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1. Yang J, Ikezoe T, Nishioka C, Tasaka T, Taniguchi A, Kuwayama Y, Komatsu N, Bandobashi K, Togitani K, Koeffler HP, Taguchi H, Yokoyama A: AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo. Blood; 2007 Sep 15;110(6):2034-40
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  • [Title] AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo.
  • We have recently shown that hematopoietic malignant cells including those from acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) aberrantly expressed Aurora A and B kinases, and ZM447439, a potent inhibitor of Aurora kinases, effectively induced growth arrest and apoptosis of a variety of leukemia cells.
  • The present study explored the effect of AZD1152, a highly selective inhibitor of Aurora B kinase, on various types of human leukemia cells.
  • AZD1152 inhibited the proliferation of AML lines (HL-60, NB4, MOLM13), ALL line (PALL-2), biphenotypic leukemia (MV4-11), acute eosinophilic leukemia (EOL-1), and the blast crisis of chronic myeloid leukemia K562 cells with an IC50 ranging from 3 nM to 40 nM, as measured by thymidine uptake on day 2 of culture.
  • Taken together, AZD1152 is a promising new agent for treatment of individuals with leukemia.
  • The combined administration of AZD1152 and conventional chemotherapeutic agent to patients with leukemia warrants further investigation.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Leukemia / drug therapy. Organophosphates / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Quinazolines / pharmacology. Tubulin Modulators / pharmacology

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  • (PMID = 17495131.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Organophosphates; 0 / Quinazolines; 0 / Tubulin Modulators; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; VC2W18DGKR / Thymidine; ZS7284E0ZP / Daunorubicin
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2. Tsuji A, Sasaki M, Ishii T, Sato S, Kanki H, Suzuki S, Takeuchi S, Fukuda T: Persistent eosinophilic infiltration of the myocardium in a child in complete remission of acute lymphoblastic leukemia and eosinophilia. Potential role in late cardiac disease? Keio J Med; 2010;59(2):64-8
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  • [Title] Persistent eosinophilic infiltration of the myocardium in a child in complete remission of acute lymphoblastic leukemia and eosinophilia. Potential role in late cardiac disease?
  • This report describes the long-term (23 years) follow-up of a pediatric patient with acute lymphoblastic leukemia and eosinophilia who underwent multiple valve replacements.
  • An 8-year-old boy with this complex disease was admitted in January 1984 and treated with 6-week course of vincristine, L-asparaginase, and prednisolone, which induced complete remission.
  • The present study indicates that a subset of patients in complete remission of acute lymphoblastic leukemia and eosinophilia can show persistent myocardial eosinophilic infiltration and are at risk of late cardiac disease.
  • [MeSH-major] Cardiomyopathies / etiology. Cardiomyopathies / pathology. Eosinophilia / complications. Eosinophilia / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


3. Qin Y, Auh S, Blokh L, Long C, Gagnon I, Hamann KJ: TNF-alpha induces transient resistance to Fas-induced apoptosis in eosinophilic acute myeloid leukemia cells. Cell Mol Immunol; 2007 Feb;4(1):43-52
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  • [Title] TNF-alpha induces transient resistance to Fas-induced apoptosis in eosinophilic acute myeloid leukemia cells.
  • Because TNF-alpha activates NF-kappaB in many cell types including inflammatory cells such as eosinophils, we examined effects of TNF-alpha signaling on the Fas-mediated killing of an eosinophilic cell line AML14.
  • This finding suggested that TNF-alpha may contribute to the prolonged survival of inflammatory cells by suppression of Fas-mediated apoptosis, the process involved with NF-kappaB transactivation, anti-apoptotic XIAP up-regulation and caspase suppression.
  • [MeSH-minor] Acute Disease. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antibodies, Monoclonal / pharmacology. Electrophoretic Mobility Shift Assay. Eosinophils / drug effects. Eosinophils / immunology. Fas Ligand Protein / antagonists & inhibitors. Humans. I-kappa B Kinase / antagonists & inhibitors. I-kappa B Kinase / metabolism. Leukemia, Myeloid. Nitriles / pharmacology. Sesquiterpenes / pharmacology. Sulfones / pharmacology. Tumor Cells, Cultured

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  • (PMID = 17349210.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL66026; United States / NHLBI NIH HHS / HL / HL79641
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies, Monoclonal; 0 / BAY 11-7085; 0 / Fas Ligand Protein; 0 / NF-kappa B; 0 / Nitriles; 0 / Sesquiterpenes; 0 / Sulfones; 0 / Tumor Necrosis Factor-alpha; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 2RDB26I5ZB / parthenolide; EC 2.7.11.10 / I-kappa B Kinase
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4. Nishioka C, Ikezoe T, Yang J, Miwa A, Tasaka T, Kuwayama Y, Togitani K, Koeffler HP, Yokoyama A: Ki11502, a novel multitargeted receptor tyrosine kinase inhibitor, induces growth arrest and apoptosis of human leukemia cells in vitro and in vivo. Blood; 2008 May 15;111(10):5086-92
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  • [Title] Ki11502, a novel multitargeted receptor tyrosine kinase inhibitor, induces growth arrest and apoptosis of human leukemia cells in vitro and in vivo.
  • Ki11502 (0.1-1 nM, 2 days) profoundly caused growth arrest, G(0)/G(1) cell-cycle arrest, and apoptosis associated with down-regulation of Bcl-2 family proteins in the eosinophilic leukemia EOL-1 cells having the activated FIP1-like 1/PDGFRalpha fusion gene.
  • In addition, Ki11502 inhibited proliferation of biphenotipic leukemia MV4-11 and acute myelogenous leukemia MOLM13 and freshly isolated leukemia cells having activating mutations in FMS-like tyrosine kinase 3 (FLT3).
  • Taken together, Ki11502 has profound antiproliferative effects on select subsets of leukemia including those possessing imatinib-resistant mutation.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Leukemia / drug therapy. Protein Kinase Inhibitors / pharmacology. Quinolines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 18309036.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ki11502; 0 / Protein Kinase Inhibitors; 0 / Quinolines; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC2384135
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5. Goiriz R, Guhl-Millán G, Peñas PF, Fernández-Herrera J, Daudén E, Fraga J, García-Diez A: Eosinophilic folliculitis following allogeneic peripheral blood stem cell transplantation: case report and review. J Cutan Pathol; 2007 Dec;34 Suppl 1:33-6
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  • [Title] Eosinophilic folliculitis following allogeneic peripheral blood stem cell transplantation: case report and review.
  • Eosinophilic folliculitis is considered a heterogeneous group of disorders, with several clinical subsets, sharing a common histopathological appearance.
  • We herein present a case of eosinophilic folliculitis that appeared in a 26-year-old woman 5 months after allogeneic peripheral blood stem cell transplantation as treatment for eosinophilic acute leukemia.
  • Our review of the published cases has shown that eosinophilic folliculitis in patients after BMT could be considered as a pattern of reaction related to immune dysregulation.
  • [MeSH-minor] Adult. Anti-Inflammatory Agents / therapeutic use. Female. Humans. Leukemia, Eosinophilic, Acute / therapy. Prednisone / therapeutic use. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17997736.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; VB0R961HZT / Prednisone
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6. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • Patients with PCM1-JAK2 disease are attractive candidates for targeted signal transduction therapy.
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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7. Kamineni P, Baptiste A, Hassan M, Dawkins FW, Zaidi S, Tefferi A, Lindsey M, Taddesse-Heath L: Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C. J Natl Med Assoc; 2006 Aug;98(8):1356-60
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  • [Title] Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C.
  • Chronic eosinophilic leukemia is a rare entity, characterized by eosinophilia of >1.5 x 10(9)/L, persisting for >6 months after exclusion of other reactive and neoplastic causes of eosinophilia, and occurring in association with a clonal cytogenetic abnormality.
  • Various chromosomal abnormalities have been associated with chronic eosinophilic leukemia.
  • Partial deletion of the long arm of chromosome 16 is a cytogenetic abnormality first reported 20 years ago in patients with acute myeloid leukemia associated with bone marrow eosinophilia (AML-M4Eo).
  • To our knowledge, this is the first case report of isolated del (16) (q22), a cytogenetic abnormality associated with AML-M4Eo, occurring in chronic eosinophilic leukemia.
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 16916138.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2569582
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8. Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS: Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up. Chang Gung Med J; 2006 Sep-Oct;29(5):532-7
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  • [Title] Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
  • Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.
  • It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).
  • Marrow aspiration showed 47% blasts and 33% eosinophils, of which 19% were morphologically abnormal with both eosinophilic and basophilic cytoplasmic granules.
  • [MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 17214400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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9. Aissi K, Rossi P, Le TB, Granel B, Bagnères D, Demoux AL, Bonin-Guillaume S, Costello R, Sebahoun G, Francès Y: [Necrotic myocarditis in acute eosinophilic lymphoblastic leukaemia]. Rev Med Interne; 2006 Nov;27(11):869-73
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  • [Title] [Necrotic myocarditis in acute eosinophilic lymphoblastic leukaemia].
  • The association between an acute lymphoblastic leukemia and hypereosinophilia was rare.
  • We report a case of a 29-year-old man who presented a heart failure secondary to necrotic myocarditis related to an acute eosinophilic lymphoblastic leukaemia.
  • The myelogram cytology showed precursor B-cell acute lymphoblastic leukaemia with hypereosinophilia.


