Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old man was diagnosed as having chronic myelogenous leukemia (CML) in chronic phase in Dec. 1985. In Dec. 1987, anemia and leukocytopenia progressed, and the percentage of blast cells increased in the bone marrow. The blast cells were lymphoblastoid and positive for TdT. It was treated as a lymphoid crisis with vincristine and prednisolone, and complete remission was achieved. However, the blasts (11%) were observed in the bone marrow in Mar. 1988, and the chromosomal analysis revealed 46, XY, t (2q-; 11q+), t (9q+; 22q-) in 13 out of 20 cells. In June, the percentage of the blasts increased again, but chromosomal analysis showed a different karyotype, 46, XY, t(2p-; 11p+), t(9q+; 22q-) which was observed in 9 out of 10 cells. Then, myeloblastoid cells increased rapidly in spite of the chemotherapy in Dec. 1988. The chromosomal analysis showed 46, XY, 2p-, 7q-, 9q+, 11p+, 22q- in all analyzed cells. The rearrangement of the bcr gene could be detected by the Southern blotting. The blasts were positive for CD7, CD11, CD13, CD33, CD36, CD41 and CD42, suggesting that the blasts had the surface phenotypes of both myeloid and megakaryocytoid-lineage. This is a case with the mixed blast crisis that changed from the lymphoid to the myelo-megakaryocytoid in nature, in which three clonal evolutions were observed during the clinical course.
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PMID:[Mixed blast crisis with the cytogenetic evidence of three clonal evolutions]. 236 40

A 46-year-old man with Werner's syndrome was admitted with epigastralgia and body weight loss. The peripheral blood findings showed anemia, thrombocytosis and eosinophilia. Bone marrow aspiration and biopsy revealed increases in eosinophils and megakaryocytes, myelodysplastic change with 6.6% myeloblast, and myelofibrosis. Chromosomal analysis revealed 46, XY, +der(1;7), -7, del(20). He was diagnosed as having myelodysplastic syndrome with myelofibrosis or essential thrombocythemia. Three months later, pancytopenia appeared with a relative increase of blasts positive for CD41 and negative for myeloperoxidase. He died of respiratory failure due to pneumonia. An autopsy revealed severe myelofibrosis with proliferation of megakaryocytes and blasts. A final diagnosis of acute megakaryoblastic leukemia was made. Werner's syndrome is rare, and it is even more unusual to have the complication of acute leukemia with der (1;7) seen in this case.
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PMID:[Werner's syndrome developing acute megakaryoblastic leukemia with der(1;7)]. 902 58

We report a case of infant leukemia with the proliferation of both erythroblast and megakaryoblast lineages. The blasts became double-positive for both erythroblastic and megakaryoblastic surface markers at the time of bone marrow relapse. A 9-month-old girl was admitted to our hospital presenting chiefly poor with weight gain and anemia. She also had splenomegaly, pleural effusion, leukocytosis, and thrombocytopenia. A bone marrow specimen showed 53.2% erythroblasts (PAS positive, alpha-NA positive, CD41 negative, MPO negative) and 20.4% megakaryoblasts with marked cytoplasmic blebs. We examined specimens by two-color flow cytometric analysis. At the onset, CD41+ glycophorin A- fraction and CD41- glycophorin A+ fraction were two major components. At the bone marrow relapse, the majority of blasts had altered to double-positive. Chromosomal analysis showed t (1; 22) (p13; q13), which has been reported to be specific for acute megakaryoblastic leukemia (M7) in infants. We reasoned that a leukemia had occurred in this patient at a progenitor cell level common to both erythroid and megakaryocytic lineages.
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PMID:[Infant leukemia with t(1;22) presenting proliferation of erythroid and megakaryocytic cell lineages]. 1022 31

Cytologic, immunologic, and cytogenetic studies were performed on the blast cells of a newborn with Down syndrome and transient myeloproliferative disease. This hematologic disorder is uncommon, and occurs primarily in infants with Down syndrome. This boy presented with a high white blood cell count and a high percentage of blast cells, without anemia or thrombocytopenia. Chromosome analysis showed a constitutional trisomy 21 without any other clonal abnormality. A three-color flow cytometric analysis was performed and revealed two different CD45 dim, CD34(+), CD117(+), CD56(+) immature subpopulations: the normal immature myeloid precursor and an immature blast cell population that expressed CD41, CD42, CD61, CD36, CD13, CD1a, and CD2. We postulate that this population could be the leukemic precursor involved in the acute megakaryoblastic leukemia frequently observed in children with Down syndrome.
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PMID:Immunophenotype of a transient myeloproliferative disorder in a newborn with trisomy 21. 1079 50

