Cases reported "Leukemia, Myeloid"

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1/92. Cytology of ascitic fluid in a patient with granulocytic sarcoma (extramedullary myeloid tumor). A case report.

    BACKGROUND: Granulocytic sarcoma (GS) is the rare extramedullary manifestation of acute myeloid leukemia that may precede or be concurrent with leukemic infiltration of bone marrow or herald blastic transformation of a chronic myeloproliferative disorder. It has been found in most body sites and shows no age or sex predilection, necessitating its inclusion in the differential diagnosis of undifferentiated neoplasms. CASE: A 36-year-old female presented with a three-year history of abdominal pain, jaundice and fluctuating abdominal girth. Cytology of the ascitic fluid revealed myeloid cells of eosinophilic lineage at all stages of differentiation, with many undifferentiated cells. Immunohistochemical studies on a cell block confirmed the diagnosis of granulocytic sarcoma, which excluded the differential diagnoses of Hodgkin's disease, non-Hodgkin's lymphoma and Langerhans histiocytosis. CONCLUSION: Granulocytic sarcoma may present as a serous effusion and can be diagnosed on a cytologic specimen.
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2/92. Extra-medullary myeloid tumour (granulocytic sarcoma) is often misdiagnosed: a study of 26 cases.

    AIMS: To describe the clinicopathological and immunophenotypic features of 26 cases of extra-medullary myeloid tumour (EMMT)/granulocytic sarcoma, which remains poorly recognized and is frequently confused with malignant lymphoma, and to discuss the main diagnostic problems experienced by the referring pathologist. methods AND RESULTS: Haematoxylin and eosin (H & E) sections of 26 cases of EMMT were re-examined. Immunostains for myeloperoxidase, lysozyme, neutrophil elastase, LCA, CD79a, CD20, CD43, CD45RO, CD3, CD30, CD15, CD68, MAC387, VS38C, MIC2, and the Leder stain for naphthol-ASD-chloroacetate esterase were performed on all cases. Clinical and follow-up data were obtained through a questionnaire to the referring pathologist or from the notes of the patients where available. In the 10 cases with known myeloproliferative disease, the initial diagnosis was correct in 10 whereas all cases presenting with EMMT without a previous history of myeloproliferative disorder had an initial incorrect diagnosis. The most common suggested diagnosis was that of a non-Hodgkin's lymphoma. The morphology of the tumours varied from well differentiated which included all stages of myeloid differentiation to poorly differentiated or blastic showing little or no evidence of myeloid differentiation. The proportion of positive cells for each stain varied. Chloroacetate esterase, myeloperoxidase and CD15 stained a large proportion of cells of the majority of the well differentiated tumours and a smaller proportion of the poorly differentiated/blastic tumours with very focal staining of some of the cases. Lysozyme and CD43 were the most sensitive of the markers staining a large proportion of cells of the majority of the tumours in both groups. Neutrophil elastase was the least sensitive of the markers of myeloid differentiation. CD79a, CD20, CD3 and CD30 were negative in all cases. CD43 was positive in all cases. CD68 stained a substantial number of cells in the majority of tumours. A smaller proportion of the tumours stained with MAC387. Four of the tumours showed positivity for MIC2. One tumour was positive for VS38C. CONCLUSION: This series documents continuing difficulties in the diagnosis of EMMT. Even well differentiated tumours are frequently mistakenly diagnosed as malignant lymphomas when they present without any history of antecedent myeloproliferative disorder. Careful evaluation of morphology for evidence of myeloid differentiation and a high index of suspicion when confronted with a less differentiated neoplasm are required to avoid this important diagnostic error. We suggest that a panel which includes chloroacetate-esterase, myeloperoxidase, lysozyme and CD43, together with other B- and T-lineage markers, in particular CD79a and CD3 should be used to confirm the diagnosis.
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3/92. Granulocytic sarcoma of the pancreas: a report of two cases and literature review.

    Granulocytic sarcomas (GS) are extramedullary tumour masses of immature myeloid cells, also known as chloroma and extramedullary myeloid cell tumour. These neoplasms usually occur simultaneously with, or follow the onset of acute myeloid leukaemia (AML). Rarely, they are the first manifestation of AML. GS may also be the first sign of transformation to AML in patients with chronic myeloproliferative disorders and myelodysplastic syndromes. GS have been reported to occur in a variety of tissues, but presentation as an abdominal mass and, in particular, infiltration of the pancreas is rare. We report two cases of pancreatic GS, review the literature, and discuss recent insights into the basic biological properties of these rare tumours.
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4/92. 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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5/92. Ultrastructure of acute myeloid leukemia arising in multiple myeloma.

