Cases reported "Leukemia, Myeloid"

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1/425. MYC amplification in two further cases of acute myeloid leukemia with trisomy 4 and double minute chromosomes.

    We report two cases of trisomy 4 with double minute chromosomes (dmin): one in a woman with acute myeloid leukemia (AML), French-American-British subtype M2, the other in a man with chronic myelomonocytic leukemia. In the former case, many cells without trisomy 4 but with dmin were present, a finding not observed in previously reported cases. In both cases, fluorescence in situ hybridization studies demonstrated the double minutes to be MYC amplicons. Ten cases of AML with trisomy 4 and dmin have now been described; in the five cases investigated, the dmin have been shown to be amplified MYC gene sequences.
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2/425. MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25).

    MLL (ALL1, Htrx, HRX), which is located on chromosome band 11q23, frequently is rearranged in patients with therapy-related acute myeloid leukemia who previously were treated with dna topoisomerase ii inhibitors. In this study, we have identified a fusion partner of MLL in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease. leukemia cells of this patient had a t(11;17)(q23;q25), which involved MLL as demonstrated by Southern blot analysis. The partner gene was cloned from cDNA of the leukemia cells by use of a combination of adapter reverse transcriptase-PCR, rapid amplification of 5' cDNA ends, and BLAST database analysis to identify expressed sequence tags. The full-length cDNA of 2.8 kb was found to be an additional member of the septin family, therefore it was named MSF (MLL septin-like fusion). Members of the septin family conserve the GTP binding domain, localize in the cytoplasm, and interact with cytoskeletal filaments. A major 4-kb transcript of MSF was expressed ubiquitously; a 1.7-kb transcript was found in most tissues. An additional 3-kb transcript was found only in hematopoietic tissues. By amplification with MLL exon 5 forward primer and reverse primers in MSF, the appropriately sized products were obtained. MSF is highly homologous to hCDCrel-1, which is a partner gene of MLL in leukemias with a t(11;22)(q23;q11.2). Further analysis of MSF may help to delineate the function of MLL partner genes in leukemia, particularly in therapy-related leukemia.
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3/425. Isolated tetrasomy 8 in minimally differentiated acute myeloid leukemia (AML-M0).

    tetrasomy 8 as a sole anomaly in hematological disorders is relatively rare. To the best of our knowledge, only 19 such cases have been described in the literature to date. Of them, acute myeloid leukemia (AML) in 13 (M1, one; M2, three; M4, one; M5, eight), acute lymphoblastic leukemia(ALL) in one, myelodysplastic syndrome(MDS) in 3, polycythemia vera(PV) and myelofibrosis(MF), one case each. Their median survival was 20 weeks. Here, we report the first case of a 29-year-old man with minimally differentiated AML (AML-M0) displaying a tetrasomy 8 clone. immunophenotyping showed positivity with CD33, CD34 and intracellular MPO, but all lymphoid markers tested were negative. Conventional cytogenetics of bone marrow cells showed 84.9% of metaphases with tetrasomy 8 in addition to 15.1% with normal diploidy. However, fluorescence in situ hybridization(FISH) using a centromeric probe specific for chromosome 8 revealed trisomy 8 in 14.2% of interphase nuclei besides tetrasomy 8 in 82.4%. The patient died four weeks after diagnosis without therapy. In conclusion, these findings suggest that tetrasomy 8 is associated with a heterogeneous group of myeloid disorders and heralds a bad prognosis. It may be a consequence of clonal evolution of trisomy 8.
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4/425. Fusion of a novel gene, BTL, to ETV6 in acute myeloid leukemias with a t(4;12)(q11-q12;p13).

    The ETV6 gene (also known as TEL) is the main target of chromosomal translocations affecting chromosome band 12p13. The rearrangements fuse ETV6 to a wide variety of partner genes in both myeloid and lymphoid malignancies. We report here 4 new cases of acute myeloid leukemia (AML) with very immature myeloblasts (French-American-British [FAB]-M0) and with a t(4;12)(q11-q12;p13). In all cases, ETV6 was found recombined to a new gene, homologous to the mouse Brx gene. The gene was named BTL (Brx-like Translocated in leukemia). Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments indicate that the expression of the BTL-ETV6 transcript, but not of the reciprocal ETV6-BTL transcript, is a common finding in these leukemias. In contrast to the majority of other ETV6 fusions, both the complete helix-loop-helix (HLH) and ETS dna binding domains of ETV6 are present in the predicted BTL-ETV6 fusion protein, and the chimeric gene is transcribed from the BTL promoter.
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5/425. Identification of amplified genes in a patient with acute myeloid leukemia and double minute chromosomes.

    A case of acute myeloid leukemia (M2) with double minute chromosomes and complex karyotypic abnormalities was analyzed cytogenetically and molecularly. comparative genomic hybridization (CGH) showed that the 8q24 region that contains the MYC oncogene was not amplified. Instead, amplification of chromosomal regions 11q23-->qter and 9p11-->pter was identified. Southern blot analysis confirmed the CGH findings and showed that the ETS1, FLI1, SRPR, NFRKB, and KCNJ5 genes located at 11q23-->24 were amplified, whereas the MLL at 11q23 was not amplified. Additionally, the IFN beta 1 and CDKN2A genes at 9p were amplified, but to a lesser degree. This is the first example of a case of acute myeloid leukemia with double minute chromosomes that has not involved amplification of either the MYC or the MLL genes.
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6/425. Transient leukemoid disorder in a newborn with down syndrome followed 19 months later by an acute myeloid leukemia: demonstration of the same structural change in both instances with clonal evolution.

