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1. Bernard F, Thomas C, Emile JF, Hercus T, Cassinat B, Chomienne C, Donadieu J: Transient hematologic and clinical effect of E21R in a child with end-stage juvenile myelomonocytic leukemia. Blood; 2002 Apr 1;99(7):2615-6
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  • [Title] Transient hematologic and clinical effect of E21R in a child with end-stage juvenile myelomonocytic leukemia.
  • Juvenile chronic myelomonocytic leukemia (JMML) is a rare leukemia where spontaneous proliferation of myeloid and monocytic precursors in patients' bone marrow cultures is dependent on GM-CSF.
  • For patients who progress after systemic chemotherapy, there are no effective therapies.
  • E21R was well-tolerated during the 3 courses of subcutaneous treatment.
  • This novel therapeutic approach clearly deserves further evaluation in JMML.
  • [MeSH-major] Granulocyte-Macrophage Colony-Stimulating Factor / genetics. Leukemia, Myelomonocytic, Acute / genetics
  • [MeSH-minor] Amino Acid Substitution. Arginine. Child. Drug Monitoring. Glutamic Acid. Humans. Male. Mutation, Missense. Treatment Outcome

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  • (PMID = 11895804.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3KX376GY7L / Glutamic Acid; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 94ZLA3W45F / Arginine
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2. Chen YC, Chou JM, Letendre L, Li CY: Clinical importance of bone marrow monocytic nodules in patients with myelodysplasia: retrospective analysis of 21 cases. Am J Hematol; 2005 Aug;79(4):329-31
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  • [Title] Clinical importance of bone marrow monocytic nodules in patients with myelodysplasia: retrospective analysis of 21 cases.
  • Bone marrow monocytic nodules (MNs) can occur in various myeloid disorders.
  • Eight patients had chronic myelomonocytic leukemia (CMML); 4 had acute myeloid leukemia (AML); and 9 had myelodysplastic/myeloproliferative diseases.
  • MNs appeared to persist even after aggressive chemotherapy, including conventional chemotherapy for 2 AML patients and high-dose chemotherapy preceding allogeneic bone marrow transplantation for 1 CMML patient.
  • Our findings demonstrate that MNs are associated with CMML, AML, myelodysplastic syndromes, and myeloproliferative diseases and suggest that MNs are resistant to intensive chemotherapy and patients with bone marrow MNs have a poor prognosis.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Acute / pathology. Leukemia, Myelomonocytic, Chronic / pathology. Myelodysplastic Syndromes / pathology. Myeloproliferative Disorders / pathology

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16044436.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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3. Soliera AR, Lidonnici MR, Ferrari-Amorotti G, Prisco M, Zhang Y, Martinez RV, Donato NJ, Calabretta B: Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells. Blood; 2008 Sep 1;112(5):1942-50
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  • Upon C/EBPalpha activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cells but only c-Myb levels decreased slightly in CD34(+) normal progenitors.
  • Ectopic c-Myb expression blocked the proliferation inhibition- and differentiation-inducing effects of C/EBPalpha, whereas c-Myb siRNA treatment enhanced C/EBPalpha-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation.
  • Ectopic GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPalpha but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPalpha induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPalpha activation.

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  • (PMID = 18550858.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / P01 78890; United States / PHS HHS / / R01 95111
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / DNA Primers; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / RNA, Small Interfering; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2518896
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4. Menillo SA, Goldberg SL, McKiernan P, Pecora AL: Intraoral psoralen ultraviolet A irradiation (PUVA) treatment of refractory oral chronic graft-versus-host disease following allogeneic stem cell transplantation. Bone Marrow Transplant; 2001 Oct;28(8):807-8
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  • [Title] Intraoral psoralen ultraviolet A irradiation (PUVA) treatment of refractory oral chronic graft-versus-host disease following allogeneic stem cell transplantation.
  • [MeSH-major] Graft vs Host Disease / drug therapy. Hematopoietic Stem Cell Transplantation / adverse effects. Mycophenolic Acid / analogs & derivatives. Oral Ulcer / drug therapy. PUVA Therapy. Transplantation, Homologous / adverse effects
  • [MeSH-minor] Adult. Drug Therapy, Combination. Humans. Hyperbilirubinemia / etiology. Immunosuppressive Agents / therapeutic use. Infection Control. Leukemia, Monocytic, Acute / therapy. Male. Prednisone / therapeutic use. Tacrolimus / therapeutic use. Xerostomia / drug therapy. Xerostomia / etiology

