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Items 1 to 19 of about 19
1. Matsuda K, Shimada A, Yoshida N, Ogawa A, Watanabe A, Yajima S, Iizuka S, Koike K, Yanai F, Kawasaki K, Yanagimachi M, Kikuchi A, Ohtsuka Y, Hidaka E, Yamauchi K, Tanaka M, Yanagisawa R, Nakazawa Y, Shiohara M, Manabe A, Kojima S, Koike K: Spontaneous improvement of hematologic abnormalities in patients having juvenile myelomonocytic leukemia with specific RAS mutations. Blood; 2007 Jun 15;109(12):5477-80
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  • [Title] Spontaneous improvement of hematologic abnormalities in patients having juvenile myelomonocytic leukemia with specific RAS mutations.
  • Of 11 children with juvenile myelomonocytic leukemia (JMML) carrying RAS mutations (8 with NRAS mutations, 3 with KRAS2 mutations), 5 had a profound elevation in either or both the white blood cells and spleen size at diagnosis.
  • Three patients had no or modest hepatosplenomegaly and mild leukocytosis at presentation but subsequently showed a marked increase in spleen size with or without hematologic exacerbation, for which nonintensive chemotherapy was initiated.
  • The other three patients with NRAS or KRAS2 glycine to serine substitution received no chemotherapy, but hematologic improvement has been observed during a 2- to 4-year follow up.
  • In the third group, all hematopoietic cell lineages analyzed had the RAS mutations at the time of hematologic improvement, whereas DNA obtained from the nails had the wild type.
  • [MeSH-major] Blood Cells / pathology. Leukemia, Myelomonocytic, Chronic / genetics. Mutation / physiology. Neoplasm Regression, Spontaneous / genetics. ras Proteins / genetics

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  • [CommentIn] Blood. 2008 Jan 15;111(2):966-7; author reply 967-8 [18182584.001]
  • (PMID = 17332249.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / ras Proteins
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2. Ohashi H, Kato C, Fukami S, Saito H, Hamaguchi M: Leukemic relapse in the central nervous system after allogeneic stem cell transplantation with complete remission in the bone marrow and donor-type chimerism: report of two cases. Am J Hematol; 2005 Jun;79(2):142-6
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  • [Title] Leukemic relapse in the central nervous system after allogeneic stem cell transplantation with complete remission in the bone marrow and donor-type chimerism: report of two cases.
  • We studied two cases with leukemia that relapsed in the central nervous system (CNS) after allogeneic stem cell transplantation.
  • One patient underwent peripheral blood stem cell transplantation (SCT) from a related, yet haplotype-mismatched, donor for chronic myelomonocytic leukemia.
  • She was kept in complete remission (CR) in the bone marrow (BM) for 7 months, until relapse in the cerebrospinal fluid (CSF) was evident.
  • In the other patient, with acute lymphoblastic leukemia, systemic relapse occurred when he was still on immunosuppression 6 months after SCT from an unrelated donor.
  • After induction chemotherapy following cessation of immunosuppression, the BM examination proved CR.
  • During consolidation chemotherapy, however, he developed leukemic dissemination in the CSF, despite the fact that the BM was in CR.
  • In both patients, the BM cells and all the fractions of the PB cells proved donor-type chimeras.
  • These results seem to suggest that the graft-versus-leukemia effects might not be as effective in the CNS as in the BM, even when complete T-lymphoid chimerism is achieved.
  • [MeSH-major] Bone Marrow / pathology. Central Nervous System Neoplasms / therapy. Leukemia / therapy. Neoplasm Recurrence, Local. Peripheral Blood Stem Cell Transplantation. Tissue Donors. Transplantation Chimera
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelomonocytic, Chronic / pathology. Leukemia, Myelomonocytic, Chronic / therapy. Male. Middle Aged. Remission Induction. Transplantation, Homologous

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  • (PMID = 15929112.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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3. Konoplev S, Huang X, Drabkin HA, Koeppen H, Jones D, Kantarjian HM, Garcia-Manero G, Chen W, Medeiros LJ, Bueso-Ramos CE: Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis. Cancer; 2009 Oct 15;115(20):4737-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis.
  • BACKGROUND: Nucleophosmin (NPM1) gene mutations are reported to predict a favorable prognosis in acute myeloid leukemia (AML) patients.
  • RESULTS: The study included 252 AML patients: 192 de novo AML, 33 AML preceded by either myelodysplastic syndrome or chronic myelomonocytic leukemia, and 27 therapy-related AML.
  • All patients received intensive chemotherapy.
  • Similar results were obtained in patients<or=60 years old with normal karyotype and wild-type FLT3 (P=.768).
  • [MeSH-major] Bone Marrow / metabolism. Cytoplasm / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism

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  • [Copyright] Copyright (c) 2009 American Cancer Society.
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  • (PMID = 19637342.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / U54 CA096300
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ NIHMS633932; NLM/ PMC4199225
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4. Tefferi A, Gotlib J, Pardanani A: Hypereosinophilic syndrome and clonal eosinophilia: point-of-care diagnostic algorithm and treatment update. Mayo Clin Proc; 2010 Feb;85(2):158-64
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  • [Title] Hypereosinophilic syndrome and clonal eosinophilia: point-of-care diagnostic algorithm and treatment update.
  • Acquired eosinophilia is operationally categorized into secondary, clonal, and idiopathic types.
  • Causes of secondary eosinophilia include parasite infections, allergic or vasculitis conditions, drugs, and lymphoma.
  • The World Health Organization classification system for hematologic malignancies recognizes 2 distinct subcategories of clonal eosinophilia: chronic eosinophilic leukemia, not otherwise specified and myeloid/lymphoid neoplasms with eosinophilia and mutations involving platelet-derived growth factor receptor alpha/beta or fibroblast growth factor receptor 1.
  • Clonal eosinophilia might also accompany other World Health Organization-defined myeloid malignancies, including chronic myelogenous leukemia, myelodysplastic syndromes, chronic myelomonocytic leukemia, and systemic mastocytosis.
  • Hypereosinophilic syndrome, a subcategory of idiopathic eosinophilia, is defined by the presence of a peripheral blood eosinophil count of 1.5 x 10(9)/L or greater for at least 6 months (a shorter duration is acceptable in the presence of symptoms that require eosinophil-lowering therapy), exclusion of both secondary and clonal eosinophilia, evidence of organ involvement, and absence of phenotypically abnormal and/or clonal T lymphocytes.
  • In the current review, we provide a simplified algorithm for distinguishing the various causes of clonal and idiopathic eosinophilia and discuss current therapy, including new drugs (imatinib mesylate, alemtuzumab, and mepolizumab).
  • [MeSH-major] Algorithms. Eosinophilia / diagnosis. Eosinophilia / drug therapy. Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Benzamides. Causality. Decision Trees. Diagnosis, Differential. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelomonocytic, Chronic / complications. Mastocytosis / complications. Mutation / genetics. Myelodysplastic Syndromes / complications. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Receptors, Platelet-Derived Growth Factor / genetics. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 20053713.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / mepolizumab; 3A189DH42V / alemtuzumab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Number-of-references] 77
  • [Other-IDs] NLM/ PMC2813824
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5. Hamidou MA, Boumalassa A, Larroche C, El Kouri D, Blétry O, Grolleau JY: Systemic medium-sized vessel vasculitis associated with chronic myelomonocytic leukemia. Semin Arthritis Rheum; 2001 Oct;31(2):119-26
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  • [Title] Systemic medium-sized vessel vasculitis associated with chronic myelomonocytic leukemia.
  • OBJECTIVE: To determine the clinical aspects of systemic vasculitis associated with chronic myelomonocytic leukemia (CMML).
  • None had viral infection or drug-associated vasculitis.
  • All patients were treated with corticosteroids, and 7 received immunosuppressive drugs.
  • CONCLUSIONS: Systemic ANCA-negative polyarteritis nodosa-type vasculitis seems closely associated to CMML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Vasculitis / etiology
  • [MeSH-minor] Aged. Aneurysm / diagnosis. Antibodies, Antineutrophil Cytoplasmic / blood. Drug Therapy, Combination. Enzyme-Linked Immunosorbent Assay. Fatal Outcome. Female. Fluorescent Antibody Technique, Indirect. Glucocorticoids / therapeutic use. Humans. Immunosuppressive Agents / therapeutic use. Male. Middle Aged. Retrospective Studies