10. Chrobák L, Voglová J: [The idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia]. Vnitr Lek; 2005 Dec;51(12):1385-93
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  • [Title] [The idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia].
  • [Transliterated title] Idiopatický hypereozinofilni syndrom a chronická eozinofilní leukemie (diferentiální diagnóza a terapie ve svetle nových poznatků).
  • HES has to be reclassified as chronic eosinophilic leukemia (CEL) when there is evidence for clonality based on the presence of chromosomal abnormalities or inactivation of X-chromosome in female patients.
  • The only exception is an acute left ventricular dysfunction which has been reported in three patients within the first week of treatment with imatinib.
  • Imatinib has been successfully used also in some patients with the constitutively activated thyrosine kinase ETV6-PDGFRbeta [1] and in systemic mast cell disease associated with eosinophilia.
  • [MeSH-minor] Chronic Disease. Humans


11. Wakabayashi S, Yamamoto K, Arai A, Miura O: [Chronic eosinophilic leukemia with complex karyotypic abnormalities including trisomy 8]. Rinsho Ketsueki; 2008 Jul;49(7):510-5
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  • [Title] [Chronic eosinophilic leukemia with complex karyotypic abnormalities including trisomy 8].
  • We report a 61-year-old man with chronic eosinophilic leukemia (CEL).
  • Although he had no obvious organ damage at diagnosis, pulmonary infiltrates in the right lung and multiple skin nodules over his whole body appeared over 4 months and progressed rapidly, accompanied by a marked increase in blasts in his peripheral blood.
  • CEL with trisomy 8 has been reported to be associated with transformation into acute leukemia and granulocytic sarcoma in the literature.
  • It is notable that the present case was associated with complex karyotypic abnormalities and the exceptionally marked disease progression.
  • Further analyses of clinical data as well as molecular genetic findings of CEL without known karyotypic abnormalities leading to constitutive activation of tyrosine-kinase genes are needed to gain insight into the pathogenesis of CEL and to develop a new disease classification and treatment strategies.
  • [MeSH-minor] Chronic Disease. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 18709984.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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12. Horigome H, Sumazaki R, Iwasaki N, Imoto N, Kinugasa H, Saito M, Matsui A: Fatal eosinophilic heart disease in a child with neurofibromatosis-1 complicated by acute lymphoblastic leukemia. Heart Vessels; 2005 May;20(3):120-2
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  • [Title] Fatal eosinophilic heart disease in a child with neurofibromatosis-1 complicated by acute lymphoblastic leukemia.
  • We present a pediatric case of neurofibromatosis-1 (NF-1) complicated by acute lymphoblastic leukemia and hypereosinophilia, which caused multiple end-organ damage.
  • When eosinophilia is diagnosed in patients with NF-1, eosinophilic end-organ damage, particularly cardiac involvement, in addition to hematological malignancies, should be screened for in order to start medical treatment at the early stage of the disease.
  • [MeSH-major] Hypereosinophilic Syndrome / complications. Neurofibromatosis 1 / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


13. Lichtman MA, Segel GB: Uncommon phenotypes of acute myelogenous leukemia: basophilic, mast cell, eosinophilic, and myeloid dendritic cell subtypes: a review. Blood Cells Mol Dis; 2005 Nov-Dec;35(3):370-83
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  • [Title] Uncommon phenotypes of acute myelogenous leukemia: basophilic, mast cell, eosinophilic, and myeloid dendritic cell subtypes: a review.
  • The potential of the transformed (leukemic) multipotential hematopoietic cell to differentiate and mature along any myeloid lineage forms the basis for the phenotypic classification of acute and chronic myelogenous leukemia.
  • Although most cases of leukemia can be classified phenotypically by the dominant lineage expressed, the genotype within each phenotype is heterogeneous.
  • The least common AML phenotypes are a reflection of the least common blood or marrow cell lineages: acute basophilic, acute mast cell, acute eosinophilic, and acute myeloid dendritic cell leukemia.
  • We discuss the features of these uncommon phenotypes and review the criteria used for their diagnosis.
  • [MeSH-major] Basophils / pathology. Dendritic Cells / pathology. Eosinophils / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mast Cells / pathology. Myeloid Cells / pathology