A 43-yr-old Japanese woman presented with mild anemia, leukocytosis and splenomegaly in May 1984. Splenomegaly and anemia gradually progressed. Sixteen years later, in October 2000, she developed inguinal lymphadenopathy. Biopsy of the lymph node revealed infiltration of blasts, megakaryocytes, fibroblasts and myeloid cells. Large blasts with basophilic cytoplasm with cytoplasmic projections appeared in the peripheral blood. These blasts were negative in peroxidase stain, positive in acid phosphatase and weakly positive in periodic acid-Schiff stain. Immunohistochemical staining with monoclonal antibodies revealed that these blasts were positive with anti-CD41 (glycoprotein IIb/IIIa) and negative with other monoclonal antibodies. So diagnosis of granulocytic sarcoma in megakaryoblastic transformation from chronic idiopathic myelofibrosis was made. A cytogenetic study revealed that bone marrow cells were 46,XX del(13)(q?) initially and additional abnormalities including der(5,5,11)(q11;q13)ins(5;?)(q11;?) were found when she developed megakaryoblastic transformation. Granulocytic sarcoma of megakaryoblastic transformation from chronic idiopathic myelofibrosis is a rare event. Immunophenotyping with monoclonal antibody for CD41(glycoprotein IIb/IIIa) confirmed the diagnosis.
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PMID:Granulocytic sarcoma of megakaryoblastic differentiation in the lymph nodes terminating as acute megakaryoblastic leukemia in a case of chronic idiopathic myelofibrosis persisting for 16 years. 1173 54

A 64-yr-old Japanese man presented with mild anemia, leukocytosis, and thrombocytosis in November 1999. A diagnosis of chronic myeloid leukemia was made with a positive Ph chromosome, and interferon alpha treatment was started, 6 million units a day. Two years later, in October 2001, the patient developed leukocytosis, an increased LDH level, and large blasts with basophilic cytoplasm with cytoplasmic projections appeared in the peripheral blood. Bone marrow aspiration revealed increased blasts (59.6%). These blasts were negative on peroxidase stain, positive on acid phosphatase, and weakly positive on alpha naphthyl butyrate esterase stain and periodic acid-Schiff stain. Immunohistochemical staining with monoclonal antibodies revealed that these blasts were strongly positive with anti-CD41 (glycoprotein IIb/IIIa), weakly positive with CD7, CD33, and CD34, and negative with other monoclonal antibodies. A diagnosis of megakaryoblastic transformation from chronic myeloid leukemia was therefore made. Two-color fluorescence in situ hybridization (FISH) for portions of the major-bcr and abl genes from bone marrow cells revealed two fused signals in 90.6% and one fused signal in 5.8% of 106 cells. A cytogenetic study revealed that bone marrow cells were 69, XYY, +6, -7, +8, -9, t(9;22)(q34;q11), +11, +13, -15, -16, dic(17;18)(p11;p11), -18, +19, +21, der(22)t(9;22) in six of nine examined cells. These findings confirmed that these megakaryoblasts originated from megakaryocytes of the chronic myeloid leukemia clone.
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PMID:Double Ph-positive megakaryoblastic transformation of chronic myeloid leukemia. 1236 19

The erythrocyte colony-forming unit (CFU-E) is a rare bone marrow (BM) progenitor that generates erythrocyte colonies in 48 hours. The existence of CFU-Es is based on these colonies, but CFU-Es have not been purified prospectively by phenotype. We have separated the "nonstem," "nonlymphoid" compartment (lineage marker [lin]-c-Kit+Sca-1-IL-7Ralpha-) into interleukin 3 receptor alpha negative (IL-3Ralpha-) and IL-3Ralpha+ subsets. Within IL-3Ralpha- but not IL-3Ralpha+ cells we have identified TER119-CD41-CD71+ erythrocyte-committed progenitors (EPs). EPs generate CFU-E colonies at about 70% efficiency and generate reticulocytes in vivo. Depletion of EPs from BM strongly reduces CFU-E frequencies. EPs lack potential for erythrocyte burst-forming unit, megakaryocyte, granulocyte (G), and monocyte (M) colonies, and for spleen colony-forming units. Chronically suppressed erythropoiesis in interferon consensus sequence-binding protein (ICSBP)-deficient BM is associated with reduced frequencies of both the EP population and CFU-E colonies. During phenylhydrazine-induced acute anemia, numbers of both the EP population and CFU-E colonies increase. Collectively, EPs (lin-c-Kit+Sca-1-IL-7Ralpha-IL-3Ralpha-CD41-CD71+) account for most, if not all, CFU-E activity in BM. As a first molecular characterization, we have compared global gene expression in EPs and nonerythroid GM progenitors. These analyses define an erythroid progenitor-specific gene expression pattern. The prospective isolation of EPs is an important step to analyze physiologic and pathologic erythropoiesis.
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PMID:Prospective isolation and global gene expression analysis of the erythrocyte colony-forming unit (CFU-E). 1552 51