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  • [Copyright] Copyright 2001 by W.B. Saunders Company
  • (PMID = 11590581.001).
  • [ISSN] 0049-0172
  • [Journal-full-title] Seminars in arthritis and rheumatism
  • [ISO-abbreviation] Semin. Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antineutrophil Cytoplasmic; 0 / Glucocorticoids; 0 / Immunosuppressive Agents
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6. Emanuel PD: Juvenile myelomonocytic leukemia. Curr Hematol Rep; 2004 May;3(3):203-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Juvenile myelomonocytic leukemia.
  • Juvenile myelomonocytic leukemia (JMML) is a rare, clonal, mixed myeloproliferative and myelodysplastic disorder afflicting young children.
  • Patients with JMML respond poorly to most standard chemotherapy regimens and, whereas stem cell transplantation is the only known curative approach, even this modality is hampered by high relapse rates.
  • Potential causative mutations or other genetic abnormalities in three genes (eg, RAS, neurofibromatosis type 1, and PTPN11), all of which are positioned in the GM-CSF/Ras signal transduction pathway, account for up to 75% of cases of JMML.
  • These pathogenetic advances are paving the way for the development and testing of mechanism-based molecularly targeted therapeutics in JMML aimed specifically at the GM-CSF signal transduction pathway through Ras.
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / etiology

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  • (PMID = 15087069.001).
  • [ISSN] 1540-3408
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 45
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7. Bennett JM: Chronic myelomonocytic leukemia. Curr Treat Options Oncol; 2002 Jun;3(3):221-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myelomonocytic leukemia.
  • Chronic myelomonocytic leukemia (CMML) has dysplastic and proliferative features.
  • Various chemotherapy regimens have been used with only modest success.
  • When the proliferative phase prevails, hydroxyurea is the treatment of choice.
  • If a donor cannot be identified, then combination acute myeloid leukemia-type therapy followed by an autologous stem cell or marrow transplant should be offered.
  • Clinical trials should be considered if available because the overall results of therapeutic interventions are far from optimal.
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Bone Marrow Transplantation. Combined Modality Therapy. Humans. Hydroxyurea / therapeutic use

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  • (PMID = 12057067.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 16
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8. Toffalini F, Kallin A, Vandenberghe P, Pierre P, Michaux L, Cools J, Demoulin JB: The fusion proteins TEL-PDGFRbeta and FIP1L1-PDGFRalpha escape ubiquitination and degradation. Haematologica; 2009 Aug;94(8):1085-93
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  • BACKGROUND: Chimeric oncogenes encoding constitutively active protein tyrosine kinases are associated with chronic myeloid neoplasms.
  • Wild-type receptor tyrosine kinases are efficiently targeted for degradation upon activation, in a process that requires Cbl-mediated monoubiquitination of receptor lysines.
  • Since protein degradation pathways have been identified as useful targets for cancer therapy, the aim of this study was to compare the degradation of hybrid and wild-type receptor tyrosine kinases.
  • RESULTS: In contrast to the corresponding wild-type receptors, which are quickly degraded upon activation, we observed that TPbeta, FPalpha and the ZNF198-FGFR1 hybrids escaped down-regulation in Ba/F3 cells.
  • The high stability of TPbeta and FPalpha hybrid proteins was confirmed in leukocytes from leukemia patients.
  • Ubiquitination of TPbeta and FPalpha was much reduced compared to that of wild-type receptors, despite marked Cbl phosphorylation in cells expressing hybrid receptors.
  • [MeSH-minor] Aged. Animals. Blotting, Western. Cell Line. Cell Proliferation. Cells, Cultured. Genotype. Humans. Hypereosinophilic Syndrome / blood. Leukemia, Myelomonocytic, Chronic / blood. Leukocytes / cytology. Leukocytes / drug effects. Leukocytes / metabolism. Male. Middle Aged. Phosphorylation. Platelet-Derived Growth Factor / pharmacology. Proto-Oncogene Proteins c-cbl / metabolism. Proto-Oncogene Proteins c-sis. Receptor, Platelet-Derived Growth Factor beta / genetics. Receptor, Platelet-Derived Growth Factor beta / metabolism. Transfection

