Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphologic and immunophenotypic findings of 36 cases of 21q22 acute myeloid leukemia (AML) and myelodysplasia (MDS) were compared, including 14 de novo t(8;21) AMLs, 11 t(8;21) therapy-related AML/MDS cases, and 11 therapy-related AML/MDS cases with other 21q22 balanced translocations [t(n;21)]. Cases were evaluated for the presence of Auer rods, distinct chunky cytoplasmic blast cell granules, promyelocyte increase, cytoplasmic perinuclear clearing (hofs) of blast cells, eosinophil increase, andfeatures of associated trilineage dysplasia. Results of immunophenotyping studies for CD19, CD34, and CD56 expression were compared. Cases of de novo and therapy-related t(8;21) disease shared common morphologic features of chunky cytoplasmic granules, perinuclear hofs, and promyelocyte increases that were not seen consistently in the t(n;21) group of t-AML/MDS cases. Immunophenotypic similarities also were observed between the 2 t(8;21) groups. De novo and therapy-related t(8;21) disease, however, differed by the frequent presence of associated dysplasia in both t-AML/MDS groups, which was infrequent in the de novo t(8;21) group. Therapy-related AMI/MDS with t(8;21) shares characteristic morphologic and immunophenotypic features with de novo t(8;21) AML, but frequently also occurs with associated myelodysplastic changes, similar to other therapy-related acute leukemias.
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PMID:Therapy-related acute myeloid leukemia/myelodysplasia with balanced 21q22 translocations. 1186 28

A 2-year-old Japanese boy who presented with multiple cervical, axillary, and inguinal lymphadenopathy was diagnosed by immunocytochemical analysis as having myeloid/natural killer (NK) cell precursor acute leukemia. Leukemic blasts in the bone marrow were positive for CD56 (NK marker), CD7 (T-cell marker), CD33 (myeloid marker), CD34, and HLA-DR. Tumor cells in a lymph node were also positive for CD2, cytoplasmic CD3 (T-cell marker), CD7, CD33, CD34, and CD56, but negative for peroxidase staining and other T-cell, NK, and myeloid markers. Southern blot analysis showed no rearrangement bands for T-cell receptor delta and immunoglobulin heavy chain. Chromosomal analysis revealed 46,XY,inv(7)(p21q21). Neither chemotherapy for acute lymphoblastic leukemia nor that for acute myeloid leukemia induced remission in this patient. However, complete remission was achieved by the administration of L-asparaginase (6,000 U/m2 for 5 days). Because the disease was considered refractory to standard chemotherapy, cord blood transplantation was performed from an HLA 1-locus mis-matched unrelated donor. The conditioning regimen consisted of total body irradiation, cytarabine, and cyclophosphamide, and cyclosporine and short-term methotrexate were employed for graft-versus-host disease (GVHD) prophylaxis. Hematological reconstitution was rapid, and only grade I acute GVHD was observed. The patient has been in remission for more than 24 months after transplantation. Our findings indicate that combination therapy with L-asparaginase and allogeneic stem cell transplantation may be useful for the treatment of myeloid/NK cell precursor acute leukemia.
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PMID:Treatment of a child with myeloid/NK cell precursor acute leukemia with L-asparaginase and unrelated cord blood transplantation. 1193 70

Allogeneic stem cell transplantation (allo-SCT) plays an important role in the treatment of infants and children with acute myelogenous leukemia (AML). Leukemic relapse after allo-SCT is responsible for a high rate of treatment failure. Extra-medullary relapse (EMR), without involvement of bone marrow, is rare compared to medullary relapse. CD56, the neural cell adhesion molecule, may contribute to the higher frequency of CNS relapse in CD56-positive AML. We observed an isolated EMR on the oculomotor nerve of a 17-month-old girl 12 weeks after cord blood transplantation (CBT), who was transplanted because of CD56-positive AML. Diagnosis of relapse was suspected clinically and confirmed by magnetic resonance imaging (MRI), and fluorescence-activated cell sorter (FACS) and chimerism analysis of cerebrospinal fluid (CSF). Therapy consisted of intra-thecal chemotherapy, CNS irradiation, and systemic immunomodulation by cyclosporin A (CsA) and basiliximab withdrawal. Twenty-one months after relapse, the patient shows full remission of symptoms and previously described oculomotor nerve infiltration.
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PMID:Unusual presentation of central nervous system relapse with oculomotor nerve palsy in a case of CD56-positive acute myeloid leukemia following allogeneic stem cell transplantation. 1210 May 14