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  • (PMID = 11781637.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; VB0R961HZT / Prednisone; WM0HAQ4WNM / Tacrolimus
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5. Hasegawa Y, Bai A, Kojima H, Komeno T, Ninomiya H, Nagasawa T: Priming effects of macrophage colony-stimulating factor on monocytic leukemia cells in combination with chemotherapy: induction of programmed cell death in vivo. Leuk Lymphoma; 2000 Feb;36(5-6):589-93

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  • [Title] Priming effects of macrophage colony-stimulating factor on monocytic leukemia cells in combination with chemotherapy: induction of programmed cell death in vivo.
  • Two elderly patients with chronic myelomonocytic leukemia were treated with cytosine arabinoside (Ara-C) and aclarubicin (ACR) under simultaneous administrations of macrophage colony-stimulating factor (M-CSF) (CAM), and both obtained good responses.
  • Examination of apoptosis using flow cytometry revealed induction of apoptotic death of leukemia cells by CAM in Patient 2, while neither induction of apoptotic death of leukemia cells nor clinical response were seen with CAG (Ara-C, ACR, and granulocyte colony-stimulating factor) given prior to CAM in Patient 1.
  • These findings suggested that chemotherapy combined with simultaneous administration of M-CSF could effectively reduce monocytic leukemia cells by inducing programmed cell death.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Apoptosis / drug effects. Leukemia, Myelomonocytic, Chronic / drug therapy. Leukemia, Myelomonocytic, Chronic / pathology. Macrophage Colony-Stimulating Factor / administration & dosage

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  • (PMID = 10784404.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 81627-83-0 / Macrophage Colony-Stimulating Factor
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6. Corazza F, Hermans C, Ferster A, Fondu P, Demulder A, Sariban E: Bone marrow stroma damage induced by chemotherapy for acute lymphoblastic leukemia in children. Pediatr Res; 2004 Jan;55(1):152-8
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  • [Title] Bone marrow stroma damage induced by chemotherapy for acute lymphoblastic leukemia in children.
  • Several studies have suggested a role of bone marrow stroma injury in long-term chemotherapy-induced hematopoietic failure.
  • To evaluate whether bone marrow microenvironment is altered by chemotherapy for acute lymphoblastic leukemia (ALL) and to determine its contribution to postchemotherapy anemia, we investigated the ability of stroma from children receiving maintenance chemotherapy for ALL to support hematopoiesis.
  • Long-term bone marrow cultures (LTBMC) were established with bone marrow cells either from ALL children under therapy (n = 24) or from control subjects (n = 19).
  • Nonadherent cells and colony forming units-granulocytic monocytic (CFU-GM) output in LTBMC did not differ between patients and controls.
  • Thus, chemotherapy for ALL induces functional deregulation within bone marrow stromal cells with an increase in the growth-inhibiting factor TGF-beta1, together with a decrease in MIP-1alpha, which might contribute to hematopoietic toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Cells / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Stromal Cells / drug effects
  • [MeSH-minor] 6-Mercaptopurine / adverse effects. Antibodies / pharmacology. Antigens, CD34 / metabolism. Antimetabolites, Antineoplastic / adverse effects. Cells, Cultured. Chemokine CCL3. Chemokine CCL4. Child. Chronic Disease. Coculture Techniques. Cytokines / immunology. Erythroid Precursor Cells / drug effects. Erythroid Precursor Cells / metabolism. Erythroid Precursor Cells / pathology. Humans. Macrophage Inflammatory Proteins / immunology. Methotrexate / adverse effects. Myeloid Progenitor Cells / drug effects. Myeloid Progenitor Cells / metabolism. Myeloid Progenitor Cells / pathology. Transforming Growth Factor beta / immunology. Transforming Growth Factor beta1

