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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proliferative activity of the haematopoietic and plasma cells in bone marrow was evaluated under normal and neoplastic conditions, by means of a sequential double immunostaining technique, using monoclonal antibody MIB-1 recognizing the cell proliferation-associated nuclear antigen Ki-67, and antibodies against glycophorin-C, myeloperoxidase, factor VIII-related antigen, and immunoglobulin light chains. Fifty-eight B5 fixed, paraffin-embedded bone marrow biopsies were analysed, including 11 normal controls. 10 cases of myelodysplasia, 14 cases of chronic myeloproliferative disorder, eight cases of acute non-lymphoid leukaemia, and 15 cases of myeloma. In normal marrows, the highest proliferative activity was noticed in the erythroid cells (75% to 95%; mean 90%), in comparison with myeloid precursors (15% to 80%; mean 38%), and megakaryocytes (10% to 20%; mean 14%): no Ki-67 positive plasma cells were found. In all investigated haematological disorders, the expression of MIB-1 by erythroid cells was similar to that observed in controls. Similarly, the percentage of MIB-1 + myeloid precursors in chronic myeloproliferative disorders and myelodysplasia largely overlapped the values observed in normals, and comparable values were also found in the blast cells from acute non-lymphoid leukaemia type M1 and M2. These findings suggest that the evaluation of either erythroid or myeloid proliferative activity is of little value in the differential diagnosis between these myeloproliferative disorders. By contrast, the obvious increase of Ki-67 expression of megakaryocytes in chronic myeloproliferative disorders, with labelling also of micro-megakaryocytes, might sustain the diagnosis in controversial cases. Since cases of mature myeloma showed less than 2% of Ki-67 positive cells, evaluation of proliferative activity is of no value in the differential diagnosis with reactive plasmacytosis. The sequential double immunophenotyping for Ki-67 antigen and for haematopoietic cell lineage-associated markers can be applied in a consistent manner to routine bone marrow biopsies to evaluate proliferating cells in normal and neoplastic conditions.
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PMID:Assessment of cell proliferation in normal and pathological bone marrow biopsies: a study using double sequential immunophenotyping on paraffin sections. 857 29

A 48-year-old Japanese man was admitted to our hospital because of general fatigue, nasal bleeding, and petechiae on his extremities. He was diagnosed with acute myelomonocytic leukemia with trilineage myelodysplasia (T-MDS). Chromosomal analysis of bone marrow cells revealed t(7;11)(p15;p15), which has been rarely reported but known to be characteristic of Japanese patients. Although t(7;11)(p15;p15) has been reported mainly in acute myelogenous leukemia (AML), it can be occasionally found in so-called stem cell diseases such as chronic myelogenous leukemia or chronic myeloproliferative disorders. Therefore, t(7;11)(p15;p15) might affect trilineage progenitors or stem cells as well as myeloid lineage cells, subsequently resulting in AML with T-MDS, as in our case reported here.
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PMID:t(7;11) and trilineage myelodysplasia in acute myelomonocytic leukemia. 861 92

The LH2 gene encodes a putative transcription factor containing two N-terminal LIM and one C-terminal HOX domains. The LH2 locus was mapped to 9q33-34.1, centromeric to the ABL gene. In a recent report, it was suggested that high levels of LH2 expression are consistently observed in chronic myeloid leukemia (CML) patients, whereas no transcription is detected in normal individuals. This led to the hypothesis that aberrant expression of LH2 may represent an additional mechanism for malignant cell proliferation in CML. We have studied the expression of LH2 in leucocytes from patients with CML or with other chronic myeloproliferative disorders (CMD), and from normal individuals, using an optimised reverse-transcription and polymerase chain reaction (PCR) technique. Twenty-seven out of 29 cDNA samples from normal individuals (93%), 49 out of 51 samples from CML patients (96%) and 20 out of 20 from Philadelphia chromosome-negative CMD showed evidence of LH2 expression. Similarly, LH2 transcription was also detected in leucocytes from CML patients in complete cytogenetic remission after treatment with interferon-alpha. Furthermore, all 36 EBV-induced lymphoblastoid cell lines established from six chronic phase CML patients showed unequivocal LH2 expression, regardless of the BCR-ABL status of the line (9 BCR-ABL positive, 27 BCR-ABL negative). We conclude that LH2 expression is not confined to CML cells, and that the t(9;22)(q34;qll) does not promote 'de novo' transcriptional activation of this gene.
Leukemia 1996 Jul
PMID:Expression of the LH2 gene in chronic myeloid leukaemia cells. 868 90