The aim of this study was to investigate the clinical, pathological and biological features of acute megakaryoblastic leukemia in childhood. The morphology of cells was observed by means of bone marrow smear; the immunophenotype was detected by flow cytometry and immunohistochemistry assay. The results indicated that the fever, hemorrhage, hepatosplenomegaly and lymphadenopathy in this case were the primary presentations accompanying by leukocytosis, anemia and thrombocytopenia. An adequate marrow aspirate could not be obtained. At the time of diagnosis, the bone marrow had more than 30% megakaryoblasts in nucleated cells. Flow cytometric analysis revealed the dual expression of CD41 and CD61 by tumor cells in bone marrow. The histopathological examination of bone marrow demonstrated infiltration of large-sized CD42b(+) cells. According to all above mentioned results, this case was diagnosed as acute megakaryoblastic leukemia. In conclusion, childhood acute megakaryoblastic leukemia is a rare and easily misdiagnosed disease with poor prognosis. Flow cytometry analysis and immunohistochemistry assay of bone marrow can help in detecting this leukemia subtype and evaluating its prognosis.
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PMID:[Childhood acute megakaryoblastic leukemia]. 1760 59

A clinically normal, 5-year-old intact female German Shepherd dog was presented to the local veterinarian to be spayed. Results of a preoperative CBC included mild nonregenerative anemia, severe thrombocytopenia, and 17% unclassified cells. On cytologic examination of aspirates from the dog's enlarged spleen and peripheral lymph nodes, a population of primitive round cells that occasionally resembled megakaryocytes was observed. A bone marrow aspirate specimen was markedly hypercellular with approximately 65% of marrow cells comprising a homogeneous population of immature hematopoietic cells similar to those found in the spleen, lymph nodes, and peripheral blood. Using immunocytochemical stains with canine-specific antibodies, all neoplastic cells strongly expressed cytoplasmic CD41 and 20-70% of the neoplastic cells expressed CD34 weakly to moderately. Rare (<0.5%) neoplastic cells weakly expressed vWF. The cells were negative for all other markers. Based on these results and the morphology of the neoplastic cells, a diagnosis of acute megakaryoblastic leukemia (AMegL) was made. In spite of treatment, results of a CBC performed 1 week later indicated progressive anemia and thrombocytopenia, and the dog was euthanized. To our knowledge, this report documents the first case of canine AMegL diagnosed with both anti-canine CD34 and CD41 antibodies.
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PMID:CD34+, CD41+ acute megakaryoblastic leukemia in a dog. 1780 80

An 11-year-old spayed-female German Shepherd dog was presented to the Veterinary Medical Teaching Hospital at Kansas State University with a history of weight loss, anorexia, depression, and lethargy for 2-3 weeks. Radiographic examination revealed a mass in the spleen and several round radiodense foci in the liver. CBC results included normocytic normochromic anemia, marked thrombocytopenia, and low numbers of neoplastic cells that frequently had cytoplasmic projections or blebs. A bone marrow aspirate contained about 80% neoplastic megakaryoblasts with the same microscopic features as those observed in peripheral blood. Using flow cytometry, cells of large size were identified in peripheral blood that expressed CD41/61, CD45, CD61, and CD62P (P-selectin) and were negative for markers of T cells, B cells, monocyte/macrophages, and dendritic cells. Because of the poor prognosis, euthanasia and subsequently necropsy were performed. On histopathologic examination, neoplastic megakaryoblasts were identified in spleen, liver, mesenteric lymph node, and the pulmonary vasculature. Using immunohistochemistry, the neoplastic megakaryoblasts weakly expressed von Willebrand factor. Based on microscopic and immunophenotypic findings, a diagnosis of acute megakaryoblastic leukemia (AMegL) was made. To our knowledge, this is the first report of AMegL in a domestic animal in which immunophenotyping by flow cytometry and a panel of antibodies against CD41/61, CD61, and CD62P were used to support the diagnosis.
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PMID:Acute megakaryoblastic leukemia in a German Shepherd dog. 1979 30


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