14. Cools J: Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia. Verh K Acad Geneeskd Belg; 2010;72(1-2):55-70
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  • [Title] Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia.
  • Insights into these mechanisms may help us to design novel strategies to treat leukemia.
  • Sorafenib was originally developed as a BRAF inhibitor, but our work demonstrates that sorafenib can also be used to treat FIP1L1-PDGFRA positive leukemia, demonstrating that new therapies to treat rare leukemias may be simply found by testing drugs that are already in use for the treatment of other diseases.
  • [MeSH-major] Hypereosinophilic Syndrome / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 20726440.001).
  • [ISSN] 0302-6469
  • [Journal-full-title] Verhandelingen - Koninklijke Academie voor Geneeskunde van België
  • [ISO-abbreviation] Verh. K. Acad. Geneeskd. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / mRNA Cleavage and Polyadenylation Factors; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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15. Khémiri M, Ouederni M, Ben Mansour F, Ben Jaballah N, Barsaoui S: [Acute respiratory failure revealing an idiopathic acute eosinophilic pneumonia: report of a pediatric case]. Ann Fr Anesth Reanim; 2008 Jun;27(6):502-4
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  • [Title] [Acute respiratory failure revealing an idiopathic acute eosinophilic pneumonia: report of a pediatric case].
  • [Transliterated title] Insuffisance respiratoire aiguë révélant un poumon aigu éosinophile idiopathique: à propos d'une observation pédiatrique.
  • Eosinophilic pneumonias are a group of heterogeneous disorders, rarely reported in children.
  • We describe a case of a 12-year-old boy hospitalized for an acute febrile respiratory failure.
  • A pulmonary eosinophilic infiltration was confirmed by a major blood eosinophilia at 33,800/mm(3) associated with increased eosinophilic rate (90%) on bronchoalveolar lavage fluid.
  • Laboratory screenings for parasitic or allergic disease were negative.
  • Bone marrow smear and medullar caryotype eliminated an acute leukemia.
  • No further visceral eosinophilic injury were found.
  • Acute eosinophilic pneumonia should be included in etiological investigation of patients with acute respiratory distress syndrome (ARDS) even in young subjects.
  • [MeSH-major] Pulmonary Eosinophilia / diagnosis. Respiratory Insufficiency / etiology
  • [MeSH-minor] Child. Humans. Male. Radiography, Thoracic. Respiration, Artificial. Respiratory Distress Syndrome, Adult / diagnosis. Respiratory Distress Syndrome, Adult / therapy. Treatment Outcome


16. Rajesh G, Sadasivan S, Hiran KR, Nandakumar R, Balakrishnan V: Acute myeloid leukemia presenting as obstructive jaundice. Indian J Gastroenterol; 2006 Mar-Apr;25(2):93-4
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  • [Title] Acute myeloid leukemia presenting as obstructive jaundice.
  • We report a 32-year-old man with acute myeloid leukemia presenting as obstructive jaundice.
  • On evaluation he was found to have the eosinophilic variant of M4 subtype acute myeloid leukemia.
  • [MeSH-minor] Adult. Common Bile Duct Diseases / complications. Humans. Leukemia, Myeloid, Acute / complications. Male

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  • (PMID = 16763341.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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17. Pardanani A, Tefferi A: Primary eosinophilic disorders: a concise review. Curr Hematol Malig Rep; 2008 Jan;3(1):37-43
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  • [Title] Primary eosinophilic disorders: a concise review.
  • Primary eosinophilic disorders include hypereosinophilic syndrome (HES); chronic eosinophilic leukemia, not otherwise categorized (CEL-NOC); platelet-derived growth factor receptor (PDGFR)-rearranged myeloid neoplasms; and other myeloid malignancies associated with prominent blood eosinophilia.
  • According to the World Health Organization consensus criteria, the diagnosis of HES requires the absence of clonal cytogenetic or molecular markers of an underlying myeloid or lymphoid neoplasm.
  • HES and CEL-NOC are considered distinct from molecularly defined eosinophilic disorders, such as those associated with activating mutations of PDGFR (PDGFRA and PDGFRB) and fibroblast growth factor receptor-1.
  • This is an important distinction because PDGFR-mutated but not other eosinophilic neoplasms are effectively treated with imatinib.
  • Current management in HES includes observation only for asymptomatic patients with no evidence of organ damage, systemic corticosteroid therapy for acute control of symptoms, and interferon-alfa-2a or hydroxyurea as steroid-sparing agents.
  • In patients with HES who are refractory to usual therapy and have life-threatening disease complications, the use of investigational drugs such as alemtuzumab or mepolizumab might be considered, but data on long-term efficacy and safety are limited.
  • [MeSH-minor] Humans. Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / pathology. Receptors, Platelet-Derived Growth Factor / genetics

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  • (PMID = 20425445.001).
  • [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
  • [Chemical-registry-number] EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Number-of-references] 69
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18. Walz C, Curtis C, Schnittger S, Schultheis B, Metzgeroth G, Schoch C, Lengfelder E, Erben P, Müller MC, Haferlach T, Hochhaus A, Hehlmann R, Cross NC, Reiter A: Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene. Genes Chromosomes Cancer; 2006 Oct;45(10):950-6
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  • [Title] Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene.
  • Here we report a female patient who presented with advanced phase of a chronic eosinophilic leukemia.
  • Despite achieving complete cytogenetic and molecular remission on imatinib, the patient relapsed with imatinib-resistant acute myeloid leukemia that was characterized by a normal karyotype, absence of detectable CDK5RAP2-PDGFRA mRNA, and a newly acquired G12D NRAS mutation.
  • [MeSH-minor] Aged. Amino Acid Sequence. Base Sequence. Benzamides. Chronic Disease. DNA Mutational Analysis. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Intracellular Signaling Peptides and Proteins / genetics. Molecular Sequence Data. Nerve Tissue Proteins / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor alpha / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16845659.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CDK5RAP2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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19. Tashiro H, Shirasaki R, Noguchi M, Gotoh M, Kawasugi K, Shirafuji N: Molecular analysis of chronic eosinophilic leukemia with t(4;10) showing good response to imatinib mesylate. Int J Hematol; 2006 Jun;83(5):433-8
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  • [Title] Molecular analysis of chronic eosinophilic leukemia with t(4;10) showing good response to imatinib mesylate.
  • A 38-year-old Japanese man was referred to our hospital in June 2003 for treatment of acute respiratory failure with severe eosinophilia.
  • However, karyotypic examination of bone marrow cells revealed that chromosomal translocation with t(4;10)(q12;p11) had occurred in 2000, and chronic eosinophilic leukemia was diagnosed.
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. Benzamides. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 4 / genetics. Chronic Disease. Enzyme Activation / drug effects. Eosinophilia / drug therapy. Eosinophilia / enzymology. Eosinophilia / genetics. Follow-Up Studies. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Imatinib Mesylate. Leukocyte Count. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Time Factors. Translocation, Genetic / genetics

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  • (PMID = 16787876.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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20. Nemoto T, Saito Y, Tokuhira M, Tomikawa A, Sagawa M, Haba Y, Hanzawa K, Sekiguchi Y, Watanabe R, Tamaru J, Itoyama S, Mori S, Kizaki M: [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy]. Rinsho Ketsueki; 2010 May;51(5):326-31
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  • [Title] [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy].
  • As plural effusion due to the underlying disease progressively worsened, she was given prednisolone and hydroxyurea, but the effect was limited.
  • The WBC count rapidly decreased, but tumor lysis syndrome led to acute renal failure and disseminated intravasucular coagulation appeared.
  • [MeSH-major] Leukemia, Eosinophilic, Acute / complications. Leukemia, Eosinophilic, Acute / drug therapy. Methylprednisolone / adverse effects. Piperazines / adverse effects. Pyrimidines / adverse effects. Tumor Lysis Syndrome / etiology
  • [MeSH-minor] Acute Kidney Injury / etiology. Aged, 80 and over. Benzamides. Disseminated Intravascular Coagulation / etiology. Drug Synergism. Fatal Outcome. Female. Humans. Hypereosinophilic Syndrome / complications. Imatinib Mesylate. Pleural Effusion / etiology. Pulse Therapy, Drug

