Cases reported "Leukemia"

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11/121. nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma.

    We describe herein a case of nephrotic syndrome (NS) following allogeneic bone marrow transplantation (allo-BMT) for natural killer cell leukemia/lymphoma. Histologic studies defined the diagnosis as crescentic glomerulonephritis with massive immunoglobulin a (IgA) deposition, which has never been reported in NS cases following allo-BMT. Most of the massive infiltrated cells in the interstice were CD3( )CD4(-)CD8( ) T cells derived from the donor. We observed mesangial deposition of haemophilus parainfluenza outer membrane (OMHP) antigen and decreased glycosylation of the IgA1 hinge in the recipient's samples is consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high as other IgA nephropathy cases. These findings suggest that NS and crescentic glomerulonephritis in this case occurred as one of the forms of chronic graft-versus-host disease (GVHD), and that IgA deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.
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12/121. Hepatosplenic microabscesses in pediatric leukemia: a report of five cases.

    Hepatosplenic microabscesses secondary to invasion by various organisms may result in life-threatening conditions, especially in patients with cancer. Whether these patients should continue ongoing cytotoxic therapy, which might result in neutropenia, with the risk of progressive abscess formation or fungemia, remains a dilemma. We report five cases of pediatric acute leukemia with hepatosplenic microabscesses in children aged 4 years to 18 years. These patients presented with prolonged fever and neutropenia after antineoplastic chemotherapy, followed by abdominal pain, hepatosplenomegaly and hepatic dysfunction. Abdominal ultrasound and computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated multiple small lesions compatible with hepatosplenic candidiasis in all of the patients. Cultures, including blood or stool cultures, were positive in only two cases. Treatment with intravenous antifungal agents, including amphotericin b, liposomal amphotericin b, and/or fluconazole were successful in two cases. These two patients remained event-free and survived for more than 24 months (20 months and 22 months after infection was diagnosed). The duration of systemic antifungal medication administration ranged from 3 months to 22 months. The serial image examinations revealed drastic reductions in small residual lesions in the two patients who survived the longest. The major issues for these patients were how long the antifungal therapy should be administered for, and how to select the optimal drug and dosage to avoid hepatic and renal toxicity. Among our patients, alternative therapy with amphotericin b, liposomal amphotericin b, and fluconazole was used according to the patients' conditions, and the duration of antifungal therapy was determined by clinical manifestations and imaging study changes.
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13/121. Midline malignant B-cell lymphoma with leukemic transformation.

    This article presents a case of lethal midline granuloma on the palate of a 44-year-old woman, which had been identified histologically as B-cell lymphoma with leukemic transformation in the terminal stages. At the first visit, physical and laboratory examinations showed no remarkable findings except for a necrotizing ulcer of the palate, and the biopsy specimens only showed massive inflammatory cell infiltration and necrosis of the granulation tissue. There was a short-term resolution after treatment with cyclophosphamide and prednisolone, but the disease reactivated and the necrotic ulcerative lesion progressively advanced into the nasal cavity. Specimens from the third biopsy exhibited histologic features that were consistent with malignant lymphoma of the diffuse, mixed B-cell type. Chemotherapy with the regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone was adopted but was interrupted after a short time because of bone marrow suppression. Subsequently, large numbers of enlarged abnormal lymphocytes with a few vacuoles in the cytoplasm appeared in the circulating blood, indicating leukemic transformation of the midline lymphoma. The patient died on the seventh day after the initiation of chemotherapy. In the presentation of this case, the authors mention clinically important matters regarding midline lethal lymphoma and briefly discuss the pathophysiology and pathogenesis.
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14/121. Recombinant human granulocyte colony-stimulating factor enhanced cytotoxicity of Ara-C in Ara-C-resistant leukemic cells from a patient with biphenotypic leukemia in cell kinetic quiescence.

    in vitro preincubation with recombinant granulocyte colony-stimulating factor(rhG-CSF, 100 ng/ml) enhanced the cytotoxicity of 1-beta-D-arabinofuranosylcytosine(Ara-C) in leukemic cells resistant to Ara-C from a patient with biphenotypic leukemia. Treatment of the cells with rhG-CSF resulted in a 17-fold increase in dna synthesis, 4.6-fold increase in percentage of S-phase, and a two-fold increase in Ara-CTP formation. Maximal effect was observed at 72 h of incubation. Combination chemotherapy with rhG-CSF and Ara-C to the patient showed remarkable cytoreduction. These results indicate that recruitment of resistant leukemic cells in cell kinetic quiescence is inducible by rhG-CSF and that it is possible enhancement of the cytotoxicity to cell cycle-specific drugs such as Ara-C.
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15/121. Leukemic reticuloendotheliosis: "hairy cell leukemia," functional and structural features of the abnormal cell in a patient with profound leukocytosis.

    The development of profound leukocytosis in a patient with leukemic reticuloendotheliosis (LRE) enabled us to obtain purified LRE cells for the investigation of their structural and functional characteristics. The LRE cells of our patient bore surface immunoglobulin and had complement receptors but did not bear Fc receptors and did not form rosettes with sheep erythrocytes. By electron microscopy, the cells were observed to contain typical ribosome lamella structures and to phagocytize both 0.81 micron latex particles and complement-coated zymosan particles. They were adherent to both glass and nylon wool fibers. The mitogenic response to erythroagglutinating phytohemagglutinin was normal to magnitude but delayed chronologically. The binding of 125I-labeled plant lectins was used to characterize the surface topography of LRE cells. Results of these studies indicated that the LRE cell surface differed significantly from the surface of normal T and B lymphocytes and chronic lymphatic leukemia cells. The LRE cells were capable of both stimulating and responding in a one-way mixed lymphocyte culture. However, the LRE cells were not active as effector cells of either cell-mediated lympholysis, a T cell function, or antibody-dependent cellular cytotoxicity, a null cell function. In contrast, they were effector cells of lectin-induced cellular cytotoxicity showing that they did possess the capacity to function as cytotoxic effector cells. These data indicated that the LRE cells in our patient had surface and functional characteristics of both lymphocytes and monocytes.
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16/121. Expression of the Tn antigen in myelodysplasia, lymphoma, and leukemia.

