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1/94. Jumping translocations involving chromosome 1q in a patient with crohn disease and acute monocytic leukemia: a review of the literature on jumping translocations in hematological malignancies and crohn disease.

    A 36-year-old man with a 10-year history of crohn disease (CD) presented with gross hematuria and blasts in his peripheral blood. A chromosome analysis revealed one normal cell and 33 abnormal cells. The stem line was 47,XY, 8. The multiple side lines also had a jumping translocation between chromosome 1q31-32 and 4, 8, 10, 17, and 18 terminal regions. A cytogenetic, morphologic, and immunophenotypic analysis of a bone marrow aspirate and biopsy demonstrated acute myeloid leukemia of monocytic lineage, AML-M5b. In this paper are reviewed (a) the unusual and rare phenomenon of jumping translocations in hematological malignancies and (b) leukemia in CD.
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2/94. Acute myeloid leukemia with t(5;11): two case reports.

    A case of acute monocytic leukemia (AMoL) with t(5;11)(q31;q23) and a case of acute myelomonocytic leukemia (AMMoL) with t(5;11)(q35;q13.1) are reported. The translocation between the long arm of chromosome 11q and that of chromosome 5q with leukemia have been rarely reported. Though breakpoint of both cases were subtlety different, they had morphologically monocytic character and showed hyperleukocytosis and chemoresistance.
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3/94. Acute monoblastic leukemia in a child following chemotherapy for neuroblastoma.

    The long-term effects of childhood cancer and its therapy are serious problems that deserve attention. One of the most important late effects is the development of secondary malignancy. We encountered a girl with neuroblastoma who developed acute monoblastic leukemia as a secondary malignancy, 32 months after starting treatment for the primary tumor at the age of 4 years and 10 months. For the primary tumor, she had received cyclophosphamide, ifosphamide, etoposide, epirubicin, cisplatin, and vincristine during a period of 20 months; no radiotherapy was given. cytogenetic analysis of the leukemic cells showed no specific changes, but a rearrangement of the mixed lineage leukemia gene (chromosome 11q23 translocation) was subsequently found by reverse transcription polymerase chain reaction. The survival time after onset of the secondary malignancy was brief. The leukemogenic hazards of cancer treatment should be weighed against their therapeutic benefits.
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4/94. tetrasomy 8 evolving into a segmental triplication 8q in a case of acute monocytic leukemia.

    We report a case of AML-M5 with tetrasomy 8 that evolved within a 7-month period to a segmental triplication 8q. Other numerical abnormalities in the initial diagnosis were not found at the relapse; however, a chromosome 1 structural abnormality was maintained, proving the clonal evolution from tetrasomy 8 to a segmental triplication of the long arm of 8. This strongly suggests that there is a functional and selective advantage for duplications and triplications of 8q in these patients.
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5/94. Multiple chromosomal associations and paracentromeric region instability in a case of acute leukemia.

    A case of acute myelomonocytic leukema is described, which was characterized cytogenetically by the presence of centromeric elongations, somatic crossovers, selective endoreduplication figures, and multiple chromosomal clusters. The demonstration of these phenomena by selective staining techniques for the chromosome bands (Q, C, G and S) and the nucleolar areas (acridine-orange, amido black B 10) raises some biological aspects involved in the proliferation of leukemic cells, such as nucleolar persistance during the metaphase and the non-separation of chromatids in the clusters during the anaphase. These structural abnormalities may represent the background for the explanation of the appearance of subclones in neoplastic disorders.
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6/94. Analysis of MLL-derived transcripts in infant acute monocytic leukemia with a complex translocation (1;11;4)(q21;q23;p16).

    It has been proposed, on the basis of cytogenetic studies and molecular analysis of MLL-derived transcripts in acute leukemia with 11q23 rearrangement, that only one fusion gene transcript present on the der(11) chromosome is critical for leukemogenesis. This view is challenged by a recent observation in a case of leukemia with a complex translocation that results in MLL being fused in-frame to two different partner genes. We investigated a case of infant monocytic leukemia with a complex translocation, (1;11;4)(q21;q23;p16). Molecular studies revealed MLL rearrangement by both fluorescence in situ hybridization and Southern blot analysis, and MLL/AF1q, but not the reciprocal message (i.e., AF1q/MLL), was amplified by polymerase chain reaction. sequence analysis of MLL/AF1q revealed an in-frame fusion between MLL exon 6 and the breakpoint located six bases upstream of the ATG start site for AF1q. Our data suggest that only one form of MLL fusion gene is implicated in leukemogenesis in our case to t(1;11;4).
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7/94. Pentasomy 8 in acute monoblastic leukemia.

    We report a case of pentasomy of chromosome 8 in 30-year-old man with de novo acute monoblastic leukemia (FAB AML M5a).
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keywords = chromosome
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8/94. Molecular analysis of the rearranged genome and chimeric mRNAs caused by the t(6;11)(q27;q23) chromosome translocation involving MLL in an infant acute monocytic leukemia.

    Chromosomal analysis of acute monocytic leukemia cells in a female infant revealed a t(6;11)(q27;q23) translocation. Southern blot analysis with a cDNA probe of the MLL gene at chromosome band 11q23 indicated that the breakpoint was in an 8.3-kb BamHI fragment that contained exons 5-11 of the MLL gene. Northern blot analysis showed a faint band corresponding to the MLL chimeric transcript. Structural analysis of a genomic clone with the rearranged MLL gene from der(11) chromosome demonstrated the breakpoint to be localized between exons 6 and 7 of the the MLL gene and to lie in an Alu sequence of this region. The partner gene fused to the 3' part of MLL was shown to be the AF6 gene on chromosome 6q27 by in situ chromosome hybridization and nucleotide sequencing of chimeric MLL cDNA clones. However, it was shown that MLL exon 5 was fused to AF6 in one clone, whereas most clones were MLL exon 6/AF6 chimeric cDNA clones. These findings indicate that exon 6 of MLL is spliced out in the process of transcription in a variant MLL/AF6. In addition, we were able to detect the splicing of exon 6 in either this chimeric MLL/AF6 or MLL transcripts from untranslocated chromosomes by reverse transcriptase-polymerase chain reaction. The detailed genetic map of AF6 was determined by in situ chromosome hybridization and radiation hybrid mapping.
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keywords = chromosome
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9/94. Acute monocytic leukemia with a novel 10;11 rearrangement resolved by fluorescence in situ hybridization.

    fluorescence in situ hybridization analysis in an adult with acute monocytic leukemia revealed the complex nature of a rearrangement between chromosomes 10 and 11, which resulted in disruption of the MLL gene. Using a combination of chromosome 10 and 11 paints, a 10 centromere-specific sequence, and a probe for the MLL locus at 11q23, the rearrangement was deduced to have involved a reciprocal translocation between chromosomes 10 and 11, followed by an inversion within the short arm of the derivative 10. To our knowledge, this novel rearrangement has not been described previously.
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10/94. FISH analysis of an AML-M5a with segmental rearrangements involving 11q23-MLL region.

    A 66-year-old man was diagnosed 10 years ago with thrombocytosis and treated with hydroxyurea. Recently, his condition deteriorated and he was found to have 68% blasts in the blood and AML-M5a. Conventional cytogenetic analysis and fluorescence in situ hybridization studies using 11-painting and MLL probes showed that chromosome 11 had duplications or triplications; the markers were also derived from the chromosome 11-MLL region. Therefore, we have demonstrated segmental rearrangement of chromosome 11 involving the MLL region resulting in multiple copies of the MLL gene.
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