Systemic mast cell disease (SMCD) can be regarded as a tumorous proliferation of tissue mast cells involving various organs. The frequency with which SMCD is found in patients with haematological disorders suggests that the association is non-random. The association includes primarily, myeloid disorders such as myelodysplastic syndromes and acute or chronic myeloproliferative disorders. Lymphoproliferative disorders may also occur but more rarely, mostly non-Hodgkin's low grade B cell lymphomas. In this report a case is described in which SMCD occurred in a patient with hairy cell leukaemia.
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PMID:Systemic mast cell disease associated with hairy cell leukaemia. 925 Aug 32

Cytogenetic aberrations resulting in deletion of 3p are common in solid tumors, indicating the presence of tumor suppressor genes (TSG) on this chromosome arm. The present study was undertaken to investigate 3p loss in hematologic disorders. Ten acute myeloid leukemias (AML), two myelodysplastic syndromes (MDS), one Philadelphia chromosome-positive chronic myeloid leukemia (CML), three acute lymphoblastic leukemias (ALL), one chronic lymphoproliferative disorder (CLD), and three non-Hodgkin's lymphomas (NHL) with abnormalities leading to 3p deletions were identified, constituting 2.9% of AML, 0.7% of MDS, 1.0% of CML with changes in addition to t(9;22), 1.5% of ALL, 4.2% of CLD, and 1.1% of NHL with cytogenetic abnormalities analyzed at our Department. Among 19042 karyotypically aberrant published cases, 1.2% of 6260 AML, 1.3% of 2285 MDS, 0.8% of 840 chronic myeloproliferative disorders (CMD), 0.7% of 1894 CML with additional aberrations to t(9;22), 0.6% of 3589 ALL 2.4% of 1602 CLD, 4.5% of 178 Hodgkin disease (HD), and 3.1% of 2394 NHL displayed partial loss of 3p (0.6-4.5%; P < 0.001); the majority occurring together with other abnormalities. The frequencies of 3p loss did not differ significantly among the MDS, ALL, and CLD morphologic subgroups, between B and T cell ALL, CLD, and NHL, among low-, intermediate-, and high-grade NHL, or between therapy-related MDS and de novo MDS, whereas the incidence of 3p deletions was higher in treatment-associated AML (P < 0.001) than in de novo AML and varied among the AML FAB groups (P < 0.001). The most frequently deleted chromosome bands were 3p25 in AML, 3p26 in MDS, 3p14 in CMD, 3p25, 3p23, and 3p21 in CML, 3p26 and 3p25 in ALL, 3p26 and 3p25 in CLD, 3p26 in HD, and 3p26 in NHL. These deletion hot spots are more distal than those reported in most solid tumor types, suggesting that different TSG are involved in hematologic malignancies and solid neoplasms.
Leukemia 1997 Aug
PMID:Deletion of chromosome arm 3p in hematologic malignancies. 926 71

Essential thrombocythemia (ET) and polycythemia vera (PV) are chronic clonal myeloid disorders that originate from the multipotential hematopoietic stem cell. They are characterized, respectively, by excessive thrombocytosis and erythrocytosis, a high incidence of thrombohemorrhagic events, vasomotor symptoms, and an inherent tendency to undergo leukemic transformation. Current standard therapies to control the excess accumulation of myeloid cells and to provide symptomatic relief carry either a persistent risk of thrombosis, as in the case of phlebotomy, or, in the case of hydroxyurea, the potential for inducing leukemia. None alter the natural history of these diseases. Interferon-alpha has been shown to have potent antiproliferative effects on the hematopoietic stem cells and bone marrow fibroblasts and, as a result, has received much attention as a therapeutic agent for chronic myeloproliferative disorders. The ability of interferon-alpha to induce hematologic and cytogenetic remission in chronic phase chronic granulocytic leukemia has further increased interest in this agent. Interferon-alpha has shown therapeutic activity in PV and ET, as demonstrated in multiple small studies and single-arm trials reviewed in this article. Reported beneficial effects include the ability to control excessive erythrocytosis and thrombocytosis and such disease-related features as vasomotor symptoms, pruritus, and splenomegaly. Recent reports of cytogenetic remission and reversal of bone marrow fibrosis after interferon therapy are of interest. Advantages over current therapeutic standards include lack of known leukemogenic and teratogenic effects and the potential to alter the underlying course of disease. Nevertheless, none of the information available allows definite therapeutic recommendations for the use of interferon-alpha in PV or ET. The available data support the need for randomized controlled trials comparing interferon-alpha with standard therapy.
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PMID:Interferon-alpha therapy in polycythemia vera and essential thrombocythemia. 938 5