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  • (PMID = 14561785.001).
  • [ISSN] 0031-3998
  • [Journal-full-title] Pediatric research
  • [ISO-abbreviation] Pediatr. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD34; 0 / Antimetabolites, Antineoplastic; 0 / Chemokine CCL3; 0 / Chemokine CCL4; 0 / Cytokines; 0 / Macrophage Inflammatory Proteins; 0 / TGFB1 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate
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7. Bennett CL, Evens AM, Andritsos LA, Balasubramanian L, Mai M, Fisher MJ, Kuzel TM, Angelotta C, McKoy JM, Vose JM, Bierman PJ, Kuter DJ, Trifilio SM, Devine SM, Tallman MS: Haematological malignancies developing in previously healthy individuals who received haematopoietic growth factors: report from the Research on Adverse Drug Events and Reports (RADAR) project. Br J Haematol; 2006 Dec;135(5):642-50
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  • [Title] Haematological malignancies developing in previously healthy individuals who received haematopoietic growth factors: report from the Research on Adverse Drug Events and Reports (RADAR) project.
  • We reviewed the findings for healthy volunteers/donors who developed haematological malignancies following PEG-rHuMGDF or G-CSF administration.
  • Mantle cell, diffuse large B-cell lymphoma and chronic lymphocytic leukaemia were diagnosed 1-5 years after PEG-rHuMGDF exposure among three volunteers.
  • For one patient, thrombocytopenia due to autoantibodies to PEG-rHuMGDF developed shortly after PEG-rHuMGDF administration and persisted until chemotherapy was administered.
  • Acute myeloid leukaemia was diagnosed 4 and 5 years after G-CSF mobilisation in two donors who underwent peripheral blood stem cell donation for sibling allogeneic haematopoietic stem cell transplantation.
  • Following intensive chemotherapy, one died from acute leukaemia and the second is in complete remission.
  • [MeSH-major] Hematologic Neoplasms / etiology. Hematopoietic Cell Growth Factors / adverse effects. Tissue Donors
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autoantibodies / immunology. Clinical Trials as Topic. Female. Granulocyte Colony-Stimulating Factor / adverse effects. Humans. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / etiology. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / etiology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / etiology. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Polyethylene Glycols / adverse effects. Recombinant Proteins / adverse effects. Thrombopoietin / adverse effects. Thrombopoietin / immunology

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  • [CommentIn] Br J Haematol. 2007 Apr;137(1):77-8; author reply 79-80 [17359373.001]
  • [CommentIn] Br J Haematol. 2007 Apr;137(1):78-9; author reply 79-80 [17359374.001]
  • [CommentIn] Br J Haematol. 2006 Dec;135(5):651-2 [17054429.001]
  • (PMID = 17054431.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA 102713-01; United States / NCI NIH HHS / CA / K23 CA109613-A1; United States / NCI NIH HHS / CA / P 30 CA60553
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Hematopoietic Cell Growth Factors; 0 / Recombinant Proteins; 0 / polyethylene glycol-recombinant human megakaryocyte growth and development factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 30IQX730WE / Polyethylene Glycols; 9014-42-0 / Thrombopoietin
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8. Sunnaram BL, Gandemer V, Sebillot M, Grandgirard N, Amiot L, Leray E, Goasguen JE: LRP overexpression in monocytic lineage. Leuk Res; 2003 Aug;27(8):755-9
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  • [Title] LRP overexpression in monocytic lineage.
  • The failure to chemotherapy is a multi factorial phenomenon and lung resistance protein (LRP) overexpression has already been discussed as implicated in drug resistance.
  • In 1996, we studied the expression of LRP and P170 (MDR) in a series of leukemias, at the time of diagnosis, by immunocytochemical (ICC) method.
  • The observation of a strong and unusual expression of LRP in acute myeloid leukemia (AML) with monocytic component led us to test (for P170 and LRP) a new series of 47 AML with different FAB subtypes.
  • We demonstrate that LRP is not correlated with clinical outcome but is statistically related to monoblastic leukemias.
  • Code 5 reaction was found in 10/13 M5 versus the other FAB subtypes (P<10(-3)).
  • The strongest LRP overexpression was also found in chronic myelomonocytic leukemia (four cases), reactive monocytosis (three cases) and in a dendritic cell line.
  • In conclusion, we report that LRP is rather a marker of monocytic lineage than a prognostic index for MDR and we suggest that detection of LRP by ICC could be an argument for the diagnosis of monoblastic and monocytic leukemias.
  • [MeSH-major] Leukemia, Myeloid / pathology. Monocytes / chemistry. Neoplasm Proteins / analysis

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  • (PMID = 12801535.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / p-170 glycoprotein, human
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9. Vural F, Ozcan MA, Ozsan GH, Demirkan F, Piskin O, Ates H, Kargi A, Undar B: Gingival involvement in a patient with CD56+ chronic myelomonocytic leukemia. Leuk Lymphoma; 2004 Feb;45(2):415-8
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  • [Title] Gingival involvement in a patient with CD56+ chronic myelomonocytic leukemia.
  • Leukemic infiltration of the gingiva is most commonly reported to be associated with monocytic subtypes of acute myeloblastic leukemia (AML) but rarely with myelodysplastic syndromes (MDS).
  • Here we report a case of CD56+ chronic myelomonocytic leukemia (CMML) who developed gingival involvement simultaneously when the leukocyte count elevated.
  • At that time no increase in peripheral or bone marrow blasts were observed.
  • Gingival hypertrophy regressed with the treatment of hydroxyurea.
  • Three months later, bone marrow blast count elevated and the patient was treated with two courses of AML-like regimen and then one course of consolidation therapy.
  • Similar to other extramedullary involvements, gingival hypertrophy in CMML can be a harbinger of the disease entering a more aggressive phase requiring systemic chemotherapy.
  • [MeSH-major] Antigens, CD56 / biosynthesis. Gingival Neoplasms / pathology. Leukemia, Myelomonocytic, Chronic / metabolism