A 29-year-old male was diagnosed as having non-Hodgkin's lymphoma (NHL, diffuse, large cell, B-cell, stage IV) in June 1999. He underwent 7 courses of chemotherapy and double autologous peripheral stem cell transplantation (total dose: CPA 13,000 mg, BUS 892 mg, L-PAM 150 mg, MCNU 870 mg, MTX 60 mg, Ara-C 160 mg, DXR 350 mg, VP-16 11,190 mg, VCR 8 mg, CBDCA 700 mg, and MIT 22 mg) for NHL and obtained complete remission in April 2000. In September 2000, he suffered from progressive general malaise. Laboratory findings showed marked leukocytosis with 85% leukemia cells, which were positive for alpha-naphthyl butyrate esterase. Surface-marker analysis of the leukemia cells showed positive results for CD11b, CD11c, CD13, CD15, CD33, CD56, CD64, CD65, CD71 and HLA-DR, and chromosomal analysis revealed add(8) (p11), add(9) (p13). He was diagnosed as having AML (M5a) and was still in complete remission for NHL. He did not respond to chemotherapy and died in December 2000, believed to be from therapy-related leukemia induced by the VP-16 used for treating NHL, judging by the patient's short clinical course and monocytic type of leukemia.
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PMID:[Therapy-related acute myeloid leukemia following double autologous peripheral blood stem cell transplantation for non-Hodgkin's lymphoma]. 1213 6

Epstein-Barr Virus-transformed B lymphoblastoid cell lines (EBV-LCLs) are routinely used for the in vitro expansion of T cells. However, these cell lines are reported to produce the cytokine IL-10, which is inhibitory for T cells. We, therefore, characterized a panel of 37 EBV-LCLs for a variety of cell surface markers, for secretion of various cytokines including IL-10 and for immunoglobulin production. These cell lines were derived from normal donors or patients with nonsmall cell lung cancer, acute myelogenous leukemia, melanoma or colon cancer. Overall, 26 lines were positive for CD19 and CD20, and 11 were negative for both. All of the lines were strongly HLA-DR+, while CD40 expression was variable. Twenty-four (65%) were both CD23+ and secreted immunoglobulin, and 33 expressed kappa and/or lambda light chains. Additionally, all of the EBV-LCLs were negative for T cell (CD3), NK cell (CD16, CD56), monocyte (CD14) and granulocyte (CD66b) surface markers. Some level of IL-10, IL-6, IL-12p40 and TNF-alpha cytokine production was detected in 33, 18, 19 and 12 EBV-LCLs, respectively. Together, these data reflect the heterogeneity of EBV-LCLs, which cautions their use nondiscriminately in various immunologic assays.
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PMID:Cell surface phenotyping and cytokine production of Epstein-Barr Virus (EBV)-transformed lymphoblastoid cell lines (LCLs). 1219 5

A case is reported of a 62-yr-old male suffering from chronic myelogenous leukemia (CML) who developed an extramedullary, para-orthic lymph-nodal blast crisis without blood or bone marrow involvement and expression of CD56/NK associated marker. The diagnosis was performed on ultrasound-guided fine-needle cytology by an immunocytochemical and flow cytometric analysis. Conventional smears showed a monomorphous population of disperse, undifferentiated cells without cytoplasm. Cells showed fragile nuclei, vesicular chromatin, and evident nucleoli. Immunocytochemistry performed on cytospin slides were negative for cytokeratin, LCA, CD20, CD45Ro, and myeloperoxidase (MPO). Flow cytometry analysis proved the myeloid origin of the tumor by expression of CD13, CD34, and CD38 and showed aberrant expression of CD56. Cytological diagnosis was confirmed by histological examination. CD56 expression is generally an expression of NK lymphoid proliferation and may be observed in acute myelogenous leukemia but has rarely been reported in CML and its related blast crisis. This unusual expression, its possible explanation, the related technical problems, and clinicopathological aspects are discussed.
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PMID:Expression of NK-associated antigens in extramedullary lymph nodal blast crisis of chronic myeloid leukemia on fine-needle cytology. 1220 63

Extramedullary myeloblastic tumors, so-called myelosarcomas (granulocytic sarcomas, chloromas) have been reported only sporadically in the pertinent literature which reflects their rather infrequent occurrence. These lesions may accompany the initial manifestation or signal relapse of acute myeloid leukemia (AML) or coincide with blastic transformation of a chronic myeloproliferative disorder. However, even more rarely, primary myelosarcomas may precede AML by months or years or may be associated with myelodysplastic syndromes (MDS) that never progress to manifest leukemia. In a retrospective evaluation a clinicopathological study on these latter two variants of isolated extramedullary manifestations of AML was performed to elucidate certain aspects of site involvement and histopathology by application of enzyme and immunohistochemistry. For this reason, we selected 6 patients presenting with a myelosarcoma in combination with MDS and 12 patients revealing only uncharacteristic reactive changes of the bone marrow. Of these patients 8 developed AML following an observation time of up to 2 years. Focal leukemic infiltrates were most often localized in the skin ( n=4), oral mucosa ( n=4), lymph nodes ( n=3), gastrointestinal tract ( n=3) or pleura and retroperitoneum ( n=3 each). Myelosarcomas were usually regarded by the clinicians as putative malignant lymphomas unless further evaluation, especially involving chloroacetate esterase reactions as well as immunostaining with a panel of antibodies reactive with lysozyme, myeloperoxidase, CD68, CD43, CD56, CD117 and CD34 proved their true nature. Although at that time bone marrow findings were inconclusive, a straightforward diagnosis was reached by considering the possibility of a (primary) myelosarcoma in these patients.
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PMID:[Extramedullary initial manifestations of acute myeloid leukemia (AML)]. 1243 91

