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Items 1 to 100 of about 147
1. Lambert F, Heimann P, Herens C, Chariot A, Bours V: A case of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia with a rare FIP1L1 breakpoint. J Mol Diagn; 2007 Jul;9(3):414-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia with a rare FIP1L1 breakpoint.
  • The idiopathic hypereosinophilic syndrome (HES) has remained for a long time a diagnosis of exclusion.
  • Differential diagnosis between the HES and the related chronic eosinophilic leukemia (CEL) relied on the identification of signs of clonality that allowed, when present, the reclassification of patients as CEL.
  • According to the World Health Organization classification, this clonal abnormality has been proposed as a new surrogate marker for chronic eosinophilic leukemia diagnosis.
  • As targeted therapy with tyrosine kinase inhibitors has dramatically changed the prognosis of FIP1L1-PDGFRA (+) CEL, false-negative results could hamper accurate diagnosis and treatment.

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  • (PMID = 17591942.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / Mutant Chimeric Proteins; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC1899422
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2. Kuk JS, Maceachern JA, Soamboonsrup P, McFarlane A, Benger A, Patterson W, Yang L, Trus MR: Chronic eosinophilic leukemia presenting with autoimmune hemolytic anemia and erythrophagocytosis by eosinophils. Am J Hematol; 2006 Jun;81(6):458-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemia presenting with autoimmune hemolytic anemia and erythrophagocytosis by eosinophils.
  • Eosinophils function primarily as secretory cells and phagocytosis by eosinophils is rarely seen.
  • We describe a case of chronic eosinophilic leukemia (CEL) in a 72-year-old male with a history of previously treated non-Hodgkin's lymphoma (NHL) presenting with erythrophagocytosis by eosinophils and an associated autoimmune hemolytic anemia (AIHA).
  • The patient's blood showed a markedly elevated eosinophil count of 16 x 10(9)/L [normal 0-0.45 x 10(9)/L] on a background of myelodysplasia and features of AIHA.
  • Prominent erythrophagocytosis by eosinophils was visualized in the blood and in the bone marrow.
  • Numerous Charcot-Leyden crystals were also seen in the bone marrow amid increased numbers of eosinophils and the presence of dysplastic granulopoiesis.
  • More significantly, this represents the first case report to describe erythrophagocytosis by eosinophils.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / pathology. Eosinophils / pathology. Hypereosinophilic Syndrome / pathology. Neoplasms, Second Primary / pathology. Phagocytosis

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  • (PMID = 16680737.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / lysolecithin acylhydrolase; EC 3.1.1.5 / Lysophospholipase
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3. Helbig G, Stella-Holowiecka B, Majewski M, Lewandowska M, Holowiecki J: Interferon alpha induces a good molecular response in a patient with chronic eosinophilic leukemia (CEL) carrying the JAK2V617F point mutation. Haematologica; 2007 Nov;92(11):e118-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interferon alpha induces a good molecular response in a patient with chronic eosinophilic leukemia (CEL) carrying the JAK2V617F point mutation.
  • The JAK2 V617F point mutation is very rare in hypereosinophilic syndrome and/or chronic eosinophilic leukemia.
  • Here we report on a patient with chronic eosinophilic leukemia and detectable JAK2 mutant clone, who achieved a good molecular response to interferon alpha-2a after 4 months of treatment.

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  • (PMID = 18024388.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a; EC 2.7.10.2 / Janus Kinase 2
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4. Yamada Y, Rothenberg ME, Cancelas JA: Current concepts on the pathogenesis of the hypereosinophilic syndrome/chronic eosinophilic leukemia. Transl Oncogenomics; 2006;1:53-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current concepts on the pathogenesis of the hypereosinophilic syndrome/chronic eosinophilic leukemia.
  • Chronic eosinophilic leukemia is a clonal disease characterized by hypereosinophilia and eosinophilia-related pathologic manifestations.
  • Several investigations have tried to dissect the mechanism of leukemogenesis and signaling induced by FIP1L1/PDGFRα in cell lines, primary human eosinophils and in murine myeloproliferative models.
  • In this review, we analyzed the current knowledge on the relationship between FIP1L1/PDGFRα-induced signaling and eosinophil proliferation, survival and activation, specially focusing on its possible role in the modulation of cytokine and chemoattractant signaling pathways.

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  • (PMID = 23662039.001).
  • [Journal-full-title] Translational oncogenomics
  • [ISO-abbreviation] Transl Oncogenomics
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3642145
  • [Keywords] NOTNLM ; FIP1L1/PDGFRα / chronic eosinophilic leukemia / hypereosinophilic syndrome eosinophils / mast cells
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5. Arora RS: Chronic eosinophilic leukemia with a unique translocation. Indian Pediatr; 2009 Jun;46(6):525-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemia with a unique translocation.
  • We report a case of chronic eosinophilic leukemia in a 9 year old girl who presented with anemia, thrombocytopenia, leucocytosis (mostly dysplastic eosinophils), lymphadenopathy and hepatosplenomegaly.
  • [MeSH-minor] Cardiomyopathies / blood. Cardiomyopathies / diagnosis. Cardiomyopathies / drug therapy. Cardiomyopathies / genetics. Child. Chronic Disease. Echocardiography. Eosinophils. Female. Glucocorticoids / therapeutic use. Humans

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  • (PMID = 19556663.001).
  • [ISSN] 0019-6061
  • [Journal-full-title] Indian pediatrics
  • [ISO-abbreviation] Indian Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Glucocorticoids
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6. Chrobák L, Voglová J: [The idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia]. Vnitr Lek; 2005 Dec;51(12):1385-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • According to World Health Organization the exclusion includes all neoplastic disorders in which eosinophils are part of the neoplastic clone.
  • 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.

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  • (PMID = 16430106.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 49
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7. Capovilla M, Cayuela JM, Bilhou-Nabera C, Gardin C, Letestu R, Baran-Marzak F, Fenaux P, Martin A: Synchronous FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and T-cell lymphoblastic lymphoma: a bilineal clonal malignancy. Eur J Haematol; 2008 Jan;80(1):81-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synchronous FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and T-cell lymphoblastic lymphoma: a bilineal clonal malignancy.
  • Several reports of successful empirical treatment of idiopathic hypereosinophilic syndrome with imatinib led to the recent identification of the FIP1L1-PDGFRA fusion gene rearrangement, which characterizes a distinctive group of chronic eosinophilic leukemias.
  • This fusion gene can be detected in eosinophils, neutrophils, mast cells, T cells, B cells and monocytes in FIP1L1-PDGFRA-positive hypereosinophilic patients suggesting a multilineage involvement.
  • In addition, a recent report noted two cases with the association of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and T-cell lymphoblastic lymphoma (T-LBL).
  • We report here the only third case of synchronous chronic eosinophilic leukemia and T-LBL, both associated with a FIP1L1-PDGFRA fusion transcript, confirming the occurrence of such disease and suggesting a clonal proliferation with two lines of differentiation probably arising from a primitive multipotent medullary stem cell.

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  • (PMID = 18028420.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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8. Lierman E, Cools J: Recent breakthroughs in the understanding and management of chronic eosinophilic leukemia. Expert Rev Anticancer Ther; 2009 Sep;9(9):1295-304
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent breakthroughs in the understanding and management of chronic eosinophilic leukemia.
  • Molecular analysis led to the identification of the clonal origin of several subgroups of HES, clearly establishing these diseases as true leukemias.
  • In cases for which clonality is clear, but no PDGFRA, PDGFRB or FGFR1 rearrangement could be demonstrated, the term 'chronic eosinophilic leukemia, not otherwise specified' is preferred.
  • For treatment of unexplained hypereosinophilia and 'chronic eosinophilic leukemia, not otherwise specified; different therapeutic strategies are currently under investigation and promising results have been obtained using humanized anti-IL-5 antibodies.

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  • (PMID = 19761433.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interleukin-5; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 80
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9. Yamada Y, Cancelas JA, Rothenberg ME: Murine model of hypereosinophilic syndromes/chronic eosinophilic leukemia. Int Arch Allergy Immunol; 2009;149 Suppl 1:102-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Murine model of hypereosinophilic syndromes/chronic eosinophilic leukemia.
  • In addition to classical HES criteria, the World Health Organization proposed a set of criteria that distinguish chronic eosinophilic leukemia (CEL) from HES.
  • Several investigations have tried to dissect the mechanism of leukemogenesis; eosinophilia and signaling induced by FIP1L1/PDGFRalpha in cell lines, bone marrow mast cells, primary human eosinophils and in murine myeloproliferative disorder models.
  • In this review, we introduce the current knowledge on the relationship between FIP1L1/PDGFRalpha and cell signaling, eosinophil proliferation, survival and activation and mastocytosis specially focusing on the evidence learned from murine models.
  • [MeSH-major] Disease Models, Animal. Eosinophils / immunology. Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / metabolism. Mice

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19494514.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 45
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10. Ishihara K, Kitamura H, Hiraizumi K, Kaneko M, Takahashi A, Zee O, Seyama T, Hong J, Ohuchi K, Hirasawa N: Mechanisms for the proliferation of eosinophilic leukemia cells by FIP1L1-PDGFRalpha. Biochem Biophys Res Commun; 2008 Feb 22;366(4):1007-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms for the proliferation of eosinophilic leukemia cells by FIP1L1-PDGFRalpha.
  • The constitutively activated tyrosine kinase Fip1-like 1 (FIP1L1)-platelet-derived growth factor receptor alpha (PDGFRalpha) causes eosinophilic leukemia EoL-1 cells to proliferate.
  • Recently, we demonstrated that histone deacetylase inhibitors suppressed this proliferation and induced the differentiation of EoL-1 cells into eosinophils in parallel with a decrease in the level of FIP1L1-PDGFRalpha.
  • In this study, we analyzed the mechanism by which FIP1L1-PDGFRalpha induces the proliferation and whether the suppression of cell proliferation triggers the differentiation into eosinophils.
  • The expression of the eosinophilic differentiation marker CCR3 was not induced by imatinib.
  • These findings suggest that FIP1L1-PDGFRalpha induces the proliferation of EoL-1 cells through the induction of c-Myc expression via ERK and JNK signaling pathways, but is not involved in the inhibition of differentiation toward mature eosinophils.

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  • (PMID = 18086564.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Butadienes; 0 / Nitriles; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyrimidines; 0 / Receptors, CCR3; 0 / U 0126; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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11. Cools J, Stover EH, Gilliland DG: Detection of the FIP1L1-PDGFRA fusion in idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia. Methods Mol Med; 2006;125:177-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of the FIP1L1-PDGFRA fusion in idiopathic hypereosinophilic syndrome and chronic eosinophilic leukemia.
  • Idiopathic hypereosinophilic syndrome (HES) and chronic eosinophilic leukemia (CEL) are related hematological malignancies characterized by sustained, unexplained hypereosinophilia (>1,500 eosinophils/microL).