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  • (PMID = 20534953.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X4W7ZR7023 / Methylprednisolone
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21. Yoshimi M, Nannya Y, Watanabe T, Asai T, Ichikawa M, Yamamoto G, Kumano K, Hangaishi A, Imai Y, Takahashi T, Chiba S, Kurokawa M: Acute eosinophilic pneumonia is a non-infectious lung complication after allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Mar;89(2):244-8
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  • [Title] Acute eosinophilic pneumonia is a non-infectious lung complication after allogeneic hematopoietic stem cell transplantation.
  • Acute eosinophilic pneumonia (AEP) is an acute febrile illness with respiratory impairment, diffuse pulmonary infiltrates, and eosinophilia in bronchoalveolar lavage (BAL) fluid.
  • We made a diagnosis of AEP and steroid was started.
  • [MeSH-minor] Graft vs Host Disease / pathology. Humans. Leukemia / complications. Leukemia / therapy. Male. Middle Aged. Pneumonia. Transplantation, Homologous

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  • (PMID = 19132457.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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22. Schaffer JV, McNiff JM, Seropian S, Cooper DL, Bolognia JL: Lichen sclerosus and eosinophilic fasciitis as manifestations of chronic graft-versus-host disease: expanding the sclerodermoid spectrum. J Am Acad Dermatol; 2005 Oct;53(4):591-601
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  • [Title] Lichen sclerosus and eosinophilic fasciitis as manifestations of chronic graft-versus-host disease: expanding the sclerodermoid spectrum.
  • Chronic cutaneous graft-versus-host disease (GVHD) is classically divided into two major clinical categories--lichenoid and sclerodermoid.
  • Eosinophilic fasciitis (EF) (a fibrosing disorder related to deep morphea) and lichen sclerosus (LS) have also been reported as manifestations of sclerodermoid GVHD.
  • EF involved the extremities (sparing the hands and feet), and was characterized clinically by an acute onset of pain and edema followed by induration with a rippled appearance.
  • [MeSH-major] Eosinophilia / etiology. Fasciitis / etiology. Graft vs Host Disease / complications. Lichen Sclerosus et Atrophicus / etiology
  • [MeSH-minor] Adult. Chronic Disease. Female. Humans. Leukemia, Myeloid, Acute / surgery. Lymphoma, Large B-Cell, Diffuse / surgery. Magnetic Resonance Imaging. Male. Middle Aged. Remission Induction. Stem Cell Transplantation


23. Doki N, Hoshino T, Irisawa H, Sakura T, Miyawaki S: [Acute myeloid leukemia complicated with pulmonary alveolar proteinosis at presentation]. Rinsho Ketsueki; 2005 Jul;46(7):522-6
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  • [Title] [Acute myeloid leukemia complicated with pulmonary alveolar proteinosis at presentation].
  • Following the results obtained from a bone marrow aspiration, he was diagnosed as having acute myeloid leukemia (AML).
  • Although the autopsy findings revealed no infectious lesions in his lungs, a PAS-positive intra-alveolar eosinophilic material, which was positive for surfactant apoprotein A staining, was present.
  • As a result of the autopsy findings, a diagnosis of secondary pulmonary alveolar proteinosis (PAP) associated with AML was made.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Pulmonary Alveolar Proteinosis / etiology

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  • (PMID = 16440746.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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24. Moralidis E, Papakonstantinou E, Arsos G, Boussios N, Koliouskas D, Karakatsanis C: Tc-99m HMPAO labeled white blood cell imaging in a child with eosinophilic lung disease. Clin Nucl Med; 2008 Jan;33(1):38-40
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  • [Title] Tc-99m HMPAO labeled white blood cell imaging in a child with eosinophilic lung disease.
  • In radiolabeled leukocyte imaging, Tc-99m HMPAO has a significantly higher selectivity for eosinophils than neutrophils, but this may be clinically meaningful in disorders with eosinophilic infiltration.
  • We present the case of a 2-year-old boy with infection who also developed drug-induced eosinophilic lung disease, as established later by bronchoalveolar lavage and discontinuation of the responsible antistaphylococcal agent.
  • These findings were consistent with eosinophilic lung infiltration and underline the importance of clinical and laboratory data in the comprehensive interpretation of Tc-99m HMPAO labeled leukocytes scans.
  • [MeSH-minor] Acetamides / adverse effects. Anti-Infective Agents / adverse effects. Child, Preschool. Humans. Leukemia, Myeloid, Acute / complications. Leukocytes. Linezolid. Magnetic Resonance Imaging. Male. Oxazolidinones / adverse effects. Staphylococcal Infections / drug therapy

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  • (PMID = 18097257.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetamides; 0 / Anti-Infective Agents; 0 / Oxazolidinones; 0 / Radiopharmaceuticals; 3B744AG22N / Technetium Tc 99m Exametazime; ISQ9I6J12J / Linezolid
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25. Ma Y, Tong HX, Deng X, Zhao Y, Liu ZG, Zhang JH: [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):12-6
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  • [Title] [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)].
  • This study was purposed to investigate the acute myeloid leukemia with complex karyotype t(2;21;8)(p12;q22;q22) (AML-M(2)) by using morphologic, immunologic, cytogenetic and molecular biologic classification technique (MICM) and to analyze the MICM characteristics of AML-M(2) and their diagnostic significance.
  • The results indicated that the bone marrow smears of case 1 showed extremely hyperplasia with myeloblasts in which a ratio of eosinophilic granulocytes and monocytes increased.

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  • (PMID = 19236738.001).
  • [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
  • [Publication-country] China
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26. Marchesi F, Minucci S, Pelicci PG, Gobbi A, Scanziani E: Immunohistochemical detection of Ym1/Ym2 chitinase-like lectins associated with hyalinosis and polypoid adenomas of the transitional epithelium in a mouse with acute myeloid leukemia. Vet Pathol; 2006 Sep;43(5):773-6
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  • [Title] Immunohistochemical detection of Ym1/Ym2 chitinase-like lectins associated with hyalinosis and polypoid adenomas of the transitional epithelium in a mouse with acute myeloid leukemia.
  • An 8-month-old PML/RARalpha knock-in female mouse developed a promyelocytic-like myeloid leukemia with an expected latency.
  • At necropsy, besides the typical findings associated with myeloid leukemia, a severe unilateral hydronephrosis was observed.
  • The epithelial cells of the polypoid adenomas showed accumulation of hyaline eosinophilic material within the cytoplasm.
  • Large amounts of extracellular eosinophilic crystals were also associated with the transitional cell adenomas.
  • Immunohistochemical analysis revealed that the eosinophilic intracytoplasmic material and the extracellular eosinophilic crystals were composed of Ym proteins.
  • A unilateral hyaline droplet tubular nephropathy was associated with the myeloid leukemia.
  • In the present PML/RARalpha knock-in female mouse, the accumulation of Ym proteins associated with the myeloid leukemia and with the polypoid adenomas of the transitional epithelium underlies 2 distinct pathogenetic mechanisms.
  • [MeSH-major] Adenoma / metabolism. Epithelium / metabolism. Glomerulosclerosis, Focal Segmental / metabolism. Lectins / metabolism. Leukemia, Myeloid, Acute / metabolism