    Expression of the normally cryptic blood group antigen Tn has occasionally been reported in hematologic disease, but the true frequency of this change is not known. A mouse monoclonal antibody (FBT3) and immunohistochemistry were used to examine expression of the Tn antigen. Expression was not detected in 35 normal bone marrow aspirates examined, but it was detected in 5 of 725 abnormal bone marrow aspirates, including 2 (3.6%) of 55 cases of de novo acute nonlymphocytic leukemia and 2 cases that terminated in acute nonlymphocytic leukemia. In two patients, one with acute myeloblastic leukemia and the other in blast transformation of chronic myeloid leukemia, the Tn antigen was expressed on 2 percent of blast cells. In one case of non-Hodgkin's lymphoma, 4 percent of normal myeloid cells expressed the antigen. In the other two cases, one of acute myelomonocytic leukemia and the other of myelodysplasia, only 2 to 8 percent of myeloid and erythroid cells initially were Tn positive. Subsequent serial immunohistochemical studies of bone marrow aspirates and peripheral blood in these two cases showed increasing numbers of Tn-positive erythroid and myeloid cells 8 to 12 months before polyagglutination was detected serologically. Tn-positive cells increased to > 90 percent in the terminal phase in both cases of both diseases. The results suggest that Tn expression in these two patients may have conferred a growth advantage to the cells and could be related to disease progression.
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17/121. Leukaemic subtype of marginal zone lymphoma: a presentation of three cases and literature review.

    The recent world health organization (WHO) classification recognizes three subtypes of marginal zone lymphoma (MZL): extranodal MZL of mucosa-associated lymphoid tissue (MALT), splenic MZL and nodal MZL. As a group, MZL share morphological and immunophenotypic features similar to that of the marginal zone B-cell in secondary B-follicles, the postulated common cell of origin. There is, however, increasing information about molecular heterogeneity between the types of MZL, suggesting different aetiology and highlighting our current incomplete understanding of this evolving entity. We describe the presentation and clinical course of three patients with MZL who do not fit the currently recognized WHO categories, and best fit the putative category of MZL, leukaemic subtype. We review the current literature on this newly described entity, highlighting the importance of its recognition.
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18/121. A t(1;9)(q23.3 approximately q25;q34) affecting the ABL1 gene in a biphenotypic leukemia.

    Recurring chromosome translocations, which are found in leukemia, can result in the inappropriate expression of oncogenes or in the formation of chimeric genes that code for structurally and functionally abnormal proteins. The chromosomal t(1;9)(q23.3 approximately q25;q34) was found in a patient with biphenotypic leukemia. fluorescence in situ hybridization (FISH) analysis revealed that the break on chromosome 9 occurred in the ABL1 gene. The breakpoint on chromosome 1 occurred distal to the PBX1 gene at 1q23.3, as shown by FISH using BAC RP11-503N16 and RP11-403P14, which flank the PBX1 locus; hence, the ABL1 gene can be fused with another gene distal to PBX1 gene.
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19/121. Burkitt transformation of mantle cell lymphoma.

    The associated poor prognosis and potentially aggressive behavior of mantle cell lymphoma and its blastoid variants make differentiation from other non-Hodgkin B-cell lymphomas especially important. We present a case of mantle cell lymphoma with a marked leukemic component, which demonstrated both a typical nodular mantle cell pattern and burkitt lymphoma within a single lymph node removed at the time of splenectomy. The presence of CD5, CD10, and Bcl-1 co-expression by immunohistochemistry and detectable t(11;14) and cMYC gene rearrangement by FISH analyses in the Burkitt region support a transformation of mantle cell lymphoma over a concomitant malignancy. A limited number of mantle cell lymphomas demonstrating dual t(11;14) and chromosome 8q24 cMYC gene rearrangements have been previously reported in the literature. They demonstrate an extremely aggressive course with a very poor prognosis. Although the accelerated terminal phase of this patient's clinical course mirrors these previous published cases; none have described the combined morphologic and immunophenotypic features of burkitt lymphoma reported here. This case provides further support for the aggressive nature of these lymphomas and demonstrates the utility of flow cytometry, immunohistochemistry, and cytogenetic techniques in avoiding potential errors in their diagnosis, prognosis, and treatment.
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20/121. clonal evolution in primary 5q-syndrome.

    Primary 5q-syndrome is a type of myelodysplastic syndrome characterized by refractory anemia, thrombocytosis, and hypolobulated megakaryocytes. The risk of leukemic transformation is low. A case of 5q- syndrome that occurred in a 42-year-old woman and was complicated by leukemic transformation 7 years after the initial diagnosis is reported. An additional clonal karyotypic anomaly, del(7q), was seen in the leukemic cells. The literature on leukemic and karyotypic evolution of primary 5q- syndrome is reviewed and the implication of karyotypic evolution is discussed.
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