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  • (PMID = 16502585.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / mRNA Cleavage and Polyadenylation Factors; 63231-63-0 / RNA; 9007-49-2 / DNA; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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12. Albano F, Anelli L, Zagaria A, Lonoce A, La Starza R, Liso V, Rocchi M, Specchia G: Extramedullary molecular evidence of the 5'KIAA1509/3'PDGFRB fusion gene in chronic eosinophilic leukemia. Leuk Res; 2008 Feb;32(2):347-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary molecular evidence of the 5'KIAA1509/3'PDGFRB fusion gene in chronic eosinophilic leukemia.
  • We report a case of chronic eosinophilic leukemia (CEL), demonstrating for the first time: (i) the association of CEL with the 5'KIAA1509/3'PDGFRB fusion gene as a consequence of a t(5;14)(q33;q32);.

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  • (PMID = 17681599.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-sis; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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13. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chronic eosinophilic leukemia with complex karyotypic abnormalities including trisomy 8].
  • We report a 61-year-old man with chronic eosinophilic leukemia (CEL).
  • He was diagnosed with CEL based on an increase in blasts and eosinophils in his peripheral blood and bone marrow, and clonal complex karyotypic abnormalities including trisomy 8.
  • 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.

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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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14. Wang W, Chen HS, Liu EB, Yang QY, Fang LH, Sun FJ, Qian LS: [Clinicopathologic studies of 13 cases of chronic eosinophilic leukemia]. Zhonghua Bing Li Xue Za Zhi; 2008 Apr;37(4):259-63

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic studies of 13 cases of chronic eosinophilic leukemia].
  • OBJECTIVE: To investigate the role of bone marrow biopsy (BMB) in diagnosis and differential diagnosis for chronic eosinophilic leukemia (CEL).
  • Most of organs and tissues were also be involved. (2) Peripheral blood counts characterized by eosinophilia (18.1 +/-16.2) x 10(9)/L, (3) BMB showed eosinophils were predominant components, others such as neutrophils, erythrocytes, megakaryocytes were decrease.
  • CONCLUSION: Combine with the clinical manifestations of CEL patients, it is important in diagnosis and differential diagnosis for CEL by observing the histomorphology features of bone marrow biopsy carefully.
  • [MeSH-major] Bone Marrow / pathology. Eosinophils / pathology. Hypereosinophilic Syndrome / diagnosis
  • [MeSH-minor] Adult. Aged. Biopsy. Chronic Disease / classification. Diagnosis, Differential. Female. Humans. Leukocyte Count / methods. Male. Middle Aged. Treatment Outcome. Young Adult

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  • (PMID = 18844036.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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15. Kumar A, Sinha S, Tripathi AK: Chronic eosinophilic leukemia: a case report and review of literature. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):112-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemia: a case report and review of literature.
  • Chronic Eosinophilic Leukemia (CEL) is a rare type of chronic myeloproliferative disorder of unknown etiology with no available true incidence.
  • An evidence of genetic clonality of eosinophils or an increase in blast cells in the blood or bone marrow is mandatory for diagnosis of CEL while no specific diagnostic tests exist for IHES; making it an entity of exclusion.
  • We add yet another case of eosinophilic leukemia along with review of available literature.

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  • (PMID = 23100928.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453119
  • [Keywords] NOTNLM ; Chronic eosinophilic leukemia / Idiopathic Hypereosinophilic syndrome
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16. Crescenzi B, Chase A, Starza RL, Beacci D, Rosti V, Gallì A, Specchia G, Martelli MF, Vandenberghe P, Cools J, Jones AV, Cross NC, Marynen P, Mecucci C: FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells. Leukemia; 2007 Mar;21(3):397-402
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells.
  • We investigated genetically affected leukemic cells in FIP1L1-PDGFRA+ chronic eosinophilic leukemia (CEL) and in BCR-ABL1+ chronic myeloid leukemia (CML), two myeloproliferative disorders responsive to imatinib.
  • Positivity was found in eosinophils, granulo-monocytes and varying percentages of erythrocytes.
  • In CML the BCR-ABL1 fusion gene was detected in CD34+/CD133+ cells, granulo-monocytes, eosinophils, erythrocytes, megakaryocytes and B-lymphocytes.
  • [MeSH-major] Fusion Proteins, bcr-abl / analysis. Hypereosinophilic Syndrome / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / enzymology. Oncogene Proteins, Fusion / analysis. Receptor, Platelet-Derived Growth Factor alpha / analysis. mRNA Cleavage and Polyadenylation Factors / analysis
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD34 / analysis. Antineoplastic Agents / therapeutic use. Benzamides. Cell Lineage. Chronic Disease. Clone Cells / enzymology. Drug Resistance. Eosinophils / enzymology. Erythrocytes / enzymology. Glycophorin / analysis. Glycoproteins / analysis. Granulocytes / enzymology. Hematopoietic Stem Cells / enzymology. Humans. Imatinib Mesylate. Immunophenotyping. Lymphocyte Subsets / enzymology. Megakaryocytes / enzymology. Monocytes / enzymology. Myeloid Cells / enzymology. Peptides / analysis. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Tumor Stem Cell Assay. X Chromosome Inactivation

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  • (PMID = 17215855.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Glycophorin; 0 / Glycoproteins; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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17. Menif S, Omri H, Hafsia R, Ben Romdhane N, Turki S, Meddeb B, Dellagi K: FIP1L1-PDGFRA positive chronic eosinophilic leukemia in Tunisian patients. Pathol Biol (Paris); 2007 Jun;55(5):242-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FIP1L1-PDGFRA positive chronic eosinophilic leukemia in Tunisian patients.
  • Hypereosinophilic syndromes (HES) are a heterogenous group of rare disorders characterized by sustained and otherwise unexplained overproduction of eosinophils with organ involvement and consecutive dysfunction.
  • Detection of the FIP1L1-PDGFRA fusion gene or the corresponding cryptic 4q12 deletion in HES supports the diagnosis of chronic eosinophilic leukemia (CEL) and provides a molecular explanation for the pathogenesis of this disorder.
  • The median age at diagnosis was 24 years (range, 18-50); one patient had a history of hypereosinophilia of more than 10 years.
  • Two patients had clinically important and symptomatic eosinophilic endomyocardial disease with thrombotic events.

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  • (PMID = 17137731.001).
  • [ISSN] 0369-8114
  • [Journal-full-title] Pathologie-biologie
  • [ISO-abbreviation] Pathol. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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18. Verstovsek S, Tefferi A, Kantarjian H, Manshouri T, Luthra R, Pardanani A, Quintás-Cardama A, Ravandi F, Ault P, Bueso-Ramos C, Cortes JE: Alemtuzumab therapy for hypereosinophilic syndrome and chronic eosinophilic leukemia. Clin Cancer Res; 2009 Jan 1;15(1):368-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab therapy for hypereosinophilic syndrome and chronic eosinophilic leukemia.
  • PURPOSE: Patients with hypereosinophilic syndrome (HES) or chronic eosinophilic leukemia (CEL) that are refractory to standard therapies are difficult to manage and have significantly shortened life expectancy.
  • EXPERIMENTAL DESIGN: CD52 is a surface glycoprotein highly expressed on eosinophils.
  • Patients with complete hematologic response (CHR; normal percent and absolute eosinophil count) were allowed to continue therapy once weekly as maintenance.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Bone Marrow / pathology. Drug Administration Schedule. Drug Evaluation. Eosinophils. Female. Humans. Leukocyte Count. Male. Middle Aged. Treatment Outcome

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  • (PMID = 19118067.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ NIHMS772843; NLM/ PMC4822510
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19. Klion AD, Robyn J, Maric I, Fu W, Schmid L, Lemery S, Noel P, Law MA, Hartsell M, Talar-Williams C, Fay MP, Dunbar CE, Nutman TB: Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing. Blood; 2007 Nov 15;110(10):3552-6
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  • [Title] Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing.
  • Although imatinib is clearly the treatment of choice for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia (CEL), little is known about optimal dosing, duration of treatment, and the possibility of cure in this disorder.
  • None developed recurrent symptoms, and eosinophil counts, serum B12, and tryptase levels remained suppressed.
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Benzamides. Biomarkers, Pharmacological / analysis. Biopsy. Chronic Disease. Dose-Response Relationship, Drug. Eosinophils / cytology. Eosinophils / drug effects. Humans. Imatinib Mesylate. Leukocyte Count. Male. Middle Aged. Recurrence. Remission Induction

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  • (PMID = 17709602.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00044304
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Pharmacological; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC2077306
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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • Bone marrow biopsy showed clonal cytogenetic abnormality consisting of deletion of the long arm of chromosome 16 (16q22).
  • The patient was treated with imatinib at 400 mg/d with improvement of symptoms, reduction of lymphadenopathy and normalization of the eosinophil count.
  • 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.
  • Whether this cytogenetic abnormality might represent a prodromal phase of AML-M4Eo is not known.
  • In addition, the role of hepatitis C in inducing clonal proliferation of eosinophils is unclear.
  • [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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21. Pardanani A, Verstovsek S: Hypereosinophilic syndrome, chronic eosinophilic leukemia, and mast cell disease. Cancer J; 2007 Nov-Dec;13(6):384-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypereosinophilic syndrome, chronic eosinophilic leukemia, and mast cell disease.
  • Hypereosinophilic syndrome (HES), chronic eosinophilic leukemia (CEL), and mast cell disease (MCD) are all considered myeloproliferative neoplasms, and diagnosis in each instance requires bone marrow examination with cytogenetic and molecular studies.
  • Diagnosis of MCD is facilitated by tryptase immunostaining and immunophenotyping to detect abnormal CD25-positive mast cells.
  • Mutation screening for KITD816V is also advised but is not essential for the diagnosis of MCD.


22. Iriuchishima H, Ogawa Y, Hoshino T, Yoshida T, Sato K, Takagi H, Toyama K, Tsukamoto N, Jinbo T: [Chronic eosinophilic leukemia with symptoms resembling Budd-Chiari syndrome due to liver infiltration]. Rinsho Ketsueki; 2007 Jun;48(6):505-9
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  • [Title] [Chronic eosinophilic leukemia with symptoms resembling Budd-Chiari syndrome due to liver infiltration].
  • A molecular biologic examination proved the clonality of the eosinophils and she was therefore diagnosed as having chronic eosinophilic leukemia (CEL).
  • The pathologic findings of a liver biopsy showed dilation of the sinusoids with infiltration of eosinophils, portal eosinophilic infiltrations with fibrosis, and biliary damage.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / pathology. Liver Neoplasms / diagnosis. Liver Neoplasms / pathology
  • [MeSH-minor] Aged. Budd-Chiari Syndrome. Chronic Disease. Diagnosis, Differential. Female. Humans. Liver / pathology. Neoplasm Invasiveness

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  • (PMID = 17633100.001).
  • [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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23. Tanaka H, Iwato K, Asou H, Kimura A: Pure red cell aplasia associated with imatinib-treated FIP1L1-PDGFRA positive chronic eosinophilic leukemia. Intern Med; 2010;49(12):1195-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pure red cell aplasia associated with imatinib-treated FIP1L1-PDGFRA positive chronic eosinophilic leukemia.
  • Then, a diagnosis of chronic eosinophilic leukemia (CEL) was made.
  • Whereas the response to the treatments with prednisolone and hydroxyurea were unsatisfactory, treatment with imatinib showed a rapid decrease of eosinophils.