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  • (PMID = 19644140.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / TEL-PDGFRbeta fusion protein, human; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / platelet-derived growth factor BB; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC2719031
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9. Kawakami M, Oka Y, Tsuboi A, Harada Y, Elisseeva OA, Furukawa Y, Tsukaguchi M, Shirakata T, Nishida S, Nakajima H, Morita S, Sakamoto J, Kawase I, Oji Y, Sugiyama H: Clinical and immunologic responses to very low-dose vaccination with WT1 peptide (5 microg/body) in a patient with chronic myelomonocytic leukemia. Int J Hematol; 2007 Jun;85(5):426-9
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  • [Title] Clinical and immunologic responses to very low-dose vaccination with WT1 peptide (5 microg/body) in a patient with chronic myelomonocytic leukemia.
  • The wild-type Wilms tumor gene, WT1, is overexpressed in myelodysplastic syndrome (MDS) as well as acute myeloid leukemia.
  • In a phase I clinical trial of biweekly vaccination with HLA-A*2402-restricted WT1 peptide for these malignancies, 2 patients with MDS developed severe leukocytopenia in association with a reduction in leukemic blast cells and levels of WT1 messenger RNA (mRNA) after only a single vaccination with 0.3 mg of WT1 peptide.
  • We describe the first trial for a 57-year-old male patient with chronic myelomonocytic leukemia who was vaccinated biweekly with a small quantity (5 microg/body) of WT1 peptide.
  • This case demonstrates for the first time that vaccination with as little as 5 microg of WT1 peptide can induce WT1-specific immune responses and resultant clinical responses.
  • [MeSH-major] Cancer Vaccines / administration & dosage. Cancer Vaccines / immunology. Leukemia, Myelomonocytic, Chronic / drug therapy. WT1 Proteins / administration & dosage. WT1 Proteins / immunology

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  • (PMID = 17562620.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / WT1 Proteins
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10. Bergstraesser E, Hasle H, Rogge T, Fischer A, Zimmermann M, Noellke P, Niemeyer CM: Non-hematopoietic stem cell transplantation treatment of juvenile myelomonocytic leukemia: a retrospective analysis and definition of response criteria. Pediatr Blood Cancer; 2007 Oct 15;49(5):629-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-hematopoietic stem cell transplantation treatment of juvenile myelomonocytic leukemia: a retrospective analysis and definition of response criteria.
  • BACKGROUND: Juvenile myelomonocytic leukemia (JMML) is a rare myeloproliferative disease of infancy.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is currently the only curative treatment modality, while the role of anti-leukemic therapy prior to HSCT is uncertain.
  • A comparative evaluation of the efficacy of different clinical protocols and great variety of anti-neoplastic drugs applied pre-HSCT is hampered by the lack of uniform criteria of response.
  • Classification schemas applied in other forms of leukemia are of little value, because in JMML therapy may result in divergent responses in solid organs compared to peripheral blood (PB).
  • PROCEDURE: We therefore defined separate response criteria for white blood count (WBC), platelet count, liver size, and spleen size.
  • We then retrospectively evaluated the efficacy of 129 treatment courses other than HSCT administered to 63 children with JMML.
  • Treatment consisted of intensive therapy according to AML-type chemotherapy, maintenance-type combination therapy, and single agent therapy.
  • To account for the variability observed in the natural course of disease, we also evaluated 32 episodes of "no therapy."
  • RESULTS: Best responses within 3 months of initiation of therapy were highly variable for the four response criteria.
  • In contrast to platelet count and liver size, there was a significant correlation between WBC or spleen size and therapy.
  • Response rates for WBC and spleen size were best for purine analogs, etoposide, and cytarabine as single agents or for maintenance-type combination therapy.
  • CONCLUSION: To rigorously test future therapeutic strategies in this rare disease an international consensus on the definition of response criteria will be helpful.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelomonocytic, Chronic / therapy
  • [MeSH-minor] Blood Cells / drug effects. Drug Evaluation. Humans. Leukocyte Count. Liver. Organ Size / drug effects. Platelet Count. Retrospective Studies. Spleen. Treatment Outcome


11. Benessahraoui M, Paratte F, Plouvier E, Humbert P, Aubin F: Demodicidosis in a child with xantholeukaemia associated with type 1 neurofibromatosis. Eur J Dermatol; 2003 May-Jun;13(3):311-2
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  • [Title] Demodicidosis in a child with xantholeukaemia associated with type 1 neurofibromatosis.
  • We report a new case of demodicidosis in a 22-month-old girl undergoing chemotherapy for chronic myelomonocytic leukaemia associated with xanthoma and type 1 neurofibromatosis.
  • The eruption cleared after oral and topical metronidazole therapy.
  • [MeSH-major] Facial Dermatoses / diagnosis. Leukemia, Myelomonocytic, Chronic / complications. Mite Infestations / diagnosis. Neurofibromatosis 1 / complications
  • [MeSH-minor] Administration, Cutaneous. Administration, Oral. Animals. Anti-Infective Agents / administration & dosage. Anti-Infective Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Female. Humans. Immunocompromised Host. Infant. Metronidazole / administration & dosage. Metronidazole / therapeutic use. Mites / classification