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  • (PMID = 15101735.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human
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10. Zhang GS, Peng HL, Dai CW, Gong FJ, Xu YX, Xiao L, Pei MF, Shen JK, Yang JJ: [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof]. Zhonghua Yi Xue Za Zhi; 2005 Dec 28;85(49):3504-8
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  • [Title] [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof].
  • OBJECTIVE: To study the clinical features and molecular genetics of acute monocytic leukemia (AML) after orthotopic liver transplantation and significance thereof.
  • METHODS: The clinical manifestations, laboratory findings, development, diagnosis, treatment, and prognosis of the first case of AML after orthotopic liver transplantation in the world, a Chinese, male, aged 46, were observed.
  • The diagnosis of chronic myelomonocytic leukemia was made.
  • Five months after the liver transplantation the disease developed to AML.
  • The patient underwent combined chemotherapy (HA or DA regimens) for 5 courses and showed a partial remission both hematologically and in bone marrow examination at first, however, became resistant to all chemotherapeutic agents.
  • RT-PCR showed absence of wild type FLT3 allele.
  • At last the patient died of infection. (2) A FLT3-ITD mutation of "insertion" type was identified in the BMMCs.
  • CONCLUSION: Orthotopic liver transplantation may be complicated with acute leukemia heterogeneous in clinical features and hematology.
  • [MeSH-major] Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Liver Transplantation / adverse effects. Postoperative Complications

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  • (PMID = 16686070.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
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11. Xu WL, Jin J, Chen ZM, Lou JY, Yu YB: [Clinical and experimental study of 38 cases with trisomy 8]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2003 Dec;20(6):528-31
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  • RESULTS: Thirty-two of 38(84.2%) cases with trisomy 8, and fourteen of 17(82.4%) cases with trisomy 8 as the sole chromosome aberration were myeloid disorders such as myelodysplastic syndrome (MDS), acute myelocytic leukemia (AML), chronic myelocytic leukemia (CML).
  • The incidence of trisomy 8 was higher in myeloid disease than in lymphocytic disease (5% vs 1.3%); the incidence of trisomy 8 was higher in acute monocytic leukemia than in other AML (6.1% vs 2.4%), and the incidence of trisomy 8 in chronic myelomonocytic leukemia( CMML) was higher than that in other myelodysplastic syndrome (MDS) (25% vs 13.2%); 17 cases had trisomy 8 as the sole chromosome aberration, 21 cases had other additional chromosome aberrations.
  • Eleven cases were treated with chemotherapy, among them only 10 cases data were available.
  • Seven cases acquired complete remission but 3 of them were M3, the other 3 cases had no response after two courses of chemotherapy.
  • Trisomy 8 might be related with differentiation abnormality of monocyte.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia / genetics. Myelodysplastic Syndromes / genetics. Trisomy

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  • (PMID = 14669224.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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12. Tolomeo M, Grimaudo S, Di Cristina A, Pipitone RM, Dusonchet L, Meli M, Crosta L, Gebbia N, Invidiata FP, Titone L, Simoni D: Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells. Cancer Lett; 2008 Jul 8;265(2):289-97
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  • [Title] Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells.
  • Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required.
  • Galangin induced an arrest of cells in G0-G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells.
  • These data suggest that galangin is an interesting candidate for a combination therapy in the treatment of imatinib-resistant leukemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm. Flavonoids / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Differentiation / drug effects. Cell Line, Tumor. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Imatinib Mesylate. K562 Cells

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  • (PMID = 18374481.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Flavonoids; 0 / Piperazines; 0 / Pyrimidines; 142FWE6ECS / galangin; 8A1O1M485B / Imatinib Mesylate
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13. Mashiyama S, Fukawa O, Mitani S, Ito S, Ito K, Asano S, Sai T: [Chronic subdural hematoma associated with malignancy: report of three cases]. No Shinkei Geka; 2000 Feb;28(2):173-8

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  • [Title] [Chronic subdural hematoma associated with malignancy: report of three cases].
  • Three cases of chronic subdural hematoma (CSH) associated with malignancy are reported.
  • Cytological examination of chronic subdural hematoma revealed abnormal white blood cells.
  • A clinical diagnosis of acute monocytic leukemia was made after the laboratory examination.
  • Remission was achieved by chemotherapy, but she died one year after the operation.
  • Cytological examination of chronic subdural hematoma revealed abnormal white blood cells.
  • A clinical diagnosis of chronic lymphocytic leukemia was made after the laboratory examination.
  • No treatment was given since there were no clinical symptoms of chronic lymphocytic leukemia.
  • [MeSH-major] Hematoma, Subdural / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Monocytic, Acute / complications
  • [MeSH-minor] Adenocarcinoma / pathology. Aged. Chronic Disease. Female. Humans. Infant