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  • (PMID = 20558942.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / FIP1L1-PDGFRA fusion protein, human; 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
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24. Maric I, Robyn J, Metcalfe DD, Fay MP, Carter M, Wilson T, Fu W, Stoddard J, Scott L, Hartsell M, Kirshenbaum A, Akin C, Nutman TB, Noel P, Klion AD: KIT D816V-associated systemic mastocytosis with eosinophilia and FIP1L1/PDGFRA-associated chronic eosinophilic leukemia are distinct entities. J Allergy Clin Immunol; 2007 Sep;120(3):680-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] KIT D816V-associated systemic mastocytosis with eosinophilia and FIP1L1/PDGFRA-associated chronic eosinophilic leukemia are distinct entities.
  • BACKGROUND: The broad and overlapping clinical manifestations of D816V KIT-associated systemic mastocytosis with eosinophilia and FIP1L1/PDGFRA-associated chronic eosinophilic leukemia (CEL), coupled with the increase in activated eosinophils and mast cells seen in both disorders, have led to confusion in the nomenclature.
  • [MeSH-major] Eosinophilia / classification. Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / physiopathology. Mastocytosis, Systemic / diagnosis. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Proteins c-kit / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism

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  • (PMID = 17628645.001).
  • [ISSN] 0091-6749
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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25. Cilloni D, Messa F, Martinelli G, Gottardi E, Arruga F, Defilippi I, Carturan S, Messa E, Fava M, Giugliano E, Rosso V, Catalano R, Merante S, Nicoli P, Rondoni M, Ottaviani E, Soverini S, Tiribelli M, Pane F, Baccarani M, Saglio G: WT1 transcript amount discriminates secondary or reactive eosinophilia from idiopathic hypereosinophilic syndrome or chronic eosinophilic leukemia. Leukemia; 2007 Jul;21(7):1442-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] WT1 transcript amount discriminates secondary or reactive eosinophilia from idiopathic hypereosinophilic syndrome or chronic eosinophilic leukemia.
  • The hybrid gene FIP1L1-PDGRFalpha was identified in a subset of patients presenting with HES or chronic eosinophilic leukemia (CEL).
  • In spite of this, the majority of HES patients do not present detectable molecular lesions and for many of them the diagnosis is based on exclusion criteria and sometimes it remains doubt.
  • For this purpose, 312 patients with hypereosinophilia were characterized at the molecular and cytogenetic level and analyzed for WT1 expression at diagnosis and during follow-up.
  • [MeSH-major] Eosinophilia / diagnosis. Hypereosinophilic Syndrome / diagnosis. RNA, Neoplasm / analysis. WT1 Proteins / genetics
  • [MeSH-minor] Adult. Aged. Chronic Disease. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Molecular Diagnostic Techniques


26. Cools J: FIP1L1-PDGFR alpha, a therapeutic target for the treatment of chronic eosinophilic leukemia. Verh K Acad Geneeskd Belg; 2005;67(3):169-76
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  • [Title] FIP1L1-PDGFR alpha, a therapeutic target for the treatment of chronic eosinophilic leukemia.
  • A diagnostic test to identify FIP1L1-PDGFRA positive HES cases (subsequently reclassified as chronic eosinophilic leukemia, CEL) is now available.

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  • (PMID = 16089297.001).
  • [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; Review
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 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] 10
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27. Gelain ME, Antoniazzi E, Bertazzolo W, Zaccolo M, Comazzi S: Chronic eosinophilic leukemia in a cat: cytochemical and immunophenotypical features. Vet Clin Pathol; 2006 Dec;35(4):454-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemia in a cat: cytochemical and immunophenotypical features.
  • A feline leukemia virus (FeLV) antigen test was positive.
  • CBC results obtained at initial presentation included severe normocytic, normochromic, nonregenerative anemia, severe thrombocytopenia, and marked leukocytosis (>100,000/microL) with 77% eosinophils.
  • After 15 days of treatment with prednisone and doxycycline, the cat had persistent severe nonregenerative anemia (HCT 3.4%), thrombocytopenia (28,000/microL), and extreme eosinophilia (total eosinophils, 123.1 x 10(3)/microL; segmented 103.0 x 10(3)/microL; immature 20.1 X 10(3)/microL).
  • Cytologic examination of aspirates from bone marrow, liver, lymph nodes, and spleen revealed a predominance of mature and immature eosinophils, many with dysplastic changes.
  • On histopathologic examination, multiple organs were infiltrated by eosinophilic granulocytes.
  • These findings were consistent with chronic eosinophilic leukemia.
  • To our knowledge, this is the first report of chronic eosinophilic leukemia in a cat associated with naturally acquired FeLV infection, in which flow cytometry was used to characterize the neoplastic cells.

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  • (PMID = 17123254.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents; N12000U13O / Doxycycline; VB0R961HZT / Prednisone
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28. Arai A, Yan W, Wakabayashi S, Hayashi S, Inazawa J, Miura O: Successful imatinib treatment of cardiac involvement of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia followed by severe hepatotoxicity. Int J Hematol; 2007 Oct;86(3):233-7
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  • [Title] Successful imatinib treatment of cardiac involvement of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia followed by severe hepatotoxicity.
  • Imatinib is highly effective for the treatment of chronic eosinophilic leukemia (CEL) caused by the FIP1L1-PDGFRA fusion gene.

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  • (PMID = 17988989.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Glucocorticoids; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / mRNA Cleavage and Polyadenylation Factors; 7LXU5N7ZO5 / Furosemide; 8A1O1M485B / Imatinib Mesylate; 9PHQ9Y1OLM / Prednisolone; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 19
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29. Florian S, Esterbauer H, Binder T, Müllauer L, Haas OA, Sperr WR, Sillaber C, Valent P: Systemic mastocytosis (SM) associated with chronic eosinophilic leukemia (SM-CEL): detection of FIP1L1/PDGFRalpha, classification by WHO criteria, and response to therapy with imatinib. Leuk Res; 2006 Sep;30(9):1201-5
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic mastocytosis (SM) associated with chronic eosinophilic leukemia (SM-CEL): detection of FIP1L1/PDGFRalpha, classification by WHO criteria, and response to therapy with imatinib.
  • We describe a case of SM with coexisting chronic eosinophilic leukemia (SM-CEL).
  • By contrast, therapy with imatinib was followed by a fast and sustained response with complete and stable regression of eosinophilia, drop in eosinophil cationic protein, and decrease of serum tryptase to normal levels.
  • This case provides further evidence for the potential of co-existence of SM with a primary eosinophilic disorder (CEL) defined by the FIP1L1/PDGFRalpha fusion gene.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hypereosinophilic Syndrome / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mastocytosis, Systemic / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Benzamides. Cardiomyopathies / blood. Cardiomyopathies / etiology. Eosinophil Cationic Protein / blood. Humans. Hydroxyurea / administration & dosage. Imatinib Mesylate. Interferon-alpha / administration & dosage. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Remission Induction. Serine Endopeptidases / blood. Tryptases. World Health Organization. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 16406018.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Interferon-alpha; 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; EC 3.1.27.- / Eosinophil Cationic Protein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases; X6Q56QN5QC / Hydroxyurea
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30. 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
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular analysis of chronic eosinophilic leukemia with t(4;10) showing good response to imatinib mesylate.
  • 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.
  • Despite treatment with steroid pulse therapy and cytarabine, the blood eosinophil count did not decrease, and the patient's respiratory condition worsened.
  • The blood eosinophil count decreased dramatically over 5 days, and the patient's condition rapidly improved, such that the patient could be discharged.

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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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31. 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
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

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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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32. Leeksma OC, de Ruiter GS, van der Hulst VP, Terpstra WE, Cools J, Vandenberghe P: [A man with FIP1L1/PDGFRA-positive chronic eosinophilic leukemia]. Ned Tijdschr Geneeskd; 2006 Sep 2;150(35):1936-43
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  • [Title] [A man with FIP1L1/PDGFRA-positive chronic eosinophilic leukemia].
  • [Transliterated title] Een man met FIP1L1-PDGFRA-positieve chronische eosinofiele leukemie.
  • He appeared to have chronic eosinophilic leukaemia that was positive for the 'FIP1-like-1-platelet-derived growth factor receptor alpha' (FIP1L1-PDGFRA) gene.
  • After 1 year of follow up, the patient was in complete haematological and molecular remission for chronic eosinophilic leukaemia.

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  • (PMID = 16999279.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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33. Lierman E, Michaux L, Beullens E, Pierre P, Marynen P, Cools J, Vandenberghe P: FIP1L1-PDGFRalpha D842V, a novel panresistant mutant, emerging after treatment of FIP1L1-PDGFRalpha T674I eosinophilic leukemia with single agent sorafenib. Leukemia; 2009 May;23(5):845-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FIP1L1-PDGFRalpha D842V, a novel panresistant mutant, emerging after treatment of FIP1L1-PDGFRalpha T674I eosinophilic leukemia with single agent sorafenib.
  • Chronic eosinophilic leukemia (CEL) is a rare myeloproliferative neoplasm characterized by the FIP1L1-PDGFRA fusion gene, variant PDGFRA fusions or other genetic lesions.

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  • (PMID = 19212337.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 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; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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34. Yamada Y, Rothenberg ME, Lee AW, Akei HS, Brandt EB, Williams DA, Cancelas JA: The FIP1L1-PDGFRA fusion gene cooperates with IL-5 to induce murine hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL)-like disease. Blood; 2006 May 15;107(10):4071-9
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  • [Title] The FIP1L1-PDGFRA fusion gene cooperates with IL-5 to induce murine hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL)-like disease.
  • Dysregulated tyrosine kinase activity by the Fip1-like1 (FIP1L1)-platelet-derived growth factor receptor alpha (PDGFRA) (F/P) fusion gene has been identified as a cause of clonal hypereosinophilic syndrome (HES), called F/P-positive chronic eosinophilic leukemia (CEL) in humans.
  • However, transplantation of F/P-transduced hematopoietic stem cells/progenitors (F/P(+) HSCs/Ps) into mice results in a chronic myelogenous leukemia-like disease, which does not resemble HES.
  • Mice that received a transplant of CD2-IL-5-transgenic F/P(+) HSC/Ps (IL-5Tg-F/P) developed intense leukocytosis, strikingly high eosinophilia, and eosinophilic infiltration of nonhematopoietic as well as hematopoietic tissues, a phenotype resembling human HES.