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  • (PMID = 12804999.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 140QMO216E / Metronidazole
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12. 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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13. Kuendgen A, Knipp S, Fox F, Strupp C, Hildebrandt B, Steidl C, Germing U, Haas R, Gattermann N: Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients with myelodysplastic syndrome and relapsed or refractory acute myeloid leukemia. Ann Hematol; 2005 Dec;84 Suppl 1:61-6
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  • [Title] Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients with myelodysplastic syndrome and relapsed or refractory acute myeloid leukemia.
  • Valproic acid (VPA) inhibits histone deacetylase activity and induces differentiation of acute myeloid leukemia (AML) blasts in vitro.
  • Median treatment duration was 4 months for VPA and 2 months for ATRA.
  • Response rates were strongly dependent on disease type according to WHO classification.
  • The response rate was 6% in refractory anemia with excess blasts (I + II), 16% in AML, and 0% in chronic myelomonocytic leukemia.
  • For patients with high-risk MDS, VPA may be combined with chemotherapy or demethylating drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Differentiation / drug effects. Female. Histone Deacetylases / drug effects. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Treatment Outcome. Tretinoin / administration & dosage


14. Emanuel PD: Mixed myeloproliferative and myelodysplastic disorders. Curr Hematol Malig Rep; 2007 Feb;2(1):9-12
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  • When the French-American-British (FAB) classification system was first devised in the 1970s for the myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML) was included in the FAB MDS classification schema.
  • In the 1990s there was ongoing discussion about distinguishing a proliferative type of CMML versus a dysplastic type of CMML, based primarily on the total white blood cell count.
  • [MeSH-minor] Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Chromosome Aberrations. Drug Delivery Systems. Female. Humans. Infant. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / classification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myelomonocytic, Chronic / classification. Leukemia, Myelomonocytic, Chronic / epidemiology. Leukemia, Myelomonocytic, Chronic / therapy. Leukemia, Myelomonocytic, Juvenile / epidemiology. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / therapy. Male. Middle Aged. Mutation. Prognosis. Sex Distribution. Translocation, Genetic

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  • (PMID = 20425383.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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15. Pandey A, Volkots DL, Seroogy JM, Rose JW, Yu JC, Lambing JL, Hutchaleelaha A, Hollenbach SJ, Abe K, Giese NA, Scarborough RM: Identification of orally active, potent, and selective 4-piperazinylquinazolines as antagonists of the platelet-derived growth factor receptor tyrosine kinase family. J Med Chem; 2002 Aug 15;45(17):3772-93
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  • A series of highly potent, specific, orally active, small molecule kinase inhibitors directed against members of PDGFR receptor have been developed through modifications of the novel quinazoline template I.
  • This analogue also inhibits autophosphorylation of Flt-3 ligand-stimulated wild-type Flt-3 and a constitutively activated Flt-3/internal tandem duplication (ITD) with IC(50) values of 30-100 nM.
  • Oral administration of 75 promotes mice survival and significantly delayed disease progression in a Flt-3/ITD-mediated leukemia mouse model and shows efficacy in a nude mouse model of chronic myelomonocytic leukemia.
  • [MeSH-minor] Administration, Oral. Animals. Biological Availability. Dogs. Female. Humans. In Vitro Techniques. Leukemia, Experimental / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Macaca fascicularis. Male. Mice. Mice, Nude. Microsomes, Liver / metabolism. Mutation. Phosphorylation. Plasma. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-kit / metabolism. Rats. Rats, Inbred Lew. Receptor Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Structure-Activity Relationship. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3