    Bone marrow from a case of multiple myeloma in which acute myeloid leukemia supervened four years after diagnosis was examined with the electron microscope. Two distinct populations of neoplastic cells, one plasmacytoid and the other myeloid, were identified in the marrow. It is concluded that the acute leukemia that developed in this patient was a distinctly new neoplasm arising from the myeloid series of cells. Since in nearly all previously reported cases, and in our patient, alkylating agents had been administered, it is thought that this may have been a factor in the development of acute myeloid leukemia.
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6/92. Fulminant septicaemic syndrome of bacillus cereus: three case reports.

    Three patients with acute leukaemia, who were severely neutropenic and iatrogenically immunosuppressed post-chemotherapy, developed rapidly fatal septicaemic shock and coma caused by bacillus cereus (B. cereus). The illness was marked by two phases: a mild febrile illness lasting 6-14 h and accompanied by subtle symptoms of autonomic sympathetic nervous system overactivity, and a second short fulminant one, marked by high fever of 40-41 degrees C accompanied by major central nervous system disturbances, and ending with deep coma and brain stem dysfunction. One patient developed the sepsis in spite of 4 days of coverage with amikacin. In the other two patients, amikacin was commenced at the earliest phase of the infection, but failed to influence the outcome. This form of B. cereus sepsis in neutropenic patients seems to be caused by strains capable of causing bacteraemia and meningitis and has the ability to produce a substance that causes leptomeningeal and neuronal necrosis. Lack of early clinical and laboratory markers inevitably leads to death. Use of antibiotics effective against B. cereus and capable of achieving high concentrations in the cerebrospinal fluid. and identification and neutralization of the necrotizing substance may hopefully help to reverse this fatal illness.
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ranking = 7.6406739014023
keywords = central nervous system, nervous system
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7/92. Relapse of acute myelogenous leukemia as a cerebellar myeloblastoma showing megakaryoblastic differentiation.

    Myeloblastomas (granulocytic sarcomas) occurring within the central nervous system (CNS) are extremely rare lesions that may develop in patients with acute or chronic myeloproliferative disorders. The majority of such lesions involve brain or spinal cord by contiguous spread from meningeal or bony sites, rather than originating within the CNS parenchyma. We describe a patient with acute myelogenous leukemia in remission, who developed a purely intraparenchymal cerebellar myeloblastoma with megakaryocytic differentiation. The neoplastic cells expressed the megakaryocytic markers factor viii-related antigen and platelet glycoprotein-IIIa (CD61), and showed ultrastructural features that were indicative of megakaryocytic differentiation. Clinically, myeloblastomas of the CNS invoke a broad differential diagnosis that includes abscess, hemorrhage, and metastatic neoplasms because of their intraparenchymal location and radiologic features. Although they are rare, myeloblastomas should be included in the histopathologic differential diagnosis of a poorly differentiated neoplasm occurring within the CNS, particularly in a patient with a history of myeloproliferative or myelodysplastic disease.
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ranking = 8.2005316335139
keywords = central nervous system, nervous system, neoplasm
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8/92. Clinically significant cardiac infiltration in acute leukemia, lymphocytic lymphoma, and plasma cell myeloma.

    Cardiac infiltration by hematologic neoplasms leading to clinically significant cardiovascular disease is rare. Three such cases are described in this report, and it is suggested that rare manifestations of hematologic neoplasms may become more common in the future since these diseases are more amenable to therapy than heretofore. Cardiac involvement with hematologic neoplasms is of more than academic interest since this complication is likely to respond to radiotherapy.
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9/92. Intracerebellar chloroma (granulocytic sarcoma): a neurosurgical complication of acute myelocytic leukemia.

    A discrete intracerebellar mass of myeloblasts was found in a 26-year-old woman with acute myelocytic leukemia in remission. This chloroma (granulocytic sarcoma) was treated successfully by surgical extirpation. An aggressive neurosurgical role seems appropriate in handling central nervous system leukemic nodules in view of the improved patient survival created by current chemotherapy regimens.
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ranking = 6.2005316335139
keywords = central nervous system, nervous system
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10/92. Amplification of the AML1(CBFA2) gene on ring chromosomes in a patient with acute myeloid leukemia and a constitutional ring chromosome 21.

    In the genesis of hematologic neoplasms gene amplification is a mechanism for illegitimate activation of proto-oncogenes. We report a phenotypically normal patient with a constitutional ring chromosome 21 who developed acute myeloid leukemia (AML). The leukemic cells revealed size-variable ring chromosomes 21 with amplification of the proto-oncogene AML1, located in the chromosomal band 21q22, within the rings. Hitherto, amplification of the proto-oncogene AML1-also in form of a ring chromosome-has been described recently only in one patient with myelodysplastic syndrome (MDS). In AML, gene amplification by ring formation has been demonstrated only in another three patients (amplification of the MLL gene in two cases and of the ETV6 gene in one case). Here we present the new evidence that the internal rearrangement of a constitutional ring chromosome 21 resulted in multiplication of a proto-oncogene in bone marrow cells and provided obviously a selective growth advantage. Moreover the amplification of ribosomal dna was observed in the ring chromosomes of the tumor cells.
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