27. Sadler GM, Halbert AR, Smith N, Rogers M: Trichodysplasia spinulosa associated with chemotherapy for acute lymphocytic leukaemia. Australas J Dermatol; 2007 May;48(2):110-4
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  • [Title] Trichodysplasia spinulosa associated with chemotherapy for acute lymphocytic leukaemia.
  • We report two boys with trichodysplasia spinulosa associated with chemotherapy for acute lymphocytic leukaemia.
  • Histopathology demonstrated hair follicles dilated by a proliferation of large eosinophilic cells containing numerous abnormal trichohyaline granules.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hair Diseases / chemically induced. Hair Follicle / virology. Immunocompromised Host. Immunosuppressive Agents / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17535200.001).
  • [ISSN] 0004-8380
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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28. Nishioka C, Ikezoe T, Yang J, Yokoyama A: Long-term exposure of leukemia cells to multi-targeted tyrosine kinase inhibitor induces activations of AKT, ERK and STAT5 signaling via epigenetic silencing of the PTEN gene. Leukemia; 2010 Sep;24(9):1631-40
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  • [Title] Long-term exposure of leukemia cells to multi-targeted tyrosine kinase inhibitor induces activations of AKT, ERK and STAT5 signaling via epigenetic silencing of the PTEN gene.
  • Imatinib induces complete molecular response in patients with chronic myeloid leukemia (CML) and chronic eosinophilic leukemia (CEL).
  • Notably, hypermethylation of the promoter region of the PTEN gene in association with the downregulation of this gene's transcripts was identified in imatinib-resistant leukemia cells isolated from individuals with CEL, CML and Philadelphia-positive acute lymphoblastic leukemia.
  • Taken together, epigenetic silence of PTEN is one of the mechanisms that cause drug resistance in individuals with leukemia after exposure to imatinib.
  • [MeSH-major] Epigenesis, Genetic. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Silencing. Hypereosinophilic Syndrome / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. PTEN Phosphohydrolase / genetics. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. STAT5 Transcription Factor / metabolism. Signal Transduction

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  • (PMID = 20596030.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Protein Kinase Inhibitors; 0 / STAT5 Transcription Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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29. Verstovsek S, Tefferi A, Cortes J, O'Brien S, Garcia-Manero G, Pardanani A, Akin C, Faderl S, Manshouri T, Thomas D, Kantarjian H: Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis. Clin Cancer Res; 2008 Jun 15;14(12):3906-15
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  • [Title] Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis.
  • Only two patients, one with SM-myelofibrosis and one with SM-chronic eosinophilic leukemia, achieved complete response (elimination of mastocytosis) lasting for 5 and 16 months, respectively.
  • Complete responses were achieved in two other patients (acute myeloid leukemia and hypereosinophilic syndrome).
  • CONCLUSION: These data show that dasatinib therapy may benefit a selected group of SM patients, primarily by improving their symptoms, but it does not eliminate the disease in the patients with KIT-D816V mutation.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Mastocytosis, Systemic / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


30. Hellmann A: Myeloproliferative syndromes: diagnosis and therapeutic options. Pol Arch Med Wewn; 2008 Dec;118(12):756-60
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  • [Title] Myeloproliferative syndromes: diagnosis and therapeutic options.
  • These syndromes include: chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, chronic eosinophilic leukemia/hypereosinophilic syndrome, chronic neutrophilic leukemia and systemic mastocytosis.
  • Diagnosis of MPS is often difficult due to need of differential diagnosis with reactive proliferation caused by primarily non-hematological factors.
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / therapy
  • [MeSH-minor] Bone Marrow. Diagnosis, Differential. Humans. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Erythroblastic, Acute / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Neutrophilic, Chronic / diagnosis. Leukemia, Neutrophilic, Chronic / therapy. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / therapy. Risk Factors. Thrombocytosis / diagnosis. Thrombocytosis / therapy

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  • (PMID = 19202955.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 19
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31. Tefferi A, Skoda R, Vardiman JW: Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics. Nat Rev Clin Oncol; 2009 Nov;6(11):627-37
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  • [Title] Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics.
  • Myeloid neoplasms are now classified into five categories: acute myeloid leukemia, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN, and myeloid and/or lymphoid malignancies associated with eosinophilia and PDGFR or FGFR1 rearrangements.
  • MPN are subclassified into eight separate entities: chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, primary myelofibrosis, systemic mastocytosis, chronic eosinophilic leukemia not otherwise specified, chronic neutrophilic leukemia, and unclassifiable MPN.
  • The diagnosis of chronic myelogenous leukemia requires the presence of BCR-ABL1, while its absence is required for all other MPN.
  • In systemic mastocytosis, presence of KIT D816V is expected but not essential for diagnosis.
  • Chronic eosinophilic leukemia not otherwise specified should be distinguished from both PDGFR-rearranged or FGFR1-rearranged neoplasms and hypereosinophilic syndrome.
  • [MeSH-major] Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Algorithms. Biomarkers, Tumor / genetics. Fusion Proteins, bcr-abl / genetics. Humans. Janus Kinase 2 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / genetics. Polycythemia Vera / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / genetics. World Health Organization

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  • (PMID = 19806146.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 77
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32. Vales A, Kondo R, Aichberger KJ, Mayerhofer M, Kainz B, Sperr WR, Sillaber C, Jäger U, Valent P: Myeloid leukemias express a broad spectrum of VEGF receptors including neuropilin-1 (NRP-1) and NRP-2. Leuk Lymphoma; 2007 Oct;48(10):1997-2007
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  • [Title] Myeloid leukemias express a broad spectrum of VEGF receptors including neuropilin-1 (NRP-1) and NRP-2.
  • We have examined the expression of five VEGF receptors (VEGR1/Flt-1, VEGFR2/KDR, Flt-4, neuropilin-1 = NRP-1, NRP-2) in leukemic cells obtained from patients with acute myeloid leukemia (n = 28), chronic myeloid leukemia (n = 14), chronic eosinophilic leukemia (n = 3), chronic myelomonocytic leukemia (n = 9), or mast cell leukemia/systemic mastocytosis (n = 3) as well as in respective cell lines.
  • In most patients, leukemic cells expressed NRP-1 mRNA and NRP-2 mRNA independent of the type of disease.
  • By contrast, transcripts for Flt-1, KDR, and Flt-4 were expressed variably without a clear correlation to the type of leukemia.
  • In conclusion, neoplastic cells in myeloid leukemias frequently express VEGFR including NRP-1 and NRP-2.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Neovascularization, Pathologic. Neuropilin-1 / biosynthesis. Neuropilin-2 / biosynthesis. Receptors, Vascular Endothelial Growth Factor / biosynthesis

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  • (PMID = 17917967.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neuropilin-2; 0 / RNA, Messenger; 144713-63-3 / Neuropilin-1; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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33. O'Shea AM, Wilson GJ, Ling SC, Minassian BA, Turnbull J, Cutz E: Lafora-like ground-glass inclusions in hepatocytes of pediatric patients: a report of two cases. Pediatr Dev Pathol; 2007 Sep-Oct;10(5):351-7
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  • Case 1 had alpha-thalassaemia major and was receiving iron chelation therapy, whereas case 2 had trisomy 21 with a history of bone marrow transplantation for acute myeloid leukemia.
  • The liver sections in both cases showed eosinophilic, periodic acid-Schiff diastase-positive intracytoplasmic inclusions that were negative for hepatitis B surface antigen.
  • Ultrastructural changes in both cases differed from classical Lafora inclusions and ruled out hepatitis B surface antigen, glycogenosis type IV, and fibrinogen storage disease.
  • Genetic analysis of the Lafora's disease genes performed in case 2 revealed no mutations.
  • Drug-induced inclusions, mimicking Lafora's disease, should be included in the differential diagnosis of hepatocyte ground-glass inclusions.
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Transplantation. Child, Preschool. Diagnosis, Differential. Down Syndrome. Humans. Immunohistochemistry. Iron. Lafora Disease / pathology. Leukemia, Myeloid, Acute / therapy. Male. Microscopy, Electron, Transmission. alpha-Thalassemia / drug therapy