A retrospective investigation of 75 EDTA-decalcified Jamshidi biopsies collected over a 2-year period at Aarhus University Hospital was performed. The biopsies originated from 75 patients suffering from idiopathic myelofibrosis, other chronic myeloproliferative disorders, or other conditions with known associations with bone marrow fibrosis. The relative volumes of trabecular and woven bone, as well as haematopoietic and non-haematopoietic tissue, were estimated histomorphometrically. The degree of fibrosis was estimated semiquantitatively. Finally, the thickness of trabecular osteons was estimated from the number of lamellae by counting. Patients with idiopathic myelofibrosis had statistically significantly more bone tissue than the other groups of patients. The osteosclerosis was primarily due to woven bone. Larger cancellous osteons also suggested a positive balance in bone remodelling. The amount of bone tissue showed furthermore a statistically significant increase through the groups of polycythaemia vera, essential thrombocythaemia, chronic myelogenous leukaemia and idiopathic myelofibrosis. Parallel to the increase in the amount of bone, an increase in the degree of marrow fibrosis was detected. The positive correlation between the amount of bone and the degree of marrow fibrosis was statistically highly significant (p=0.0008).
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PMID:A histomorphometric study of haematological disorders with respect to marrow fibrosis and osteosclerosis. 963 73

Using a multiparameter flow cytometry assay enumerating cells positive for CD13, CD14 and CD66 antigens, we determined the asynchronous CD14/CD66 co-expression in unselected bone marrow and peripheral blood samples with suspected malignant blood disorders. CD14/CD66 co-expression > or = 5% were found in 131/691 bone marrow samples. Only 55 of these exhibited an identifiable population in 2-parameter flow cytometry histograms. Of the 55 samples 43 (78%) came from patients with myeloid disorders; e.g. 11 with myelodysplastic syndromes, 15 with chronic myeloproliferative disorders and 17 with acute myeloid leukaemia. Only one of these 17 cases was a de novo case, while 8 were secondary to another malignant haematological disease and 8 were from the period after cytoreductive therapy. Notably, CD14/CD66 co-expression patterns were related to disease categories; e.g. in chronic myelomonocytic leukaemia and acute myeloid leukaemia following a dysplastic phase the co-expression displayed two subsets in peripheral blood, low-avidity CD14 and low-avidity CD66, respectively. The latter disease category also exhibited these 2 subsets in bone marrow. In all other cases, the CD14/CD66 co-expression in bone marrow was heterogeneous. In conclusion, abnormal CD14/CD66 co-expression might be a valuable parameter in defining asynchronous myelopoiesis in malignant myeloid disorders, especially myeloproliferative disorders and secondary acute myeloid leukemias.
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PMID:Flow cytometric identification of myeloid disorders by asynchronous expression of the CD14 and CD66 antigens. 985 50

Flt-3 ligand (FL) is a growth factor (GF) which might have clinical use as a mobilizer of stem and progenitor cells into peripheral blood (PB) in autologous transplantations of various malignant haematological diseases, unless FL stimulates the growth of malignant cells in these diseases. The present study evaluated the effects of FL on the proliferation of granulocytemacrophage (GM) progenitor cells collected from PB of 24 patients with chronic myeloproliferative disorders (MPDs) by using a methylcellulose assay in serum-free culture conditions. It was shown that FL as a single factor had no stimulatory effect on GM colony formation either in the whole MPD group or in the MPD subgroups, which comprised 9 patients with essential thrombocythaemia, 7 with polycythaemia vera and 8 with chronic myelogenous leukaemia. No increase in GM colony formation was observed, either, when FL was used in combination with other GFs, such as mast cell growth factor (MGF), granulocyte-colony stimulating factor (G-CSF), GM-CSF or interleukin-3 (IL-3). GM-CSF and IL-3 were the only single GFs which significantly increased GM colony formation in the whole MPD group. As a conclusion, FL does not seem to induce GM colony formation of MPDs alone or in combination with G-CSF in in vitro colony assays.
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PMID:Flt-3 ligand does not induce the growth of peripheral blood granulocyte-macrophage colony-forming cells in myeloproliferative disorders. 1005 13

The effects of thrombopoietin (TPO) on cell proliferation and differentiation, and the relation between these effects and the expression of c-mpl on leukemia cells were studied in seven acute myelogeneous leukemia cell lines and seven myelogeneous blast cell preparations from patients with chronic myeloproliferative disorders (CMPDs) and myelodysplastic syndrome (MDS). Among the leukemia cells, five preparations of megakaryoblastic leukemia cells from patients and one megakaryoblastic cell line, CMK 11.5, proliferated in response to TPO in vitro. CMK 11.5 and the blastic cells from one patient diagnosed with MDS with myelofibrosis differentiated with increasing expression of CD41a in response to TPO. However, TPO had no effect on the cells lacking megakaryocytic characteristics. Some patients with CMPD and MDS develop acute transformation with blasts demonstrating megakaryocytic features, and some of these cells show growth in response to TPO. Therefore, in vivo administration of TPO should be considered carefully for patients with CMPD or MDS, since TPO may induce leukemic cell proliferation.
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PMID:Thrombopoietin activates the growth of megakaryoblasts in patients with chronic myeloproliferative disorders and myelodysplastic syndrome. 1077 93


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