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  • (PMID = 10666738.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] JAPAN
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14. Drexler HG, Matsuo Y, MacLeod RA: Malignant hematopoietic cell lines: in vitro models for the study of erythroleukemia. Leuk Res; 2004 Dec;28(12):1243-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A panel of leukemia cell lines has been assembled over the last 30 years representing a spectrum of erythroid cells arrested at various stages of differentiation.
  • Most cell lines have been established from acute myeloid leukemia M6 or chronic myeloid leukemia in blast crisis and generally express immunoprofiles typically seen in immature erythroid cells.
  • Several cell lines may be induced to differentiate along the erythroid, megakaryocytic or monocytic pathway by treatment with pharmacological or physiological reagents.
  • [MeSH-major] Cell Line, Tumor. Erythroid Cells / pathology. Leukemia, Erythroblastic, Acute / pathology
  • [MeSH-minor] Cell Differentiation. Cytogenetic Analysis. Cytokines. Humans. Immunophenotyping. Leukemia, Megakaryoblastic, Acute / pathology

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  • (PMID = 15475063.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 67
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15. Pogrebniak A, Hasmann M, Schemainda I, Pelka-Fleischer R, Nuessler V: Cytoprotective features of selenazofurin in hematopoietic cells. Int J Clin Pharmacol Ther; 2002 Aug;40(8):368-75
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  • OBJECTIVES: Antineoplastic activity of tiazofurin (Tz) and selenazofurin (Se) depends on their conversion to substances which are analogs of NAD.
  • The therapeutic potential of modulating intracellular NAD levels and activity of NAD-dependent enzymes by concomitant administration of conventional anticancer agents merits further research.
  • Our aim was to investigate the cytotoxic effects of Tz and Se in hematopoietic cells and to test their ability to potentiate the effects of DNA strand-disrupting agents.
  • MATERIAL: THP-1, a cell line, derived from human acute monoblastic leukemia, was used.
  • METHODS: The WST-l test was used to detect the function of NAD(P)-dependent dehydrogenases after exposure of THP-1 cells to Tz or Se.
  • Cytotoxicity of Tz, Se, MNNG and chlorambucil was assessed using the membrane permeability assay (PI test).
  • RESULTS: THP-1 cells were sensitive to cytotoxic effects of Tz and Se, with IC50 values of 2.5 x 10(-5) M for Tz and 2 x 10(-6) M for Se, as determined with the WST-1 test; 10 microM Se induced cell membrane disruption in more than 20% of THP-1 cells 48 hours after commencement of treatment, whereas the same concentration of Tz failed to increase membrane permeability.
  • Pretreatment of THP-1 cells with 0.5 - 1.5 microM Se had no effect on the time course of cell death, induced by treatment with the DNA-damaging agent 1-methyl-3-nitro-1 - nitrosoguanidinium (MNNG) for 36 hours.
  • However, when incubation of THP-1 cells with MNNG was prolonged (72 hours) without changing the incubation medium, pretreatment with Se had the following effects: the relative number of cells that died spontaneously decreased, and the cytotoxicity of MNNG was diminished.
  • CONCLUSIONS: Contrary to other investigations, we here demonstrate that preincubation with Se may partially protect cells from cell death induced by the alkylating agents MNNG and chlorambucil in the THP-1 cell line and in CLL lymphocytes presumably by affecting spontaneous cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Organoselenium Compounds / pharmacology. Organoselenium Compounds / therapeutic use. Ribavirin / analogs & derivatives. Ribonucleosides / pharmacology. Ribonucleosides / therapeutic use
  • [MeSH-minor] Cell Death / drug effects. Cell Line. Cell Survival / drug effects. Chlorambucil / pharmacology. Dose-Response Relationship, Drug. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Monocytic, Acute / drug therapy. Methylnitronitrosoguanidine / pharmacology