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  • (PMID = 17929993.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; E1UOL152H7 / Iron; J06Y7MXW4D / Deferoxamine
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34. Panigrahi I, Naithani R: Imatinib mesylate: A designer drug. J Assoc Physicians India; 2006 Mar;54:203-6
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  • Imatinib, a specific tyrosine kinase inhibitor, since its inception in 1990s, has become the first-line drug in management of chronic myelogenous leukemia (CML) chronic phase.
  • It has also shown promising results in treatment of gastro-intestinal stromal tumors, clonal eosinophilic disorders and Philadelphia chromosome positive acute lymphatic leukemia.
  • [MeSH-minor] Benzamides. Eosinophilia / drug therapy. Gastrointestinal Stromal Tumors / drug therapy. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16800347.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 31
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35. Tefferi A, Gilliland G: Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system. Best Pract Res Clin Haematol; 2006;19(3):365-85
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  • In turn, myeloid malignancies are broadly categorized into either acute myeloid leukemia (AML) or chronic myeloid disorder (CMD), depending on the presence or absence, respectively, of AML-defining cytomorphologic and cytogenetic features.
  • It has now become evident that most CMD represent clonal stem cell processes where the primary oncogenic event has been characterized in certain instances; Bcr/Abl in chronic myeloid leukemia, FIP1L1-PDGFRA or c-kit(D816V) in systemic mastocytosis, rearrangements of PDGFRB in chronic eosinophilic leukemia, and rearrangements of FGFR1 in stem cell leukemia/lymphoma syndrome.
  • In addition, Bcr/Abl-negative classic myeloproliferative disorders are characterized by recurrent JAK2(V617F) mutations, whereas other mutations affecting the RAS signaling pathway molecules have been associated with juvenile myelomonocytic leukemia.
  • [MeSH-minor] Fusion Proteins, bcr-abl / genetics. Genes, abl. Humans. Janus Kinase 2. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / classification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

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  • (PMID = 16781478.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 232
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36. Bain BJ: Clinical applications of molecular haematology: an overview. J Assoc Physicians India; 2007 Jul;55:503-6
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  • The molecular understanding has helped in fine-tuning the diagnosis, prognosis and management.
  • Following is an overview of clinical applications of molecular haematology, especially in the field of chronic myeloid leukaemia, chronic eosinophilic leukaemia, bcr abl negative chronic myeloproliferative disorders and acute promyelocytic leukaemia.
  • [MeSH-minor] Humans. Hypereosinophilic Syndrome / diagnosis. Janus Kinase 2 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Promyelocytic, Acute. Molecular Biology. Myeloproliferative Disorders / diagnosis. Prognosis

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  • (PMID = 17907501.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 16
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37. Ikezoe T, Nishioka C, Tasaka T, Yang Y, Komatsu N, Togitani K, Koeffler HP, Taguchi H: The antitumor effects of sunitinib (formerly SU11248) against a variety of human hematologic malignancies: enhancement of growth inhibition via inhibition of mammalian target of rapamycin signaling. Mol Cancer Ther; 2006 Oct;5(10):2522-30
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  • We studied antitumor effects of receptor tyrosine kinase inhibitor sunitinib (formerly SU11248) against a variety of hematologic malignancies including the following leukemias: eosinophilic (EOL-1), acute myeloid (THP-1, U937, Kasumi-1), biphenotypic (MV4-11), acute lymphoblastic (NALL-1, Jurkat, BALL-2, PALL-1, PALL-2), blast crisis of chronic myeloid (KU812, Kcl-22, K562), and adult T-cell (MT-1, MT-2, MT-4), as well as non-Hodgkin's lymphoma (KS-1, Dauji, Akata) and multiple myeloma (U266).
  • In addition, sunitinib inhibited the proliferation of freshly isolated leukemia cells from patients possessing mutations in FLT3 gene.
  • Interestingly, rapamycin analogue RAD001 enhanced the ability of sunitinib to inhibit the proliferation of leukemia cells and down-regulate levels of mammalian target of rapamycin effectors p70 S6 kinase and eukaryotic initiation factor 4E-binding protein 1 in these cells.
  • Taken together, sunitinib may be useful for treatment of individuals with leukemias possessing activation mutation of tyrosine kinase, and the combination of sunitinib and RAD001 represents a promising novel treatment strategy.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Adaptor Proteins, Signal Transducing / biosynthesis. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Everolimus. Humans. Leukemia / metabolism. Leukemia / pathology. Mutation. Phosphoproteins / antagonists & inhibitors. Phosphoproteins / biosynthesis. Receptor Protein-Tyrosine Kinases / genetics. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / biosynthesis. Signal Transduction. Sirolimus / analogs & derivatives. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 17041096.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / EIF4EBP1 protein, human; 0 / Indoles; 0 / Phosphoproteins; 0 / Pyrroles; 0 / sunitinib; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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38. Gérard J, Berdin B, Portier G, Godon A, Tessier-Marteau A, Geneviève F, Zandecki M: [Bone marrow necrosis in two patients with neoplastic disorders]. Ann Biol Clin (Paris); 2007 Nov-Dec;65(6):636-42
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  • Diagnosis is done on characteristic cytological pattern of the bone marrow aspiration and/or biopsy.
  • An haematological malignancy was suspected after observation of a few peripheral blood blast cells, but necrosis was found on the bone marrow aspiration and could not lead to further haematological diagnosis.
  • Within next days, the white blood cell count and the number of blasts increased, leading to the diagnosis of acute monoblastic leukaemia.
  • The second patient, aged 28, has been hospitalized for severe bleeding a few days after the diagnosis of a metastatic gastric tumour.
  • According to literature, bone marrow necrosis is in most instances secondary to either an haematological malignancy (60%) or to a solid tumour (30%), but only at times observed with a non-malignant disorder.
  • Bone pain, fever, cytopenias and elevated serum lactic dehydrogenase and alkaline phosphatase are frequently reported, but are mostly non specific of the diagnosis in these malignant conditions.
  • Examination of the bone marrow leads to the diagnosis: cells are pycnotic, scarcely recognizable in a background of amorphous extracellular eosinophilic proteinaceous material, and histology shows disappearance of fat spaces with preservation of the bone tissue.
  • Tissue hypoxemia due to microcirculation failure may be the main mechanism leading to the necrosis, whatever the related disorder.
  • Supportive care together with specific therapy of the causal disease must be started promptly.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Monocytic, Acute / pathology. Stomach Neoplasms / pathology