    A transient leukemoid disorder (TLD) was observed in a newborn with down syndrome (DS), demonstrating a clonal abnormality: 47,XX,der(X;15)(p10;q10), 21(c). Spontaneous remission was observed, but 19 months later an acute leukemia from the myeloid series was discovered. Cytogenetic study revealed the same structural change as at birth, with karyotypic evolution corresponding to addition of one chromosome 8 and a fourth chromosome 21. These findings demonstrate, at least in our patient, that TLD and the subsequent acute leukemia are closely related and that TLD, closely related to DS, must be viewed as a preleukemic disorder undergoing spontaneous remission. A review of literature data shows that most cytogenetic studies reported so far are related to either TLD or acute leukemia in DS. Serial studies performed in the same patient are quite infrequent and, to the best of our knowledge, there is only one other report demonstrating a cytogenetic relation between TLD and the subsequent acute leukemia.
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7/425. Identification of novel chromosomal rearrangements in acute myelogenous leukemia involving loci on chromosome 2p23, 15q22 and 17q21.

    Chromosomal translocations are frequently linked to multiple hematological malignancies. The study of the resulting abnormal gene products has led to fundamental advances in the understanding of cancer biology. This is the first report of t(2;15)(p23;q22) and t(2;17)(p23;q21) translocations in human malignancy. Patient 1, a 73-year-old male, was diagnosed with myeloblastic (FAB M1 sub-type) AML. cytogenetic analysis showed a 47,XY,t(2;15)(p23;q22), 13 karyotype. Fluorescent in situ hybridization (FISH) showed that the PML gene was transferred intact to the short arm of chromosome 2 while the ALK gene on chromosome 2p23 was passively transferred to the long arm of chromosome 15. Patient 2 was a 60-year-old male diagnosed with monocytic (FAB M4-type) AML. cytogenetic analysis showed 46,XY,t(2;17)(p23;q21) karyotype. FISH analysis showed that neither RARalpha nor ALK were disrupted by the translocation. None of the coding region of the three genes studied were translocated in these patients. This raises the possibilities that other neighboring genes could be involved or that noncoding regulatory sequences of the studied genes could be put in contact and deregulate expression of other genes. Alternatively, displacement of ALK, RARalpha and PML to novel positions could lead to loss of their normal regulation
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8/425. Extramedullary myeloid cell tumor of the urinary bladder in a patient with myelodysplastic syndrome.

    We report a case of extramedullary myeloid cell tumor of the urinary bladder in an elderly male with a three year history of myelodysplastic syndrome (refractory anemia with excess blasts), noninvasive papillary transitional cell carcinoma of the urinary bladder, and in situ transitional cell carcinoma of the left ureter. light microscopy demonstrated a poorly differentiated neoplasm composed of medium to large cells with eosinophilic cytoplasm. The tumor cells showed immunohistochemical expression of myeloperoxidase, lysozyme, CD15, CD68 and CD43. bone marrow examination following cystectomy demonstrated refractory anemia with excess blasts (6-10%) and a normal karyotype. cytogenetics, approximately 1 year after cystectomy, demonstrated a deletion of the short arm of chromosome number 12. Four years after presentation, the patient succumbed to pulmonary aspergillosis.
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9/425. A new translocation, t(2;4;12)(p21;q12;p13), in CD7-positive acute myeloid leukemia: a variant form of t(4;12).

    We describe a 41-year-old man with CD7-positive acute myeloid leukemia (AML-M0) with trilineage-myelodysplasia. Chromosome analysis of the bone marrow cells showed 46.XY.t(2;4;12) (p21;q12;p13). Cytological and clinical features of our case were quite similar to those of AML with t(4;12)(q11-12;p13). The karyotypic interpretation was confirmed by fluorescence in situ hybridization (FISH) by using the whole-chromosome painting probes specific for chromosomes 2, 4, and 12. FISH analysis with the use of the YAC 936e2 probe, which covers the TEL gene, did not show the split signal, suggesting that a gene other than TEL was involved in the leukemogenesis of the present case. Our case with AML with t(2;4;12)(p21;q12;p13) appears to be the first case of a variant type of AML with t(4;12) (q11-12;p13).
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10/425. Cytogenetic studies of the spleen in chronic granulocytic leukaemia.

    Using a technique of short-term in vitro culture, cytogenetic studies were performed on splenic tissue from 12 patients with chronic granulocytic leukaemia. In eight patients the disease was in its chronic phase and had been treated with busulphan (seven cases) or splenic irradiation (one case). In five of these patients, small numbers of dividing cells possessing the philadelphia (Ph1) chromosome were observed; in one, only Ph1 -negative metaphases, presumably those of lymphocytes, occurred, and in two patients no dividing cells were obtained. In four patients chronic granulocytic leukaemia had undergone metamorphosis to an acute phase: in two of these patients no dividing cells were observed in splenic cultures with or without added phytohaemagglutinin: this result may have been attributable to prior cytotoxic therapy. In cultures from the other two patients in metamorphosis, almost all dividing cells were Ph1 -positve and many cells possessed two Ph1 chromosomes. Full cytogenetic analysis in one of these cases showed that the spleen contained several closely related cell lines, apparently reflecting progressive tumour cell evolution.
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