyotype. Like HL-60, the new line shows some surface-antigenic-T cell characteristics. Despite an antigenic pattern most consistent with that of helper-inducer T cells (T4+, D44+/-, 4B4+, 2H4-, TQ1+/-), HL-T cells and their conditioned culture medium suppress antigen, mitogen, and mixed-leukocyte-culture-mediated lymphocyte proliferation.
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PMID:HL-T, a new cell line derived from HL-60 promyelocytic leukemia cell cultures expressing terminal transferase and secreting suppressor activity. 330 49

A translocation involving the short arm of chromosome #1 and the short arm of chromosome #7, [t(1;7)(p11;p11)] was present in four patients with myelodysplastic syndrome (MDS). Two of these patients had prior lymphoproliferative disorders and developed MDS following prolonged therapy with alkylating agents. One of the patients with prior therapy history has two additional independent abnormal clones: one with a partial deletion of the long arm of #7 and the other with t(1;7)(q21;q11). A third patient had a family history of leukemia in both the father and a brother, both of whom developed acute nonlymphocytic leukemia following an MDS phase. The last patient was an elderly woman with no predisposing features.
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PMID:Four patients with myelodysplastic syndrome with translocation (1;7)(p11;p11) including one patient with independent clones del(7)q22) [corrected] and t(1;7)(q21;q11) 342 49

A putative isochromosome of the long arm of chromosome #17 was identified in bone marrow cells from each of six patients with leukemia. Adequate sample was available for detailed study in four patients, and in each of these four cases examination with multiple staining techniques implied that the rearrangement is a dicentric chromosome, dic(17)(p11.2). An asymmetry of constriction at the two centromeric regions suggested that one centromere was inactive. The data presented here suggest that many of the presumed i(17q) markers observed in leukemia may actually represent dicentric rearrangements.
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PMID:Dicentric chromosome 17 in patients with leukemia. 346 78

The YK-M2 cell line was established from the peripheral blood of a patient with acute monoblastic leukemia in whom an anterior mediastinal tumor preceded the peripheral blood manifestation. The established cells grew in a single cell suspension with a doubling time of 60 h and consisted of primitive monoblastic cells. The cells were 52% positive for peroxidase staining and manifested strongly positive activity of alpha-naphthyl acetate esterase, which was completely inhibited by sodium fluoride. The cells showed strong expression of Fc gamma receptors and phagocytosed sensitized ox erythrocytes. When the cells were incubated with 1 alpha,25-dihydroxy-vitamin D3, they were induced to differentiate into mature monocyte-macrophage-like cells, which reduced the nitroblue tetrazolium dye and released a small amount of the superoxide anion. Cytogenetic studies revealed that the cells had a near-triploid karyotype with a modal chromosome number of 68, and the short arm of one No. 17 chromosome was deleted [del(17)(p11)]. The YK-M2 cell line is particularly unique in that the cells retained the polyploid karyotype that may be an initial cytogenetic change in the malignant transformation of the parent leukemia cells.
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PMID:Establishment of a novel acute monoblastic leukemia cell line (YK-M2) having a near-triploid karyotype. 346 38


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