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  • (PMID = 18039608.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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39. Tefferi A, Elliott MA, Pardanani A: Atypical myeloproliferative disorders: diagnosis and management. Mayo Clin Proc; 2006 Apr;81(4):553-63
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  • [Title] Atypical myeloproliferative disorders: diagnosis and management.
  • The World Health Organization system for classification of tumors of the hematopoietic system divides myeloid disorders into acute myeloid leukemia and chronic myeloid disorders based on the presence or absence, respectively, of acute myeloid leukemia--defining morphological and cytogenetic features including the presence of 20% or more myeloblasts in either the bone marrow or the peripheral blood.
  • Classic MPD includes polycythemia vera, essential thrombocythemia, myelofibrosis with myeloid metaplasia, and chronic myeloid leukemia.
  • The current review focuses on the diagnosis and treatment of both molecularly defined and clinicopathologically assigned categories of atypical MPD: chronic myelomonocytic leukemia, juvenile myelomonocytic leukemia, chronic neutrophilic leukemia, chronic basophilic leukemia, chronic eosinophilic leukemia, idiopathic eosinophilia including hypereosinophilic syndrome, systemic mastocytosis, unclassified MPD, and eosinophilic/mast cell disorders associated with mutations of platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB), FGFR1, and KIT.
  • [MeSH-minor] Biomarkers, Tumor / genetics. Bone Marrow / pathology. Diagnosis, Differential. Humans

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  • (PMID = 16610578.001).
  • [ISSN] 0025-6196
  • [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 / Biomarkers, Tumor
  • [Number-of-references] 173
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40. Niedzielska E, Wójcik D, Barg E, Pietras W, Sega-Pondel D, Doroszko A, Niedzielska M, Skarzyńska M, Chybicka A: [Evaluation of selected endocrine complications in patients treated with auto- and allo-haematopoietic stem cell transplantation]. Med Wieku Rozwoj; 2008 Jul-Sep;12(3):761-6
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  • MATERIAL AND METHODS: The investigated group consisted of: I. 16 patients after auto-HSCT (6 girls, 10 boys) aged 3-20 years (average 10,8+/-) because of acute myelogenous leukaemia (n=5), non Hodgkin lymphoma (n=3), neuroblastoma (n=3), embryonal cancer (n=2), medulloblastoma (n=1), Ewing's sarcoma/PNET (n=1), hyper eosinophilic syndrome (n=1).
  • Indication for HSCT was acute lymphoblastic leukaemia (n=11), acute myelogenous leukaemia (n=5), chronic myeloid leukaemia-CML (n=6), myelodysplastic syndromes (n=2), non Hodgkin lymphoma (n=1), juvenile myelomonocytic leukemia (n=1), severe aplastic anaemia (n=1), Blackfan-Diamond anaemia (n=1), severe combined immune deficiency (n=1), rhabdomyosarcoma (n=1).
  • [MeSH-major] Endocrine System Diseases / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia / therapy


41. Zhang Y, He Q, Huang XJ, Jiang H, Yang SM, Lu J, Qing YZ, Shi Y, Dang H, Qiu JY, Lu DP: [Cytogenetic study on eosinophilia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):454-7
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  • The aim of study was to investigate the importance of chromosome aberration in differential diagnosis of eosinophilia and the chromosomal aberrations involved in patients with clonal eosinophilia.
  • Combining clinical, hematological and cytogenetical data, the 5 patients were diagnosed as acute myeloid leukemia with eosinophilia, chronic eosinophilic leukemia, 8p11 myeloproliferative syndrome, chronic myeloid leukemia in acute phase and acute myeloid leukemia-M(4Eo) respectively.
  • In conclusion, cytogenetical detection is very important in differential diagnosis of clonal eosinophilic disorders and chronic eosinophilic leukemia, which is suggested to be done routinely in clinic.

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  • (PMID = 17605843.001).
  • [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
  • [Publication-country] China
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42. Bogucka-Kocka A, Smolarz HD, Kocki J: Apoptotic activities of ethanol extracts from some Apiaceae on human leukaemia cell lines. Fitoterapia; 2008 Dec;79(7-8):487-97
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  • [Title] Apoptotic activities of ethanol extracts from some Apiaceae on human leukaemia cell lines.
  • The apoptotic activities of seven ethanol extracts from fruits of seven species of Apiaceae, Eryngium planum, Archangelica officinalis, Pastinaca sativa, Heracleum sibiricum, Carum carvi, Foeniculum vulgare, Levisticum officinale against ML-1--human acute myeloblastic leukaemia, J-45.01--human acute T cell leukaemia, EOL--human eosinophilic leukaemia, HL-60--human Caucasian promyelocytic leukaemia, 1301--human T cell leukaemia lymphoblast, C-8166--human T cell leukaemia, U-266B1--human myeloma, WICL--human Caucasian normal B cell, and H-9--human T cell, were investigated.
  • [MeSH-major] Apiaceae / chemistry. Apoptosis / drug effects. Leukemia / drug therapy. Phytotherapy. Plant Extracts / pharmacology

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  • (PMID = 18672039.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Plant Extracts
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43. Metzelder SK, Reinke C, Walthers EM, Barth P, Vogelmeier C, Neubauer A, Bals R: ["Malignant" ARDS]. Internist (Berl); 2009 Oct;50(10):1272, 1274-7
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  • Acute respiratory failure and the "acute respiratory distress syndrome" (ARDS) are frequent medical conditions in critically ill patients.
  • The first patient was diagnosed with an acute myeloic leukemia M5 (FAB).
  • These case reports show that in addition to the classical causes of ARDS, specific disease entities can mimic this form of respiratory failure.
  • Beside solid cancers and lymphomas, acute and progressive forms of inflammatory, parenchymal lung diseases (such as acute interstitial pneumonitis, acute eosinophilic pneumonia, diffuse alveolar hemorrhagia, and acute hypersensitivity pneumonitis) can manifest with this picture.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Lung Diseases, Interstitial / complications. Lung Diseases, Interstitial / diagnosis. Lung Neoplasms / complications. Lung Neoplasms / diagnosis. Respiratory Distress Syndrome, Adult / diagnosis. Respiratory Distress Syndrome, Adult / etiology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 19562262.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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44. Lavastre V, Chiasson S, Cavalli H, Girard D: Viscum album agglutinin-I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils. Br J Haematol; 2005 Aug;130(4):527-35
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  • [Title] Viscum album agglutinin-I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils.
  • VAA-I was found to induce apoptosis in eosinophilic AML14.3D10 (3D10) cells and that these cells expressed caspases-1, -2, -3, -4, -7, -8, -9 and -10.
  • [MeSH-major] Caspases / metabolism. Cytoskeletal Proteins / metabolism. Leukemia, Myeloid / metabolism. Plant Preparations / pharmacology. Plant Proteins / pharmacology. Toxins, Biological / pharmacology
  • [MeSH-minor] Acute Disease. Apoptosis. Caspase 3. Caspase 8. Cell Line, Tumor. DNA Fragmentation. Eosinophils / metabolism. Gelsolin / analysis. Gelsolin / metabolism. Humans. Laminin / metabolism. Paxillin. Phosphoproteins / analysis. Phosphoproteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Ribosome Inactivating Proteins. Vimentin / analysis. Vimentin / metabolism

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  • (PMID = 16098066.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Gelsolin; 0 / LAMB1 protein, human; 0 / Laminin; 0 / PXN protein, human; 0 / Paxillin; 0 / Phosphoproteins; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Toxins, Biological; 0 / VAA-I protein, Viscum album; 0 / Vimentin; EC 3.2.2.22 / Ribosome Inactivating Proteins; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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45. Roufosse F, Goldman M, Cogan E: Hypereosinophilic syndrome: lymphoproliferative and myeloproliferative variants. Semin Respir Crit Care Med; 2006 Apr;27(2):158-70
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  • Idiopathic hypereosinophilic syndrome is a largely heterogeneous disorder defined as persistent, marked hypereosinophilia of unknown origin complicated by end-organ damage.
  • As far as prognosis of these disease variants is concerned, hypereosinophilic syndrome patients with the FIP1L1-PDGFRalpha fusion gene may develop acute myelogenous (eosinophilic) leukemia, whereas those with clonal interleukin-5-producing T-cells have an increased risk of developing T-cell lymphoma.
  • [MeSH-major] Hypereosinophilic Syndrome / classification. Hypereosinophilic Syndrome / diagnosis. Lymphoproliferative Disorders / diagnosis. Myeloproliferative Disorders / diagnosis