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  • (PMID = 16418325.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL069974; United States / NIDDK NIH HHS / DK / R01 DK062757; United States / NHLBI NIH HHS / HL / 1P01 HL 69974; United States / NIDDK NIH HHS / DK / 1R01 DK 062757
  • [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 / FIP1L1-PDGFRA fusion protein, human; 0 / Interleukin-5; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC1895281
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35. Lee JS, Kim IS: Leukotactin-1/CCL15 induces cell migration and differentiation of human eosinophilic leukemia EoL-1 cells through PKCdelta activation. Mol Biol Rep; 2010 Jun;37(5):2149-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukotactin-1/CCL15 induces cell migration and differentiation of human eosinophilic leukemia EoL-1 cells through PKCdelta activation.
  • Although eosinophils express both receptors, the role of Lkn-1 in immature eosinophils remains to be elucidated.
  • In this present study, we investigated the contribution of the CCR1-binding chemokines to chemotactic activity and in the differentiation in the human eosinophilic leukemia cell line EoL-1.
  • Lkn-1 enhanced the butyric acid-induced differentiation via PKCdelta after binding to the increased CCR1 because Lkn-1 caused EoL-1 cells to change morphologically into mature eosinophil-like cells.
  • Likewise, Lkn-1 increased the expression of both eosinophil peroxidase (EPO) and the major basic protein (MBP).
  • This finding contributes to an understanding of CC chemokines in eosinophil biology and to the development of novel therapies for the treatment of eosinophilic disorders.
  • This study suggests the pivotal roles of Lkn-1 in the regulation of the movement and development of eosinophils.

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  • (PMID = 19669929.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CCL15 protein, human; 0 / Chemokines, CC; 0 / Macrophage Inflammatory Proteins; 0 / Receptors, CCR1; 107-92-6 / Butyric Acid; EC 2.7.11.13 / Protein Kinase C-delta; EC 3.1.4.- / Type C Phospholipases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go
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36. Luo RM, Wu SL, Tong CR, Qiu JY, Wu P, Lu DP: [FIP1L1/PDGFRalpha fusion gene-negative chronic eosinophilic leukemia with t(5;12)(q31;p13): a case report and review of literatures]. Zhonghua Nei Ke Za Zhi; 2008 Nov;47(11):919-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [FIP1L1/PDGFRalpha fusion gene-negative chronic eosinophilic leukemia with t(5;12)(q31;p13): a case report and review of literatures].
  • OBJECTIVE: To deepen the understanding of chronic eosinophilic leukemia (CEL).
  • METHODS: The course of diagnosis and treatment in a case of FIP1L1/PDGFRalpha fusion gene negative CEL was reported.
  • Trephine biopsy showed a hypercellular marrow with eosinophilic proliferation and moderate reticular fibrosis.
  • Eosinophilic infiltration was found in lung and spleen and embolism was also found in spleen.
  • She had a clonal chromosomal abnormality t(5;12)(q31;p13).
  • It is noteworthy that clonal CD(3)(-), CD(4)(-), CD(8)(+)T-cell abnormality is related to the pathogenesis of CEL.

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  • (PMID = 19080234.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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37. Wang LN, Pan Q, Fu JF, Shi JY, Jin J, Li JM, Hu J, Zhao WL, Chen Z, Chen SJ: FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib. Chin Med J (Engl); 2008 May 20;121(10):867-73
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  • [Title] FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib.
  • BACKGROUND: The FIP1L1-PDGFRalpha fusion gene plays an important role in the pathogenesis of chronic eosinophilic leukemia (CEL) and is a direct therapeutic target of the tyrosine kinase inhibitor imatinib mesylate.
  • The FIP1L1-PDGFRalpha-associated patients diagnosed with CEL, frequently had hepatosplenomegaly, eosinophil-related tissue damage, anemia, thrombocytopenia, myelofibrosis and a short overall survival time.
  • Detection of the FIP1L1-PDGFRalpha fusion gene is valid for both CEL diagnosis and therapy surveillance.

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  • (PMID = 18706197.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Oncogene Proteins v-abl; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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38. Fletcher S, Abdalla S, Edwards M, Bain BJ: Case 32. Eosinophilia: reactive or neoplastic? Leuk Lymphoma; 2007 Jan;48(1):174-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A diagnosis of eosinophilic leukemia was suspected in a patient who presented with eosinophilia and a mild macrocytic anemia and was found to have trisomy 8.
  • Further tests and the subsequent clinical course permitted an accurate diagnosis.
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 8. Female. Humans. Trisomy / diagnosis

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  • (PMID = 17325861.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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39. Lee JS, Yang EJ, Kim IS: The roles of MCP-1 and protein kinase C delta activation in human eosinophilic leukemia EoL-1 cells. Cytokine; 2009 Dec;48(3):186-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The roles of MCP-1 and protein kinase C delta activation in human eosinophilic leukemia EoL-1 cells.
  • Idiopathic hypereosinophilc syndrome is a disorder associated with clonally eosinophilic proliferation.
  • In this study, we investigated the contribution of monocyte chemoattractant protein-1 (MCP-1)/CCL2 to chemotactic activity and protein kinase C delta (PKC delta in the human eosinophilic leukemia cell line EoL-1.
  • MCP-1 induces strong migration of EoL-1 cells and the chemotaxis signal in response to MCP-1 involves a G(i)/G(o) protein, phospholipase C (PLC), PKC delta, p38 MAPK and NF-kappaB.
  • The increase in the basal expression and activity of PKC delta in EoL-1 cells, compared to normal eosinophils, inhibits apoptosis in EoL-1 cells.
  • This study contributes to an understanding of MCP-1 in eosinophil biology and pathogenic mechanism of eosinophilic disorders.
  • [MeSH-minor] Apoptosis. Blotting, Western. Cell Line, Tumor. Enzyme Activation. Eosinophils / enzymology. Eosinophils / metabolism. Flow Cytometry. Humans. Hypereosinophilic Syndrome / enzymology. Hypereosinophilic Syndrome / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 19664934.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL2; 0 / NF-kappa B; EC 2.7.11.13 / Protein Kinase C-delta
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40. Bain BJ, Fletcher SH: Chronic eosinophilic leukemias and the myeloproliferative variant of the hypereosinophilic syndrome. Immunol Allergy Clin North Am; 2007 Aug;27(3):377-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemias and the myeloproliferative variant of the hypereosinophilic syndrome.
  • In many of these patients a diagnosis of eosinophilic leukemia can be made.
  • Prompt diagnosis of such cases is important since specific tyrosine kinase inhibitor therapy is indicated.
  • [MeSH-minor] Chronic Disease. Cytokines / metabolism. Hematologic Neoplasms / diagnosis. Hematologic Neoplasms / genetics. Hematologic Neoplasms / physiopathology. Hematologic Neoplasms / therapy. Humans. Leukemia / diagnosis. Leukemia / genetics. Leukemia / physiopathology. Leukemia / therapy. Myeloproliferative Disorders / genetics. Myeloproliferative Disorders / physiopathology. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / physiology. mRNA Cleavage and Polyadenylation Factors / genetics. mRNA Cleavage and Polyadenylation Factors / physiology

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  • (PMID = 17868855.001).
  • [ISSN] 0889-8561
  • [Journal-full-title] Immunology and allergy clinics of North America
  • [ISO-abbreviation] Immunol Allergy Clin North Am
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 57
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41. Vigna E, Lucia E, Gentile M, Mazzone C, Bisconte MG, Gentile C, Armentano A, Ottaviani E, Rondoni M, Martinelli G, Morabito F: PDGFRalpha/FIP1L1-positive chronic eosinophilic leukemia presenting with retro-orbital localization: efficacy of imatinib treatment. Cancer Chemother Pharmacol; 2008 Apr;61(4):713-6
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  • [Title] PDGFRalpha/FIP1L1-positive chronic eosinophilic leukemia presenting with retro-orbital localization: efficacy of imatinib treatment.
  • CASE REPORT: A 53-year-old male presented an absolute eosinophil count of 25,000/mm(3), anemia (Hb 10.2 g/dl) and a moderate increase in the platelet count (571,000/mm(3)).
  • Imatinib mesylate (IM) was started and, after 7 days of treatment eosinophil count significantly declined along with a dramatic reduction of the left exophthalm.
  • CONCLUSION: In our case, the diagnosis of FIPIL1-PDGFRA-positive CEL and IM therapy has allowed the patient to experience an excellent clinical therapeutic result, avoiding surgical treatment of the retro-orbital mass.

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  • (PMID = 17549478.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 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
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42. 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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43. Robert C, Delva L, Balitrand N, Nahajevszky S, Masszi T, Chomienne C, Papp B: Apoptosis induction by retinoids in eosinophilic leukemia cells: implication of retinoic acid receptor-alpha signaling in all-trans-retinoic acid hypersensitivity. Cancer Res; 2006 Jun 15;66(12):6336-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis induction by retinoids in eosinophilic leukemia cells: implication of retinoic acid receptor-alpha signaling in all-trans-retinoic acid hypersensitivity.
  • We show that all-trans-retinoic acid (ATRA) inhibits eosinophil colony formation of HES-derived bone marrow cells and is a powerful inducer of apoptosis of the EoL-1 cell line.
  • Unlike in other ATRA-sensitive myeloid leukemia models, apoptosis was rapid and was not preceded by terminal cell differentiation.
  • [MeSH-major] Apoptosis / drug effects. Drug Hypersensitivity / pathology. Eosinophils / drug effects. Hypereosinophilic Syndrome / pathology. Receptors, Retinoic Acid / metabolism. Tretinoin / pharmacology

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  • (PMID = 16778211.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / Receptors, Retinoic Acid; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy].
  • CBC showed extremely elevated WBC count (186,300/microl), in which the population of blastic eosinophils was over 90%.
  • The eosinophils expressed CD7/13/33/34/DR, and the karyotype demonstrated 47,XX,+8.
  • [MeSH-major] Leukemia, Eosinophilic, Acute / complications. Leukemia, Eosinophilic, Acute / drug therapy. Methylprednisolone / adverse effects. Piperazines / adverse effects. Pyrimidines / adverse effects. Tumor Lysis Syndrome / etiology

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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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45. Jovanovic JV, Score J, Waghorn K, Cilloni D, Gottardi E, Metzgeroth G, Erben P, Popp H, Walz C, Hochhaus A, Roche-Lestienne C, Preudhomme C, Solomon E, Apperley J, Rondoni M, Ottaviani E, Martinelli G, Brito-Babapulle F, Saglio G, Hehlmann R, Cross NC, Reiter A, Grimwade D: Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. Blood; 2007 Jun 1;109(11):4635-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia.

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  • (PMID = 17299092.001).
  • [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] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / DNA Primers; 0 / FIP1L1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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46. Tanaka Y, Kurata M, Togami K, Fujita H, Watanabe N, Matsushita A, Maeda A, Nagai K, Sada A, Matsui T, Takahashi T: Chronic eosinophilic leukemia with the FIP1L1-PDGFRalpha fusion gene in a patient with a history of combination chemotherapy. Int J Hematol; 2006 Feb;83(2):152-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic eosinophilic leukemia with the FIP1L1-PDGFRalpha fusion gene in a patient with a history of combination chemotherapy.
  • Although a number of similar eosinophilic cases have been reported, our patient may be the first such patient with a history of chemotherapy.