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  • (PMID = 12467305.001).
  • [ISSN] 0946-1965
  • [Journal-full-title] International journal of clinical pharmacology and therapeutics
  • [ISO-abbreviation] Int J Clin Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoselenium Compounds; 0 / Ribonucleosides; 12H3O2UGSF / Methylnitronitrosoguanidine; 18D0SL7309 / Chlorambucil; 49717AWG6K / Ribavirin; 83705-13-9 / selenazofurin; ULJ82834RE / tiazofurin
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16. Guan M, Chen SC, Ge CW: [Long-term effects of androgen combined with low dose all-trans-retinoic acid on myelodysplastic syndrome: follow-up of 60 cases]. Zhonghua Yi Xue Za Zhi; 2009 Apr 7;89(13):919-22
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  • METHODS: Sixty-two MDS patients, 48 with RA, 2 of RAS, 9 with RA with excess of blasts (RAEB), 2 with RAEB-transformation (RAEB-t ), and 1 with chronic myelogenous-monocytic leukemia (CMML) according to the FAB subtype standard, received stanazolol (6 mg/d) or danazol (600 mg/d) and low dose all-trans-retinoic acid (ATRA 10 mg/d).
  • Three months later the treatment was discontinued on 22 patients that showed ineffective and 2 more patients withdrew from the treatment due to exacerbation.
  • The remaining 36 patients were treated according to the original protocol, and the doses of these 2 drugs were reduced by half until the condition was exacerbated.
  • RESULTS: After 6 months of treatment, complete remission (CR) was seen in 1 patient, partial remission (PR) in 6 patients, and hematologic Improvement (HI) in 19 of the 60 patients evaluated with a response rate of 43.3% (26/60) in all patients, 50% (24/48) in RA/RAS group, and 16.7% (2/12) in RAEB/RAEB-t/CMML group.
  • There were not significant differences in cellularity, dysplastic hematopoiesis, and myeloblast before and after treatment among the RA/RAS patients.
  • After 12 months of treatment, CR was seen in 1 patient, PR in 7, and HI in 9, with a response rate of 28.3% (17/60) in all patients, 35.4% (17/48) in the RA/RAS group, and 0% (0/12) in the RAEB/RAEB-t/CMML group.
  • Adverse effects were mild and did not require discontinuance of the therapy.
  • The survival time of the 19 patients in the RA group that responded well to treatment was 54 months (41, 66), significantly longer than that of the 20 patients without good outcomes [23 months (13,32), chi2=4.72, P=0.025].
  • CONCLUSION: Effective, economic, and safe, stanozolol or danazol with low-dose all-trans-retinoic acid improves the life quality and prolongs the survival time of the MDS patients who respond well.
  • [MeSH-major] Androgens / therapeutic use. Myelodysplastic Syndromes / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Drug Therapy, Combination. Follow-Up Studies. Humans. Middle Aged. Time. Treatment Outcome. Young Adult


17. Saydam G, Aydin HH, Sahin F, Selvi N, Oktem G, Terzioglu E, Buyukkececi F, Omay SB: Involvement of protein phosphatase 2A in interferon-alpha-2b-induced apoptosis in K562 human chronic myelogenous leukaemia cells. Leuk Res; 2003 Aug;27(8):709-17
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  • [Title] Involvement of protein phosphatase 2A in interferon-alpha-2b-induced apoptosis in K562 human chronic myelogenous leukaemia cells.
  • Interferon-alpha (IFN-alpha)-2b is known to have antiproliferative effects on hematological malignant cells, especially chronic myelogenous leukaemia (CML).
  • Also during interferon therapy, resistance can emerge in the CML clones.
  • It can be induced to differentiate to granulocytic and/or monocytic lineages with certain molecules.
  • Apoptosis assay by the mono-oligonucleosome detection and acridine orange/propidium iodide dye revealed marked apoptosis underlying cytotoxicity.
  • [MeSH-major] Apoptosis / drug effects. Interferon-alpha / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Phosphoprotein Phosphatases / physiology
  • [MeSH-minor] Cell Differentiation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Inhibitory Concentration 50. K562 Cells. Kinetics. Protein Phosphatase 2. Protein Subunits / analysis. Recombinant Proteins

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  • (PMID = 12801529.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Interferon-alpha; 0 / Protein Subunits; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
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18. Yan Z, Yang B, Wang QS, Wang LL, Han XP, Ren F, Yu L: [Clinical pathological features of the 8p11 myeloproliferative syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1321-6
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  • This study was aimed to investigate the clinico-pathological features, diagnosis and treatment of the 8p11 (eight p11) myeloproliferative syndrome (EMS).
  • The results indicated that EMS was a relatively rare disease characterized by the occurrence of a bcr/abl-negative myeloproliferative disorder and a T-cell lymphoblastic lymphoma (T-LBL).
  • At the molecular level, all cases carried a chromosomal abnormality involving the fibroblast growth factor receptor 1 (FGFR1) at chromosome 8p11.
  • Majority of patients terminate in acute myeloid leukemia which is resistant to conventional chemotherapy.
  • It is usually misdiagnosed as T-LBL, atypical chronic myeloid leukemia (aCML) or chronic myelogenous-monocytic leukemia (CMML).