Hematopoietic neoplasm coexpressing CD4 and CD56 includes a subset of acute myeloid leukemia with myelomonocytic differentiation, plasmacytoid monocyte tumor, and other immature hematopoietic neoplasms of undefined origin. Herein, we report a CD4+CD56+CD68+ hematopoietic tumor that was thought to be a tumor of plasmacytoid monocytes. This case is unique in the absence of accompanying myelomonocytic leukemia and the faint expression of cCD3 on the tumor cells. The patient was a 22-yr old man presented with multiple lymphadenopathy and an involvement of the bone marrow. Tumor cells were large and monomorphic with an angulated eosinophilic cytoplasm of moderate amount. Nuclei of most tumor cells were eccentric and round with one or two prominent nucleoli. Rough endoplasmic reticulum was prominent in electron microscopic examination. Tumor cells expressed CD4, CD7, CD10, CD45RB, CD56, CD68, and HLA-DR and were negative for CD1a, CD2, sCD3, CD5, CD13, CD14, CD20, CD33, CD34, CD43, CD45RA, TIA-1, S-100, and TdT. cCD3 was not detected in the immunostaining using paraffin tissue, but was faintly expressed in flow cytometry and immunostaining using a touch imprint slide. T-cell receptor gene rearrangement analysis and EBV in situ hybridization showed negative results. Cytochemically, myeloperoxidase, Sudan black B, and alpha naphthyl butyrate esterase were all negative.
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PMID:CD4+CD56+CD68+hematopoietic tumor of probable plasmacytoid monocyte derivation with weak expression of cytoplasmic CD3. 1248 12

In order to investigate the expression of CD56 on acute leukemia cells and its clinical significance, samples from 70 patients with acute leukemia were analyzed with multicolor flow cytometry to determine the CD56 and other leukocyte differentiation antigens. The results showed that 16 of 70 cases (22.86%) were identified to express CD56, of which 1/35 (2.86%) patient with acute lymphocytic leukemia (ALL) and 15/31 (48.39%) with acute myelocytic leukemia (AML) were CD56 positive. The positive rate of CD56 in AML was significantly higher than that in ALL (P < 0.01). The expression of CD56 varied in AML subtypes. The positive rate (11/15) of CD56 in AML-M(0), -M(1) and -M(2) was significantly higher than that in AML-M(3), -M(4) and -M(5) (4/16) (P = 0.013). 13 of 15 AML with CD56 expression were also positive for HLA-DR (41.94%), and a significant positive correlation was found between the expression of CD56 and HLA-DR (r = 0.439, P = 0.014). It was concluded that CD56 mainly expressed in AML cells. The analysis of CD56 expression on acute leukemia is of great value in the diagnosis, prognosis prediction and monitoring of minimal residual disease in AML patients.
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PMID:[Expression of CD56 in acute leukemia and its clinical significance]. 1251 82

The megakaryoblastic leukemia cell line MOLM-16 was established at relapse from the peripheral blood of a 77-year-old Japanese woman with minimally differentiated acute myeloid leukemia (AML-M0). Immunophenotyping of the fresh leukemic cells revealed a myeloid/NK precursor phenotype being positive for CD7, CD13, CD33, CD34, and CD56. In addition, megakaryocyte-associated antigens CD41 and CD61 were found to be positive. The established cell line designated MOLM-16 was proliferatively responsive to the treatment with various cytokines including EPO, GM-CSF, IL-3, PIXY-321, and TPO. MOLM-16 revealed characteristics of the megakaryocytic lineage in terms of immunophenotyping being positive for CD9, CD31, CD36, CD41, CD61, CD62P, CD63, CD110, CD151, thrombospondin, von Willebrand factor (vWf), and fibrinogen. Electron microscopic analysis showed positivity for ultrastructural platelet peroxidase in the nuclear envelope. The karyotype analysis of MOLM-16 revealed various numerical and structural abnormalities including t(6;8)(q21;q24.3), t(9;18)(q13;q21) and marker chromosomes. The extensive immunological, cytogenetic and functional characterization of MOLM-16 suggests that this cell line may represent a scientifically significant in vitro model which could facilitate the evaluation of megakaryocytic differentiation.
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PMID:Megakaryoblastic leukemia cell line MOLM-16 derived from minimally differentiated acute leukemia with myeloid/NK precursor phenotype. 1252 22


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