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  • (PMID = 16513534.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 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
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47. Ishihara K, Takahashi A, Kaneko M, Sugeno H, Hirasawa N, Hong J, Zee O, Ohuchi K: Differentiation of eosinophilic leukemia EoL-1 cells into eosinophils induced by histone deacetylase inhibitors. Life Sci; 2007 Mar 6;80(13):1213-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differentiation of eosinophilic leukemia EoL-1 cells into eosinophils induced by histone deacetylase inhibitors.
  • EoL-1 cells differentiate into eosinophils in the presence of n-butyrate, but the mechanism has remained to be elucidated.
  • Because n-butyrate can inhibit histone deacetylases, we hypothesized that the inhibition of histone deacetylases induces the differentiation of EoL-1 cells into eosinophils.
  • In this study, using n-butyrate and two other histone deacetylase inhibitors, apicidin and trichostatin A, we have analyzed the relationship between the inhibition of histone deacetylases and the differentiation into eosinophils in EoL-1 cells.
  • It was demonstrated that apicidin and n-butyrate induced a continuous acetylation of histones H4 and H3, inhibited the proliferation of EoL-1 cells without attenuating the level of FIP1L1-PDGFRA mRNA, and induced the expression of markers for mature eosinophils such as integrin beta7, CCR1, and CCR3 on EoL-1 cells, while trichostatin A evoked a transient acetylation of histones and induced no differentiation into eosinophils.
  • These findings suggest that the continuous inhibition of histone deacetylases in EoL-1 cells induces the differentiation into mature eosinophils.
  • [MeSH-major] Cell Differentiation / drug effects. Enzyme Inhibitors / pharmacology. Eosinophils / drug effects. Histone Deacetylase Inhibitors. Hypereosinophilic Syndrome / drug therapy

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  • (PMID = 17258775.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Butyrates; 0 / Enzyme Inhibitors; 0 / FIP1L1 protein, human; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Peptides, Cyclic; 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / apicidin; 0 / mRNA Cleavage and Polyadenylation Factors; 3X2S926L3Z / trichostatin A; EC 3.5.1.98 / Histone Deacetylases
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48. Bletry O, Kahn JE, Ackermann F, Charles P, Legrand F: [New insights into hypereosinophilic syndromes]. Bull Acad Natl Med; 2010 Mar;194(3):547-59; discussion 559-60
Genetic Alliance. consumer health - Hypereosinophilic syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • HES can directly affect the eosinophil lineage (often linked to a fusion gene FIP1L1-PDGFRA, and corresponding in this case to chronic eosinophilic leukemia), or the lymphoid lineage, where eosinophilia is secondary to expansion of a T cell subset overproducing interleukin-5, a cytokine involved in eosinophilopoiesis.
  • These recent discoveries have legitimized the use of tyrosine kinase inhibitors such as imatinib, which, by inhibiting PDGFRA, have transformed the prognosis of chronic eosinophilic leukemia, and also the use of monoclonal anti-IL-5 antibodies, which are promising treatment for steroid-dependent HES.

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  • (PMID = 21171248.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Cytokines; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Interleukin-5; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / mepolizumab; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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49. Baumgartner C, Gleixner KV, Peter B, Ferenc V, Gruze A, Remsing Rix LL, Bennett KL, Samorapoompichit P, Lee FY, Pickl WF, Esterbauer H, Sillaber C, Superti-Furga G, Valent P: Dasatinib inhibits the growth and survival of neoplastic human eosinophils (EOL-1) through targeting of FIP1L1-PDGFRalpha. Exp Hematol; 2008 Oct;36(10):1244-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib inhibits the growth and survival of neoplastic human eosinophils (EOL-1) through targeting of FIP1L1-PDGFRalpha.
  • OBJECTIVE: Chronic eosinophilic leukemia (CEL) is a myeloproliferative disorder characterized by molecular and/or cytogenetic evidence of clonality of eosinophils, marked eosinophilia, and organ damage.
  • Therefore, several attempts have been made to identify other TK inhibitors that counteract growth of neoplastic eosinophils.
  • MATERIALS AND METHODS: We provide evidence that dasatinib, a multi-targeted kinase inhibitor, blocks the growth and survival of EOL-1, an eosinophil leukemia cell line carrying FIP1L1-PDGFRalpha.
  • CONCLUSIONS: Dasatinib inhibits the growth of leukemic eosinophils through targeting of the disease-related oncoprotein FIP1L1-PDGFRalpha.
  • [MeSH-major] Cell Division / drug effects. Cell Survival / drug effects. Eosinophils / physiology. Hypereosinophilic Syndrome / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. Thiazoles / pharmacology. mRNA Cleavage and Polyadenylation Factors / physiology

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  • (PMID = 18619723.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / mRNA Cleavage and Polyadenylation Factors; RBZ1571X5H / Dasatinib; VC2W18DGKR / Thymidine
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50. Fletcher S, Bain B: Diagnosis and treatment of hypereosinophilic syndromes. Curr Opin Hematol; 2007 Jan;14(1):37-42
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  • [Title] Diagnosis and treatment of hypereosinophilic syndromes.
  • PURPOSE OF REVIEW: The aim of this article is to provide an update of causes of hypereosinophilia, including advances in knowledge of eosinophilic leukemia, and to outline an approach to investigation.
  • We also aim to discuss in more detail the diagnosis and management of various hypereosinophilic syndromes including the clonal eosinophilias and those driven by abnormal cytokine-secreting T cells.
  • RECENT FINDINGS: Our understanding of the causative genetic abnormalities in eosinophilic leukemia is increasing, as is the repertoire of techniques available to detect them.
  • New treatments on the horizon include further tyrosine kinase inhibitors for use in eosinophilic leukemia, which should provide an alternative to imatinib for those patients who develop resistance.

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  • (PMID = 17133098.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 33
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51. Ishihara K, Hong J, Zee O, Ohuchi K: Mechanism of the eosinophilic differentiation of HL-60 clone 15 cells induced by n-butyrate. Int Arch Allergy Immunol; 2005;137 Suppl 1:77-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of the eosinophilic differentiation of HL-60 clone 15 cells induced by n-butyrate.
  • n-Butyrate is one of the most powerful chemical inducers of the differentiation of human eosinophilic leukemia HL-60 clone 15 cells into mature eosinophils.
  • We have recently reported that the mechanism by which HL-60 clone 15 cells differentiate into eosinophils by n-butyrate is that n-butyrate continuously inhibits histone deacetylase activity as a histone deacetylase inhibitor, resulting in continuous acetylation of histones.
  • In this review, we discuss roles of histone acetyltransferase, histone deacetylase and histone deacetylase inhibitors in the differentiation of HL-60 clone 15 cells into eosinophils.
  • [MeSH-major] Butyrates / pharmacology. Cell Differentiation / drug effects. Eosinophils / drug effects

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  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 15947489.001).
  • [ISSN] 1018-2438
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histone Deacetylase Inhibitors; 0 / Histones; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / Histone Acetyltransferases; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 41
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52. Chim CS, Ma SK: Eosinophilic leukemic transformation in polycythemia rubra vera (PRV). Leuk Lymphoma; 2005 Mar;46(3):447-50
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  • [Title] Eosinophilic leukemic transformation in polycythemia rubra vera (PRV).
  • We report a rare case of eosinophilic leukemia transformation in a patient with polycythemia rubra vera on hydroxycarbamide (hydroxyurea) therapy only.
  • Cytogenetic study showed complex abnormalities including -5, -7, +8, suggestive of a secondary leukemia.

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  • (PMID = 15621837.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] X6Q56QN5QC / Hydroxyurea
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53. Sheikh J, Weller PF: Clinical overview of hypereosinophilic syndromes. Immunol Allergy Clin North Am; 2007 Aug;27(3):333-55
Genetic Alliance. consumer health - Hypereosinophilic syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Based on recent advances in molecular and genetic diagnostic techniques and increasing experience with differences in clinical features and prognosis, some subtypes of HES have been defined, such as myeloproliferative variants, including chronic eosinophilic leukemia, and lymphocytic variants, but other subtypes remain undefined.

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  • (PMID = 17868853.001).
  • [ISSN] 0889-8561
  • [Journal-full-title] Immunology and allergy clinics of North America
  • [ISO-abbreviation] Immunol Allergy Clin North Am
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 111
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54. 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
MedlinePlus Health Information. consumer health - Eosinophilic Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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55. Klco JM, Vij R, Kreisel FH, Hassan A, Frater JL: Molecular pathology of myeloproliferative neoplasms. Am J Clin Pathol; 2010 Apr;133(4):602-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The current 2008 World Health Organization system recognizes 8 types of MPN: chronic myelogenous leukemia, chronic neutrophilic leukemia, polycythemia vera, primary myelofibrosis, essential thrombocythemia, chronic eosinophilic leukemia, mastocytosis, and myeloproliferative neoplasm, unclassifiable.
  • [MeSH-minor] Diagnosis, Differential. Humans. Signal Transduction / genetics

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  • (PMID = 20231614.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 144
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56. Tefferi A, Skoda R, Vardiman JW: Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics. Nat Rev Clin Oncol; 2009 Nov;6(11):627-37
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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57. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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58. Mesa RA: Imatinib and tyrosine kinase inhibition, in the management of BCR-ABL negative myeloproliferative disorders. Biologics; 2007 Jun;1(2):129-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The MPDs (which include polycythemia vera (PV), essential thrombocythemia (ET), chronic eosinophilic leukemia (CEL), primary myelofibrosis (PMF), chronic myelomonocytic leukemia (CMML), and systemic mast cell disease (SMCD)) exclude chronic myeloid leukemia (CML) because of the pathognomic importance of the BCR-ABL translocation for the diagnosis and treatment of this disorder with imatinib mesylate.

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  • (PMID = 19707323.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2721304
  • [Keywords] NOTNLM ; essential thrombocythemia / myelofibrosis / myeloproliferative diseases / polycythemia vera / therapy
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59. Thiele J: Philadelphia chromosome-negative chronic myeloproliferative disease. Am J Clin Pathol; 2009 Aug;132(2):261-80
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for chronic myeloproliferative disease .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The presented and submitted cases highlighted some important issues and also impending problems associated with the diagnosis and classification.
  • Cases included predominantly rare entities like chronic eosinophilic leukemia and related disorders, chronic neutrophilic leukemia, and others with specific genetic abnormalities that allowed molecularly targeted therapy.
  • In this context, the distinctive role of a positive JAK2(V617F) mutation for the diagnosis of Ph- MPD was underscored, including entities with a low allele burden and the discrimination from reactive disorders (autoimmune myelofibrosis, reactive thrombocytosis).
  • Although novel genetic and molecular approaches have significantly improved the way we classify Ph- MPD, a combined clinicopathologic approach, including representative bone marrow specimens, still remains the yardstick for diagnosis.

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  • (PMID = 19605821.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 183
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60. Robert C, Apàti A, Chomienne C, Papp B: All-trans-retinoic acid enhances apoptosis induction by tyrosine kinase inhibitors in the eosinophilic leukemia-derived EoL-1 cell line. Leuk Res; 2008 Feb;32(2):343-6
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] All-trans-retinoic acid enhances apoptosis induction by tyrosine kinase inhibitors in the eosinophilic leukemia-derived EoL-1 cell line.
  • Imatinib and retinoids induce apoptosis in FIP1L1/PDGFRalpha-positive EoL-1 leukemia cells.
  • In order to enhance the potency of the molecularly targeted therapy of eosinophilic leukemia, we investigated the effect of retinoids combined with tyrosine kinase inhibitors on EoL-1 cells.