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  • (PMID = 21129285.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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19. Gyurkocza B, Plescia J, Raskett CM, Garlick DS, Lowry PA, Carter BZ, Andreeff M, Meli M, Colombo G, Altieri DC: Antileukemic activity of shepherdin and molecular diversity of hsp90 inhibitors. J Natl Cancer Inst; 2006 Aug 2;98(15):1068-77
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  • Inhibitors of Hsp90 are being examined as cancer therapeutic agents, but the molecular mechanism of their anticancer activity is still unclear.
  • We investigated Hsp90 as a therapeutic target for acute myeloid leukemia (AML) by use of the Hsp90 inhibitor shepherdin (a novel peptidyl antagonist of the interaction between Hsp90 and survivin, which is a regulator of cell proliferation and cell viability in cancer).
  • Apoptosis, Hsp90 client protein expression, and mitochondrial dysfunction were evaluated in AML types (myeloblastic, monocytic, and chronic myelogenous leukemia in blast crisis), patient-derived blasts, and normal mononuclear cells.
  • Organ tissues were examined histologically.
  • Cell-permeable shepherdin[79-83] induced rapid (within 30 minutes) and complete (with concentrations inducing 50% cell death of 24-35 microM) killing of AML types and blasts, but it did not affect normal mononuclear cells.
  • Shepherdin[79-83] made contact with unique residues in the ATP pocket of Hsp90 (Ile-96, Asp-102, and Phe-138), did not increase Hsp70 levels in AML cells, disrupted mitochondrial function within 2 minutes of treatment, and eliminated the expression of Hsp90 client proteins.
  • [MeSH-major] Antineoplastic Agents / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Microtubule-Associated Proteins / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Peptide Fragments / pharmacology

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  • (PMID = 16882944.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / CA78810; United States / NCI NIH HHS / CA / CA90917; United States / NHLBI NIH HHS / HL / HL54131
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / HSP90 Heat-Shock Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / shepherdin; K3Z4F929H6 / Lysine; TE7660XO1C / Glycine
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20. Athanasiadou A, Saloum R, Gaitatzi M, Anagnostopoulos A, Fassas A: Isolated pentasomy of chromosome 8 in erythroleukemia. Leuk Lymphoma; 2001 Nov-Dec;42(6):1409-12

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  • Only 2 such cases, one in acute monocytic leukemia and one in chronic myelomonocytic leukemia have been described in the literature to date.
  • The patient died three days after diagnosis without chemotherapy.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia, Erythroblastic, Acute / genetics

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  • (PMID = 11911427.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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21. Tirado CA, Valdez F, Klesse L, Karandikar NJ, Uddin N, Arbini A, Fustino N, Collins R, Patel S, Smart RL, Garcia R, Doolittle J, Chen W: Acute myeloid leukemia with inv(16) with CBFB-MYH11, 3'CBFB deletion, variant t(9;22) with BCR-ABL1, and del(7)(q22q32) in a pediatric patient: case report and literature review. Cancer Genet Cytogenet; 2010 Jul 1;200(1):54-9
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  • [Title] Acute myeloid leukemia with inv(16) with CBFB-MYH11, 3'CBFB deletion, variant t(9;22) with BCR-ABL1, and del(7)(q22q32) in a pediatric patient: case report and literature review.
  • Coexistence of inv(16) and t(9;22) is a rare chromosomal aberration, one that has been described in chronic myelogenous leukemia (CML), mainly in myeloid blast crisis, and de novo acute myeloid leukemia (AML).
  • Here we present the case of a 13-year-old boy with a new diagnosis of AML with some features of monocytic differentiation.
  • The patient was treated with standard AML chemotherapy plus gemtuzumab as part of a clinical trial.
  • To the best of our knowledge, this is the first description of a pediatric case of de novo AML with a stemline showing inv(16) along with 3'CBFB deletion, an abnormal clone revealing in addition a del(7)(q22q32), and another clone with a t(9;22;19)(q34;q11.2;p13.1) as an additional abnormality.
  • [MeSH-major] Chromosome Deletion. Chromosome Inversion. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. Fusion Proteins, bcr-abl / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20513535.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 16
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22. Au WY, Ma SK, Wan TS, Man C, Kwong YL: Pentasomy 8q in therapy-related myelodysplastic syndrome due to cyclophosphamide therapy for fibrosing alveolitis. Cancer Genet Cytogenet; 2003 Feb;141(1):79-82
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  • [Title] Pentasomy 8q in therapy-related myelodysplastic syndrome due to cyclophosphamide therapy for fibrosing alveolitis.
  • Trisomy 8/8q is a common cytogenetic event in myelocytic malignancies, ranging from myelodysplastic syndrome (MDS) to acute myelocytic leukemia (AML) to blastic transformation of chronic myelocytic leukemia.
  • A patient with fibrosing alveolitis on prolonged cyclophosphamide treatment developed therapy-related MDS.
  • The clinical features of 11 cases of myelocytic leukemia with pentasomy and hexasomy 8/8q were summarized.
  • Compared with trisomy and tetrasomy 8, significant features included reduced median survival (90 days), treatment refractoriness (even with transplantation), monocytic differentiation, trilineage dysplasia, and radiation or toxin exposure.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Pulmonary Fibrosis / complications. Pulmonary Fibrosis / drug therapy