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  • (PMID = 16612767.001).
  • [ISSN] 1069-3424
  • [Journal-full-title] Seminars in respiratory and critical care medicine
  • [ISO-abbreviation] Semin Respir Crit Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CD52 antigen; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Glucocorticoids; 0 / Glycoproteins; 0 / Immunologic Factors; 0 / Interleukin-5; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 70
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46. Qiu Z, Dyer KD, Xie Z, Rådinger M, Rosenberg HF: GATA transcription factors regulate the expression of the human eosinophil-derived neurotoxin (RNase 2) gene. J Biol Chem; 2009 May 8;284(19):13099-109
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  • The transcription factors GATA-1 and GATA-2 have been implicated in promoting differentiation of eosinophilic leukocytes.

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  • (PMID = 19279013.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ FJ785402
  • [Grant] United States / NIAID NIH HHS / AI / AI00941; United States / NIAID NIH HHS / AI / AI00942; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.1.- / Eosinophil-Derived Neurotoxin; EC 3.1.27.5 / RNASE2 protein, human
  • [Other-IDs] NLM/ PMC2676042
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47. Chu KH, Lee CC, Hsin SC, Cai BC, Wang JH, Chiang BL: Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma. Cell Mol Immunol; 2010 Sep;7(5):375-80
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  • The clinical hallmarks of asthma include elevated serum levels of immunoglobulin E (IgE), eosinophilic inflammation and airway hyper-responsiveness (AHR).
  • Today, As2O3 is used as one of the standard therapies for acute promyelocytic leukemia (APL).
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bronchoalveolar Lavage Fluid / immunology. Cells, Cultured. Disease Models, Animal. Female. Immunoglobulin E / blood. Interleukin-5 / immunology. Mice. Mice, Inbred BALB C

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  • (PMID = 20495578.001).
  • [ISSN] 2042-0226
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Interleukin-5; 0 / Oxides; 37341-29-0 / Immunoglobulin E; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4002675
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48. González-Vela MC, Val-Bernal JF, Mayorga M, Cagigal ML, Fernández F, Mazorra F: Myeloid sarcoma of the extrahepatic bile ducts presenting as obstructive jaundice. APMIS; 2006 Sep;114(9):666-8
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  • We report a rare case of myeloid sarcoma (MS) of the extrahepatic bile ducts presenting as obstructive jaundice in a patient without leukemia at time of diagnosis.
  • These cells exhibited medium-sized round nuclei with central nucleoli and eosinophilic cytoplasm, and were strongly positive for myeloperoxidase, CD68, lysozyme, CD45, CD117 (c-kit protein) and CD43.
  • Eight months following surgery the patient presented with multiple cutaneous nodules and bone marrow trephine biopsy showed acute myelomonocytic leukemia.
  • MS should be taken into consideration in the differential diagnosis of a patient with obstructive jaundice.
  • Immunohistochemistry is essential for a correct diagnosis.

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  • (PMID = 16948823.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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49. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
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  • Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes.
  • Treatment of hypereosinophilic patients depends on the variant of disease, presence of end organ damage, molecular targets, and the overall situation in each case.
  • [MeSH-major] Eosinophilia / diagnosis. Eosinophilia / drug therapy. Eosinophils / metabolism. Myeloproliferative Disorders / complications

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  • (PMID = 19246139.001).
  • [ISSN] 1532-1681
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 74
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50. Vega F, Medeiros LJ, Davuluri R, Cromwell CC, Alkan S, Abruzzo LV: t(8;13)-positive bilineal lymphomas: report of 6 cases. Am J Surg Pathol; 2008 Jan;32(1):14-20
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  • Approximately 75% of EMS patients present with or develop precursor T-cell lymphoblastic lymphoma, and most subsequently develop acute myeloid leukemia.
  • Histologically, each tumor was composed of 2 distinct cellular components: small to medium-sized T cells with scant cytoplasm that resembled lymphoblasts, and larger immature-appearing cells with more abundant eosinophilic cytoplasm that resembled myeloblasts, a subset of which expressed myeloid antigens.
  • We believe that these bilineal neoplasms of mixed T-cell and myeloid lineages, which present as lymphoma, are analogous to bilineal leukemias.

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  • (PMID = 18162765.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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51. Abramson N: Chronic eosinophilic leukemia/hypereosinophilic syndrome and acute leukemia. J Clin Oncol; 2006 Apr 1;24(10):1647
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  • [Title] Chronic eosinophilic leukemia/hypereosinophilic syndrome and acute leukemia.
  • [MeSH-major] Hypereosinophilic Syndrome / complications. Leukemia / etiology
  • [MeSH-minor] Acute Disease. Humans

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  • [CommentOn] J Clin Oncol. 2005 Sep 10;23(26):6285-95 [16155011.001]
  • (PMID = 16575017.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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52. Shvidel L, Sigler E, Shtalrid M, Berrebi A, Resnitzky P: Hybrid eosinophilic-basophilic acute myeloid leukaemia diagnosed by electron microscopy. Br J Haematol; 2007 May;137(4):381-3
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  • [Title] Hybrid eosinophilic-basophilic acute myeloid leukaemia diagnosed by electron microscopy.
  • [MeSH-major] Basophils / ultrastructure. Eosinophils / ultrastructure. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 17456060.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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53. Tasaka T, Matsuhashi Y, Ohnishi H, Kubota Y: Eosinophilic cystitis following cord blood transplantation: a form of acute GVHD. A variant of hemorrhagic cystitis after hematopoietic SCT or drug-induced? Bone Marrow Transplant; 2008 Oct;42(7):495-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eosinophilic cystitis following cord blood transplantation: a form of acute GVHD. A variant of hemorrhagic cystitis after hematopoietic SCT or drug-induced?
  • [MeSH-major] Cord Blood Stem Cell Transplantation / adverse effects. Cystitis / etiology. Graft vs Host Disease / diagnosis. Hematopoietic Stem Cell Transplantation / adverse effects. Hemorrhage / etiology. Leukemia, Myelomonocytic, Acute / surgery


54. Gower WA, Collaco JM, Ellis CL, Halbower AC, Mogayzel PJ: A previously healthy adolescent with evolving infiltrates and progressive respiratory distress. Thorax; 2009 Apr;64(4):290, 364
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Leukemia, Eosinophilic, Acute / complications. Respiratory Insufficiency / etiology
  • [MeSH-minor] Acute Disease. Adolescent. Humans. Male

  • MedlinePlus Health Information. consumer health - Respiratory Failure.
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  • (PMID = 19329730.001).
  • [ISSN] 1468-3296
  • [Journal-full-title] Thorax
  • [ISO-abbreviation] Thorax
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / K23 RR024257; United States / NCRR NIH HHS / RR / M01 RR000069
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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