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  • (PMID = 17915318.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Protein-Tyrosine Kinases
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61. Stover EH, Chen J, Folens C, Lee BH, Mentens N, Marynen P, Williams IR, Gilliland DG, Cools J: Activation of FIP1L1-PDGFRalpha requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent. Proc Natl Acad Sci U S A; 2006 May 23;103(21):8078-83
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The unique interstitial deletion on chromosome 4q12 that leads to expression of the FIP1L1-PDGFRalpha fusion tyrosine kinase was recently identified as a cause of chronic eosinophilic leukemia.
  • [MeSH-minor] Animals. Bone Marrow Transplantation. Cell Line, Tumor. Cells, Cultured. Dimerization. Humans. Leukemia / enzymology. Leukemia / metabolism. Mice. Protein Binding. Protein Structure, Tertiary

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  • (PMID = 16690743.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [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 / FIP1L1 protein, human; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC1472432
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62. Tefferi A, Elliott MA, Pardanani A: Atypical myeloproliferative disorders: diagnosis and management. Mayo Clin Proc; 2006 Apr;81(4):553-63
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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63. Haferlach T, Bacher U, Kern W, Schnittger S, Haferlach C: The diagnosis of BCR/ABL-negative chronic myeloproliferative diseases (CMPD): a comprehensive approach based on morphology, cytogenetics, and molecular markers. Ann Hematol; 2008 Jan;87(1):1-10
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The diagnosis of BCR/ABL-negative chronic myeloproliferative diseases (CMPD): a comprehensive approach based on morphology, cytogenetics, and molecular markers.
  • Recent years showed significant progress in the molecular characterization of the chronic myeloproliferative disorders (CMPD) which are classified according to the WHO classification of 2001 as polycythemia vera (PV), chronic idiopathic myelofibrosis (CIMF), essential thrombocythemia (ET), CMPD/unclassifiable (CMPD-U), chronic neutrophilic leukemia, and chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome, all to be delineated from BCR/ABL-positive chronic myeloid leukemia (CML).
  • After 2001, the detection of the high frequency of the JAK2V617F mutation in PV, CIMF, and ET, and of the FIP1L1-PDGFRA fusion gene in CEL further added important information in the diagnosis of CMPD.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cytogenetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / diagnosis. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics

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  • (PMID = 17938925.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 69
  • [Other-IDs] NLM/ PMC2082654
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64. Wadleigh M, Tefferi A: Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteria. Int J Hematol; 2010 Mar;91(2):174-9
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  • [Title] Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteria.
  • The classic MPNs were polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF) and chronic myelogenous leukemia.
  • (3) the reorganization of the eosinophilic disorders into a molecularly defined category of PDGFRA, PDGFRB and FGFR1-associated myeloid and lymphoid neoplasms with eosinophilia and chronic eosinophilic leukemia, not otherwise specified; and (4) refinement of the diagnostic criteria for PV, ET and PMF incorporating recently described molecular markers, JAK2V617F, JAK2 exon 12 mutations and MPL mutations.
  • [MeSH-major] Myeloproliferative Disorders / classification. Myeloproliferative Disorders / diagnosis. World Health Organization

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  • (PMID = 20191332.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 50
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65. Kim DW, Shin MG, Yun HK, Kim SH, Shin JH, Suh SP, Ryang DW: [Incidence and causes of hypereosinophilia (corrected) in the patients of a university hospital]. Korean J Lab Med; 2009 Jun;29(3):185-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Eosinophilia and hypereosinophilia were defined when absolute eosinophil count was greater than 500/microL and 1,500/microL, respectively.
  • We also found a rare case of FIP1L1-PDGFRalpha positive chronic eosinophilic leukemia combined with light chain multiple myeloma.
  • A rare case of clonal eosinophilia (chronic eosinophilic leukemia) associated with multiple myeloma was confirmed using molecular studies.

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  • [ErratumIn] Korean J Lab Med. 2010 Apr;30(2):202
  • (PMID = 19571614.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / FIP1L1 protein, human; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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66. Rodzaj M, Gałazka K, Majewski M, Zduńczyk A: A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report. Pol Arch Med Wewn; 2009 Dec;119(12):838-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic myeloid neoplasm with eosinophilia and abnormalities of platelet-derived growth factor receptor alpha (PDGFRA), referred to until 2008 as chronic eosinophilic leukemia, is distinguished from hypereosinophilic syndrome (HES), if accompanied by genetic abnormalities that enable to determine eosinophil clonality.
  • Its product is a protein showing tyrosine kinase activity leading to malignant proliferation of eosinophil precursors.
  • Differential diagnosis of HES is often difficult because hypereosinophilia may also be reactive and may occur in many nonhematological as well as hematological disorders.
  • It was impossible to unequivocally determine the type of bone marrow disease based on histologic criteria, and a wide spectrum of molecular tests differentiating the type of myeloid proliferation were necessary to establish the diagnosis.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oncogene Proteins, Fusion / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism

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  • (PMID = 20010473.001).
  • [ISSN] 1897-9483
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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67. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
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  • [Title] Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.
  • In stem cell- and myelopoietic neoplasms, eosinophils are derived from the malignant clone, whereas in lymphoid neoplasms and reactive states, eosinophilia is usually triggered by eosinopoietic cytokines.
  • 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.
  • [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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68. 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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69. Jung YJ, Woo SY, Jang MH, Miyasaka M, Ryu KH, Park HK, Seoh JY: Human eosinophils show chemotaxis to lymphoid chemokines and exhibit antigen-presenting-cell-like properties upon stimulation with IFN-gamma, IL-3 and GM-CSF. Int Arch Allergy Immunol; 2008;146(3):227-34
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  • [Title] Human eosinophils show chemotaxis to lymphoid chemokines and exhibit antigen-presenting-cell-like properties upon stimulation with IFN-gamma, IL-3 and GM-CSF.
  • BACKGROUND: Eosinophils are multifunctional leukocytes.
  • Here, we report that a human eosinophilic leukemia cell line, EoL-1, and human peripheral blood (PB) eosinophils become reactive to the lymphoid chemokines CCL21 and CCL25 upon stimulation.
  • The eosinophil fraction was purified from normal human adult PB and incubated for 1 day with the same cytokine combination.
  • Human PB eosinophils also showed chemotactic responsiveness to CCL21 and CCL25 upon stimulation with IFN-gamma, IL-3 and GM-CSF.
  • CONCLUSIONS: These in vitro observations raise the possibility that eosinophils may utilize lymphoid chemokines to enter LNs and serve antigen-presenting functions in the LN under certain inflammatory conditions.
  • [MeSH-major] Antigen Presentation / immunology. Chemotaxis / immunology. Eosinophils / drug effects. Eosinophils / immunology. Receptors, CCR / immunology. Receptors, CCR7 / immunology

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18268391.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CC chemokine receptor 9; 0 / CCR7 protein, human; 0 / Interleukin-3; 0 / Receptors, CCR; 0 / Receptors, CCR7; 82115-62-6 / Interferon-gamma; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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70. Sada A, Katayama Y, Yamamoto K, Okuyama S, Nakata H, Shimada H, Oshimi K, Mori M, Matsui T, Japanese Elderly Leukemia and Lymphoma Study Group: A multicenter analysis of the FIP1L1-alphaPDGFR fusion gene in Japanese idiopathic hypereosinophilic syndrome: an aberrant splicing skipping the alphaPDGFR exon 12. Ann Hematol; 2007 Dec;86(12):855-63
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  • To study the clinical characteristics of hypereosionophilic syndrome and chronic eosinophilic leukemia (HES/CEL) in Japan, the clinical data of 29 HES/CEL patients throughout the country were surveyed.
  • Considering the relatively low incidence of the FIP1L1-alphaPDGFR transcript positive case, extreme care must therefore be taken when making a diagnosis using RT-PCR before imatinib therapy.

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  • (PMID = 17701174.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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71. De Keersmaecker K, Cools J: Chronic myeloproliferative disorders: a tyrosine kinase tale. Leukemia; 2006 Feb;20(2):200-5
The Lens. Cited by Patents in .

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  • The archetype of this class of hematological diseases is chronic myeloid leukemia (CML), characterized by the presence of the Philadelphia (Ph) chromosome, the result of t(9;22)(q34;q11), and the associated BCR-ABL1 oncogene.
  • The majority of Ph-negative CMPDs, however, such as chronic eosinophilic leukemia, polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis are not characterized by the presence of recurrent chromosomal abnormalities.
  • Genome-wide screenings to identify novel tyrosine kinase abnormalities in CMPDs may contribute to further improvement of the diagnosis and the treatment of these diseases.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / enzymology. Myeloproliferative Disorders / genetics. Protein-Tyrosine Kinases / genetics


72. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • The CMD are traditionally classified by their morphologic appearances into discrete clinicopathologic entities based primarily on subjective technologies.
  • 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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73. Terakawa M, Tomimori Y, Goto M, Hayashi Y, Oikawa S, Fukuda Y: Eosinophil migration induced by mast cell chymase is mediated by extracellular signal-regulated kinase pathway. Biochem Biophys Res Commun; 2005 Jul 15;332(4):969-75
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  • [Title] Eosinophil migration induced by mast cell chymase is mediated by extracellular signal-regulated kinase pathway.
  • Mast cell chymase is known to induce eosinophil migration in vivo and in vitro.
  • In the present study, we investigated possible involvement of mitogen-activated protein (MAP) kinases; extracellular signal-regulated kinase (ERK), c-Jun amino-terminal kinase (JNK), and p38, in the chymase-induced eosinophil migration.
  • Human chymase induced a rapid phosphorylation of ERK1/2 and p38 in human eosinophilic leukemia EoL-1 cells, while no phosphorylation was detected in JNK.
  • Similar results were obtained in the experiments using mouse chymase and eosinophils.
  • U0126 (the inhibitor for MAP/ERK kinase) suppressed chymase-induced migration of EoL-1 cells and mouse eosinophils.
  • It is suggested therefore that chymase activates ERK and p38 probably through G-protein-coupled receptor, and that ERK but not p38 cascade may have a crucial role in chymase-induced migration of eosinophils.
  • [MeSH-major] Eosinophils / cytology. Eosinophils / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Mast Cells / enzymology. Serine Endopeptidases / chemistry

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  • (PMID = 15919053.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracenes; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Nitriles; 0 / Pyridines; 0 / Receptors, G-Protein-Coupled; 0 / SB 203580; 0 / U 0126; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; 107-92-6 / Butyric Acid; EC 2.4.2.31 / Pertussis Toxin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.39 / Chymases
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74. Mithraprabhu S, Grigoriadis G, Khong T, Spencer A: Deactylase inhibition in myeloproliferative neoplasms. Invest New Drugs; 2010 Dec;28 Suppl 1:S50-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The MPNs include eight haematological disorders: chronic myelogenous leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF), systemic mastocytosis (SM), chronic eosinophilic leukemia, not otherwise specified (CEL, NOS), chronic neutrophilic leukemia (CNL), and unclassifiable MPN (MPN, U).