23. Guan M, Chen SC, Li RS, Ge CW, Zhu HL: [Low dose all-trans retinoic acid and androgen therapy for patients with myelodysplastic syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2004 Dec;12(6):774-8
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  • [Title] [Low dose all-trans retinoic acid and androgen therapy for patients with myelodysplastic syndrome].
  • To explore therapeutic efficacy of androgens and low dose all-trans retinoic acid (ATRA) for myelodysplastic syndrome (MDS) patients, 55 patients of MDS were observed, including 41 cases of refractory anemia (RA), 11 cases of refractory anemia with excess of blasts (RAEB), 2 cases of refractory anemia with excess of blasts in transformation (RAEB-t) and 1 case of chronic myeloic-monocytic leukemia (CMML).
  • The results showed that according to MDS international working group response criteria, at the end of three months,complete remission (CR) was seen in 1 patient, partial remission (PR) was found in 2 patients.
  • In conclusion, danazol or stanazol in combination with low dose ATRA are partialy effective in therapy for patients with low-risk myelodysplastic syndrome.

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  • (PMID = 15631659.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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24. Zhang C, Liang MY, Wang SM: [Clinical analysis of bicytopenia and pancytopenia during pregnancy]. Zhonghua Fu Chan Ke Za Zhi; 2009 Jul;44(7):488-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To investigate the diagnosis, management, pregnancy outcome and prognosis of bicytopenia or pancytopenia during pregnancy.
  • METHODS: Retrospective chart review was conducted on 24 pregnancies who were found bicytopenia or pancytopenia during pregnancy for the first time.
  • RESULTS: According to the clinical data and laboratory findings, the latter including complete blood cell count, reticulocyte count, peripheral smear, serum folate and vitamin B12 level, autoimmune antibody screening, bone marrow smear and biopsy, thirteen patients were diagnosed as having chronic aplastic anemia (CAA), six as having myelodysplastic syndromes (MDS), two as having megaloblastic anemia (MA), one as having paroxysmal nocturnal hemoglobinuria (PNH), one as having Evan's syndrome and one as having acute leukemia.
  • The patient with acute leukemia died of recurrence six months postpartum.
  • Of the 6 patients with MDS, one achieved partial remission, four no remission, and one transformed into acute monocytic leukemia, then refused chemotherapy and was lost follow-up.
  • Diagnosis should be made as soon as possible through appropriate and reasonable laboratory examinations.
  • [MeSH-major] Anemia, Aplastic / therapy. Blood Transfusion. Pancytopenia / therapy. Pregnancy Complications, Hematologic / diagnosis. Pregnancy Complications, Hematologic / therapy. Pregnancy Outcome
  • [MeSH-minor] Adult. Biopsy, Needle. Bone Marrow / pathology. Bone Marrow Examination. Female. Folic Acid / therapeutic use. Follow-Up Studies. Humans. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Pregnancy. Prognosis. Retrospective Studies. Young Adult


25. Germeshausen M, Schulze H, Kratz C, Wilkens L, Repp R, Shannon K, Welte K, Ballmaier M: An acquired G-CSF receptor mutation results in increased proliferation of CMML cells from a patient with severe congenital neutropenia. Leukemia; 2005 Apr;19(4):611-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment with pharmacological doses of recombinant human granulocyte colony-stimulating factor (rh-G-CSF) stimulates neutrophil production and decreases the risk of major infectious complications.
  • We report a CN patient with chronic myelomonocytic leukemia (CMML) who never received rh-G-CSF.
  • In vitro culture revealed a G-CSF-dependent proliferation of CMML cells, which subsequently differentiated along the monocytic/macrophage lineage.
  • Our results provide direct evidence for the in vivo expression of a truncated G-CSFR in leukemic cells, which emerged in the absence of rh-G-CSF treatment and transduces proliferative signals.
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Neutropenia / genetics. Neutropenia / pathology. Receptors, Granulocyte Colony-Stimulating Factor / genetics

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  • (PMID = 15729385.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA72614
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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