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  • (PMID = 12166950.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; E1IO3ICJ9A / tandutinib; EC 2.7.1.- / PDGF receptor tyrosine kinase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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16. Depil S, Deconinck E, Milpied N, Sutton L, Witz F, Jouet JP, Damaj G, Yakoub-Agha I, Société Française de Greffe de Moelle et Thérapie cellulaire: Donor lymphocyte infusion to treat relapse after allogeneic bone marrow transplantation for myelodysplastic syndrome. Bone Marrow Transplant; 2004 Mar;33(5):531-4
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  • Donor lymphocyte infusion has become established as a salvage therapy for patients with hematological disorders relapsing after allogeneic bone marrow transplantation (BMT).
  • Between July 1993 and October 2001, 14 patients with MDS relapsing after allogeneic BMT received DLI as salvage therapy.
  • At the time of BMT, one patient had RA, nine had RAEB, of whom three were in CR after induction-type chemotherapy, two had RAEB-T, one had CMML and one had AML.
  • At the time of relapse, the median marrow blast count was 9%.
  • With a median follow-up of 49 months, six patients were alive, of whom two were in CR after DLI alone and remained disease-free, two were in CR after a second BMT and two had active disease.
  • Although DLI alone seems to be effective in a small number of patients with MDS, other treatment strategies, including prior debulking chemotherapy, deserve investigation.
  • [MeSH-major] Bone Marrow Transplantation. Lymphocyte Transfusion. Myelodysplastic Syndromes / immunology. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adult. Anemia, Refractory, with Excess of Blasts / therapy. Female. Graft vs Host Disease. Humans. Leukemia, Myeloid / therapy. Leukemia, Myelomonocytic, Chronic / therapy. Male. Middle Aged. Recurrence. Tissue Donors. Transplantation, Homologous. Treatment Outcome


17. Jilani I, Estey E, Huh Y, Joe Y, Manshouri T, Yared M, Giles F, Kantarjian H, Cortes J, Thomas D, Keating M, Freireich E, Albitar M: Differences in CD33 intensity between various myeloid neoplasms. Am J Clin Pathol; 2002 Oct;118(4):560-6
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  • We measured the concentration of CD33 antigen on the surface of cells in 315 bone marrow (BM) samples and 114 corresponding peripheral blood (PB) samples from patients with various leukemias (acute myeloid leukemia [AML], chronic myelogenous leukemia [CML], myeloproliferative disorder [MPD] other than CML, myelodysplastic syndrome [MDS]) and from control subjects.
  • CD33 intensity in total BM CD33+ cells differed significantly with the type of disease.
  • There was no correlation between CD33 intensity and response to therapy or overall survival in 35 patients treated with protocols including Mylotarg.
  • [MeSH-major] Aminoglycosides. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Bone Marrow Cells / immunology. Leukemia / immunology
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. Immunotoxins. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / immunology. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / pathology. Prospective Studies. Reproducibility of Results. Sialic Acid Binding Ig-like Lectin 3. Single-Blind Method. Survival Analysis. Survival Rate. Treatment Outcome

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  • (PMID = 12375643.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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18. Novitzky N: Myelodysplastic syndromes in children. A critical review of the clinical manifestations and management. Am J Hematol; 2000 Apr;63(4):212-22
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  • This study also included children with juvenile chronic myelomonocytic leukaemia (JCML) and monosomy 7 (Mo7).
  • Amid those with Mo7, the clinical and laboratory characteristics as well as survival, closely followed their FAB type.
  • Of the treatment options described, survival was significantly higher in those who underwent bone marrow transplant (BMT) (46.9%; P = 0.00021).
  • Among children with JMML (CMML/JCML) not receiving a BMT, time to death was shortest in those best described as JCML (absence of constitutional and karyotypic derangement, thrombocytopenia and elevated Hb F).
  • Finally, BMT remains the treatment of choice for those with primary MDS, as intensive chemotherapy is no better than supportive measures.

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10706766.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
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19. Tilly-Gentric A, Malo JP, Marion V: Primary myelodysplasia: management and outcome at 3 years in 45 patients age 65 and older. J Am Geriatr Soc; 2001 Oct;49(10):1358-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MEASUREMENTS: Clinical presentation, initial hematological features, type of myelodysplasia (French American British classification), treatment, and evolution at 36 months were studied.
  • Refractory anemia was diagnosed in 20 patients; 11 patients presented with refractory anemia with excess blast cells, eight with chronic myelomonocytic leukemia.
  • Thirty-one patients received erythrocyte transfusions, no patient received chemotherapy.
  • The median survival (22 months) was lower than in other reported series even in types of myelodysplasia with a classically better prognosis.
  • CONCLUSION: Myelodysplasia is probably underdiagnosed in older people and has a poor prognosis (median survival 22 months), and no effective treatment is available in older patients.
  • [MeSH-major] Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Diagnosis, Differential. Female. France / epidemiology. Humans. Male. Prognosis. Survival Analysis. Treatment Outcome

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  • (PMID = 11890496.001).
  • [ISSN] 0002-8614
  • [Journal-full-title] Journal of the American Geriatrics Society
  • [ISO-abbreviation] J Am Geriatr Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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