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  • (PMID = 21127942.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC3003795
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75. Yamada Y, Cancelas JA: FIP1L1/PDGFR alpha-associated systemic mastocytosis. Int Arch Allergy Immunol; 2010;152 Suppl 1:101-5
Genetic Alliance. consumer health - Systemic mastocytosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Since the identification of the FIP1L1/PDGFRA fusion gene as a pathogenic cause of the hypereosinophilic syndrome (HES), the importance of the molecular classification of HES leading to the diagnosis of chronic eosinophilic leukemia (CEL) has been recognized.
  • FIP1L1/PDGFR alpha-positive disorders are characterized by clonal hypereosinophilia, multiple organ dysfunctions due to eosinophil infiltration, systemic mastocytosis (SM) and a dramatic response to treatment with imatinib mesylate.

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  • [Copyright] (c) 2010 S. Karger AG, Basel.
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  • (PMID = 20523072.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL087159; United States / NHLBI NIH HHS / HL / R42 HL080759; United States / NHLBI NIH HHS / HL / HL080759; United States / NHLBI NIH HHS / HL / HL080759-01A2S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 25
  • [Other-IDs] NLM/ PMC2917731
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76. Jain N, Cortes J, Quintás-Cardama A, Manshouri T, Luthra R, Garcia-Manero G, Kantarjian H, Verstovsek S: Imatinib has limited therapeutic activity for hypereosinophilic syndrome patients with unknown or negative PDGFRalpha mutation status. Leuk Res; 2009 Jun;33(6):837-9
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • With a molecular/cytogenetic clonality marker, the disease is classified as chronic eosinophilic leukemia (CEL).

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  • (PMID = 19013640.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS684505; NLM/ PMC4422052
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77. Fukushima K, Matsumura I, Ezoe S, Tokunaga M, Yasumi M, Satoh Y, Shibayama H, Tanaka H, Iwama A, Kanakura Y: FIP1L1-PDGFRalpha imposes eosinophil lineage commitment on hematopoietic stem/progenitor cells. J Biol Chem; 2009 Mar 20;284(12):7719-32
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FIP1L1-PDGFRalpha imposes eosinophil lineage commitment on hematopoietic stem/progenitor cells.
  • Although leukemogenic tyrosine kinases (LTKs) activate a common set of downstream molecules, the phenotypes of leukemia caused by LTKs are rather distinct.
  • Here we report the molecular mechanism underlying the development of hypereosinophilic syndrome/chronic eosinophilic leukemia by FIP1L1-PDGFRalpha.
  • Importantly, FIP1L1-PDGFRalpha but not TEL-PDGFRbeta enhanced the development of Gr-1(+)IL-5Ralpha(+) eosinophil progenitors from c-Kit(high)Sca-1(+)Lineage(-) cells.
  • FIP1L1-PDGFRalpha also promoted eosinophil development from common myeloid progenitors.
  • Furthermore, when expressed in megakaryocyte/erythrocyte progenitors and common lymphoid progenitors, FIP1L1-PDGFRalpha not only inhibited differentiation toward erythroid cells, megakaryocytes, and B-lymphocytes but aberrantly developed eosinophil progenitors from megakaryocyte/erythrocyte progenitors and common lymphoid progenitors.
  • As for the mechanism of FIP1L1-PDGFRalpha-induced eosinophil development, FIP1L1-PDGFRalpha was found to more intensely activate MEK1/2 and p38(MAPK) than TEL-PDGFRbeta.
  • In addition, a MEK1/2 inhibitor and a p38(MAPK) inhibitor suppressed FIP1L1-PDGFRalpha-promoted eosinophil development.
  • In addition, short hairpin RNAs against C/EBPalpha and GATA-2 and GATA-3KRR, which can act as a dominant-negative form over all GATA members, inhibited FIP1L1-PDGFRalpha-induced eosinophil development.
  • Together, these results indicate that FIP1L1-PDGFRalpha enhances eosinophil development by modifying the expression and activity of lineage-specific transcription factors through Ras/MEK and p38(MAPK) cascades.
  • [MeSH-major] Cell Differentiation. Eosinophils / enzymology. Hypereosinophilic Syndrome / enzymology. MAP Kinase Signaling System. Oncogene Proteins, Fusion / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism

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  • (PMID = 19147501.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Cytokines; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / GATA1 Transcription Factor; 0 / GATA2 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Gata2 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / proto-oncogene protein Spi-1; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.1.- / MAP2K2 protein, human; EC 2.7.1.- / Map2k1 protein, mouse; EC 2.7.1.- / Map2k2 protein, mouse; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 2.7.12.2 / MAP Kinase Kinase 2
  • [Other-IDs] NLM/ PMC2658066
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78. 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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  • 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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79. Score J, Curtis C, Waghorn K, Stalder M, Jotterand M, Grand FH, Cross NC: Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia. Leukemia; 2006 May;20(5):827-32
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  • Idiopathic hypereosinophilic syndrome (IHES) is a disease that is difficult to classify, and diagnosis is one of exclusion.
  • The identification of a cytogenetically invisible interstitial deletion resulting in the fusion of FIP1-Like-1 (FIP1L1) to platelet-derived growth factor receptor alpha (PDGFRA) has enabled many IHES cases to be reclassified as chronic eosinophilic leukemia.

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  • (PMID = 16498388.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 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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80. Hirota R, Roger NN, Nakamura H, Song HS, Sawamura M, Suganuma N: Anti-inflammatory effects of limonene from yuzu (Citrus junos Tanaka) essential oil on eosinophils. J Food Sci; 2010 Apr;75(3):H87-92
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  • [Title] Anti-inflammatory effects of limonene from yuzu (Citrus junos Tanaka) essential oil on eosinophils.
  • We investigated in vitro anti-inflammatory effects of limonene from yuzu peel on human eosinophilic leukemia HL-60 clone 15 cells.
  • These results suggest that limonene may have potential anti-inflammatory efficacy for the treatment of bronchial asthma by inhibiting cytokines, ROS production, and inactivating eosinophil migration.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Citrus / chemistry. Cyclohexenes / pharmacology. Eosinophils / drug effects. Fruit / chemistry. Oils, Volatile / chemistry. Terpenes / pharmacology

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  • (PMID = 20492298.001).
  • [ISSN] 1750-3841
  • [Journal-full-title] Journal of food science
  • [ISO-abbreviation] J. Food Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / CCL2 protein, human; 0 / Chemokine CCL2; 0 / Cyclohexenes; 0 / DNA-Binding Proteins; 0 / NF-kappa B; 0 / Oils, Volatile; 0 / Reactive Oxygen Species; 0 / Terpenes; 9MC3I34447 / limonene; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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81. Gotlib J: Eosinophilic myeloid disorders: new classification and novel therapeutic strategies. Curr Opin Hematol; 2010 Mar;17(2):117-24
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  • [Title] Eosinophilic myeloid disorders: new classification and novel therapeutic strategies.
  • PURPOSE OF REVIEW: The aim of this brief review is to evaluate recent developments in the classification and treatment of eosinophilic myeloid disorders in the context of reactive, lymphocyte-variant, and idiopathic eosinophilias.
  • RECENT FINDINGS: The revised 2008 WHO classification recognizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, or FGFR1') and undefined (chronic eosinophilic leukemia, not otherwise specified) eosinophilic myeloid disorders.
  • Although studied in idiopathic hypereosinophilic syndrome, the therapeutic niche of anti-interleukin-5 (mepolizumab) and anti-CD52 (alemtuzumab) antibody therapy in eosinophilic myeloid diseases has yet to be established.
  • SUMMARY: Molecular/genetic analysis is now mandatory for the diagnosis, classification, and treatment of eosinophilic myeloid disorders.
  • [MeSH-major] Hypereosinophilic Syndrome / drug therapy. Leukemia, Myeloid / drug therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 20071982.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Number-of-references] 59
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82. Chou CW, Hsu SP, Chen MT, Chen MH, Shih YH, Lee LS, Lin CF: Idiopathic hypereosinophilic syndrome with infiltration of cerebrospinal fluid by immature eosinophils: a case report and literature review. Surg Neurol; 2007;68 Suppl 1:S52-5; discussion S55
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  • [Title] Idiopathic hypereosinophilic syndrome with infiltration of cerebrospinal fluid by immature eosinophils: a case report and literature review.
  • It has been recognized that eosinophils can induce varying degrees of neural damage.
  • There are only a few reports in the literature regarding CSF by eosinophils, and the relationship between hypereosinophilic syndrome and eosinophilic leukemia remains unclear.
  • CASE DESCRIPTION: We report a case of IHS with CSF infiltration by immature eosinophils and significant subdural effusion with underlying brain parenchyma compression.
  • Respiratory distress and pulmonary infiltration with eosinophils developed.
  • Cerebrospinal fluid infiltration by immature eosinophils is a rare condition in IHS and may lead to poor prognosis, as observed in this patient, despite improved medical management (steroid and imatinib mesylate) and adequate surgical shunting for the subdural effusion.
  • [MeSH-major] Eosinophils / pathology. Hypereosinophilic Syndrome / cerebrospinal fluid. Hypereosinophilic Syndrome / physiopathology. Intracranial Hypertension / physiopathology. Subdural Effusion / physiopathology. Subdural Space / physiopathology

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  • (PMID = 17963925.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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83. Lierman E, Folens C, Stover EH, Mentens N, Van Miegroet H, Scheers W, Boogaerts M, Vandenberghe P, Marynen P, Cools J: Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. Blood; 2006 Aug 15;108(4):1374-6
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  • The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib.

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  • [Cites] Blood. 2003 Jun 15;101(12):4660-6 [12676775.001]
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  • (PMID = 16645167.001).
  • [ISSN] 0006-4971
  • [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 / Benzamides; 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 25X51I8RD4 / Niacinamide; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC1895882
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84. 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.
  • 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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85. Starosta V, Pazdrak K, Boldogh I, Svider T, Kurosky A: Lipoxin A4 counterregulates GM-CSF signaling in eosinophilic granulocytes. J Immunol; 2008 Dec 15;181(12):8688-99

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lipoxin A4 counterregulates GM-CSF signaling in eosinophilic granulocytes.
  • Eosinophils are granulated leukocytes that are involved in many inflammation-associated pathologies including airway inflammation in asthma.
  • Resolution of eosinophilic inflammation and return to homeostasis is in part due to endogenous chemical mediators, for example, lipoxins, resolvins, and protectins.
  • In view of the importance of lipoxins (LXs) in resolving inflammation, we investigated the molecular basis of LXA(4) action on eosinophilic granulocytes stimulated with GM-CSF employing the eosinophilic leukemia cell line EoL-1 as well as peripheral blood eosinophils.
  • Microscopic imaging showed that treatment of EoL-1 cells or blood eosinophils with GM-CSF resulted in the reorganization of actin and the translocation of alpha-fodrin from the cytoplasm to the plasma membrane.
  • Thus, the mechanism of LXA(4) action likely involves prevention of activation of eosinophilic granulocytes by GM-CSF through inhibition of protein tyrosine phosphorylation and modification of some cytoskeletal components.
  • [MeSH-major] Eosinophils / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / antagonists & inhibitors. Granulocyte-Macrophage Colony-Stimulating Factor / physiology. Lipoxins / physiology. Signal Transduction / immunology

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  • (PMID = 19050289.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / N01HV28184; United States / NIAID NIH HHS / AI / P01 AI062885; United States / NIEHS NIH HHS / ES / P30-ES006676; United States / NHLBI NIH HHS / HV / N01-HV-28184; United States / NHLBI NIH HHS / HV / N01 HV028184-13; United States / NHLBI NIH HHS / HV / HHSN268201000037C; United States / NIEHS NIH HHS / ES / P30 ES006676; United States / NHLBI NIH HHS / HV / N01 HV028184
  • [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 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / Inflammation Mediators; 0 / Lipoxins; 0 / Microfilament Proteins; 0 / Recombinant Proteins; 0 / fodrin; 0 / lipoxin A4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS695521; NLM/ PMC4465225
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86. Kanda R, Tsuji S, Ohmachi Y, Ishida Y, Ban N, Shimada Y: Rapid and reliable diagnosis of murine myeloid leukemia (ML) by FISH of peripheral blood smear using probe of PU. 1, a candidate ML tumor suppressor. Mol Cytogenet; 2008;1:22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid and reliable diagnosis of murine myeloid leukemia (ML) by FISH of peripheral blood smear using probe of PU. 1, a candidate ML tumor suppressor.
  • BACKGROUND: Murine myeloid leukemia (ML) provides a good animal model to study the mechanisms of radiation-induced leukemia in humans.
  • For the rapid diagnosis of ML, this study reports a FISH method using spleen cells and peripheral blood smears from ML mice exposed to gamma rays and neutrons with PU.1, a candidate ML tumor suppressor, as a probe.
  • Mice with very low frequencies of cells showing the loss of one copy of PU.1 (one-PU.1 frequency) were later diagnosed pathologically not with ML but with blastic or eosinophilic leukemia.
  • CONCLUSION: The FISH method was capable of detecting aberration of copy number of the PU.1 gene on murine chromosome 2, and using a peripheral blood smear is more practical and less invasive than conventional pathological diagnosis or the cytogenetic examination of spleen cells.

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  • (PMID = 18922187.001).
  • [ISSN] 1755-8166
  • [Journal-full-title] Molecular cytogenetics
  • [ISO-abbreviation] Mol Cytogenet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2572613
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87. Dinić-Uzurov V, Lalosević V, Milosević I, Urosević I, Lalosević D, Popović S: [Current differential diagnosis of hypereosinophilic syndrome]. Med Pregl; 2007 Nov-Dec;60(11-12):581-6
Genetic Alliance. consumer health - Hypereosinophilic syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Current differential diagnosis of hypereosinophilic syndrome].
  • Despite specific therapy, eosinophilia may persist for over a year after diagnosis, and decreases slowly.
  • We had two patients with clinical and histological features resembling chronic eosinophilic leukemia, and many others with T-cell lymphoma, planocellular or adenocarcinoma etc. where eosinophilia persisted DRUG-INDUCED EOSINOPHILIA: Drugs associated with eosinophilia include penicillins, tetracyclines, especially minocycline, clarithromycin, tetrazepam, mefloquine, and many, others.
  • HYPEREOSINOPHILIA WITH ORGAN DYSFUNCTION: Many severe diseases, such as sarcoidosis, Churg-Strauss syndrome, pemphigus vulgaris, eosinophilic gastrointestinal diseases, inflammatory bowel disease and many others are associated with hypereosinophilia and target organ damage, e.g. involvement of the heart, lungs, skin, or nervous tissue.
  • If the differential diagnosis of hypereosinophilia fails to resolve the etiology succesfully, the diagnosis of idiopathic HES remains.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Eosinophilia / diagnosis. Eosinophilia / etiology. Humans

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  • (PMID = 18666600.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
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88. Rajnai H, Bödör C, Reiniger L, Timár B, Csernus B, Szepesi A, Csomor J, Matolcsy A: [Novel method in diagnosis of chronic myeloproliferative disorders--detection of JAK2 mutation]. Orv Hetil; 2006 Nov 12;147(45):2175-9
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  • [Title] [Novel method in diagnosis of chronic myeloproliferative disorders--detection of JAK2 mutation].
  • The WHO classification describes six major groups of chronic myeloproliferative disorders, as follows: chronic myeloid leukemia, chronic neutrophilic leukemia, chronic eosinophilic leukemia, polycythemia vera, essential thrombocythemia and chronic idiopathic myelofibrosis.
  • The diagnosis of chronic myeloid leukemia and certain types of chronic eosinophilic leukemia are based on the detection of fusion genes (in chronic myeloid leukemia the BCR/ABL fusion gene, and in chronic eosinophilic leukemia the FIP1L1-PDGFRalpha gene).
  • [MeSH-major] Janus Kinase 2 / genetics. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics. Point Mutation
  • [MeSH-minor] Alleles. Amino Acid Sequence. Base Sequence. Biomarkers, Tumor / analysis. Genetic Markers. Humans. Leukemia / diagnosis. Leukemia / genetics. Molecular Sequence Data. Phenylalanine. Polycythemia Vera / diagnosis. Polycythemia Vera / genetics. Polymerase Chain Reaction / methods. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / genetics. Signal Transduction. Thrombocytopenia / diagnosis. Thrombocytopenia / genetics. Valine

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  • (PMID = 17402211.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 47E5O17Y3R / Phenylalanine; EC 2.7.10.2 / Janus Kinase 2; HG18B9YRS7 / Valine
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89. Kishimoto S, Oka S, Gokoh M, Sugiura T: Chemotaxis of human peripheral blood eosinophils to 2-arachidonoylglycerol: comparison with other eosinophil chemoattractants. Int Arch Allergy Immunol; 2006;140 Suppl 1:3-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotaxis of human peripheral blood eosinophils to 2-arachidonoylglycerol: comparison with other eosinophil chemoattractants.
  • Recently, we found that human eosinophilic leukemia EoL-1 cells and human peripheral blood eosinophils express the CB2 receptor.
  • In this study, we investigated whether the 2-AG-induced migration of human eosinophils is due to chemotaxis or chemokinesis.
  • We also compared the ability of 2-AG to induce the migration of eosinophils with those of other eosinophil chemoattractants.
  • METHODS: Eosinophils were separated from the peripheral blood of healthy donors.
  • The migration of eosinophils to various stimulants was examined using Transwell inserts.
  • RESULTS: 2-AG ether induced the migration of human eosinophils, like 2-AG.
  • The 2-AG ether-induced migration was reduced by the coincubation of eosinophils with 2-AG ether in the upper compartment of the Transwell inserts, indicating that the migration is attributable to chemotaxis.
  • The concentration of 2-AG required to induce the eosinophil migration appears to be pathophysiologically relevant, although the order of the pharmacologically effective concentration of 2-AG was approximately ten times lower than those of platelet-activating factor, RANTES and eotaxin.
  • CONCLUSION: These results strongly suggest that 2-AG is involved in the infiltration of eosinophils during allergic inflammation.
  • [MeSH-major] Arachidonic Acids / pharmacology. Chemotactic Factors, Eosinophil / pharmacology. Chemotaxis, Leukocyte / drug effects. Eosinophils / drug effects. Glycerides / pharmacology

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16772720.001).
  • [ISSN] 1018-2438
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Arachidonic Acids; 0 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Chemokine CCL5; 0 / Chemokines, CC; 0 / Chemotactic Factors, Eosinophil; 0 / Endocannabinoids; 0 / Glycerides; 0 / Platelet Activating Factor; 0 / Receptor, Cannabinoid, CB2; 53847-30-6 / 2-arachidonylglycerol
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90. Gotlib J, Cross NC, Gilliland DG: Eosinophilic disorders: molecular pathogenesis, new classification, and modern therapy. Best Pract Res Clin Haematol; 2006;19(3):535-69
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  • [Title] Eosinophilic disorders: molecular pathogenesis, new classification, and modern therapy.
  • Before the 1990s, lack of evidence for a reactive cause of hypereosinophilia or chronic eosinophilic leukemia (e.g. presence of a clonal cytogenetic abnormality or increased blood or bone marrow blasts) resulted in diagnosticians characterizing such nebulous cases as 'idiopathic hypereosinophilic syndrome (HES)'.
  • However, over the last decade, significant advances in our understanding of the molecular pathophysiology of eosinophilic disorders have shifted an increasing proportion of cases from this idiopathic HES 'pool' to genetically defined eosinophilic diseases with recurrent molecular abnormalities.
  • Rearrangements involving PDGFRA and PDGFRB in eosinophilic chronic myeloproliferative disorders, and of fibroblast growth factor receptor 1 (FGFR1) in the 8p11 stem cell myeloproliferative syndrome constitute additional examples of specific genetic alterations linked to clonal eosinophilia.
  • This recent revival in understanding the biologic basis of eosinophilic disorders has permitted more genetic specificity in the classification of these diseases, and has translated into successful therapeutic approaches with targeted agents such as imatinib mesylate and recombinant anti-IL-5 antibody.

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  • (PMID = 16781488.001).
  • [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
  • [Number-of-references] 219
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91. Salemi S, Yousefi S, Simon D, Schmid I, Moretti L, Scapozza L, Simon HU: A novel FIP1L1-PDGFRA mutant destabilizing the inactive conformation of the kinase domain in chronic eosinophilic leukemia/hypereosinophilic syndrome. Allergy; 2009 Jun;64(6):913-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel FIP1L1-PDGFRA mutant destabilizing the inactive conformation of the kinase domain in chronic eosinophilic leukemia/hypereosinophilic syndrome.
  • BACKGROUND: The Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) gene fusion is a common cause of chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES), and patients suffering from this particular subgroup of CEL/HES respond to low-dose imatinib therapy.
  • The identification of novel drug-resistant FIP1L1-PDGFRA variants may help to develop the next generation of target-directed compounds for CEL/HES and other leukemias.

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  • (PMID = 19210352.001).
  • [ISSN] 1398-9995
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Benzamides; 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 25X51I8RD4 / Niacinamide; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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92. Pardanani A: Systemic mastocytosis: bone marrow pathology, classification, and current therapies. Acta Haematol; 2005;114(1):41-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The diagnosis of systemic MCD is most commonly established by a thorough histological and immunohistochemical examination of a bone marrow (BM) trephine specimen.
  • In cases with pathognomonic perivascular and -trabecular aggregates of morphologically atypical MC and significant BM involvement, the diagnosis may be relatively straightforward.
  • In contrast, when a sparse, loose pattern of MC infiltration predominates, or when MCs are obscured by an associated non-MC hematological neoplasm, a high index of suspicion and use of adjunctive tests, including special stains, such as tryptase and CD25, may be necessary to reach a diagnosis.
  • Some cases, however, such those with Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA)(+) clonal eosinophilia associated with elevated serum tryptase levels, with features that overlap MCD and chronic eosinophilic leukemia, may not be easy to categorize on the basis of this classification.

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 15995324.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Interferon-alpha; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Interleukin-2; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
  • [Number-of-references] 120
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93. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • [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

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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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94. Pardanani A, Tefferi A: Primary eosinophilic disorders: a concise review. Curr Hematol Malig Rep; 2008 Jan;3(1):37-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [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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95. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • [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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96. La Starza R, Specchia G, Cuneo A, Beacci D, Nozzoli C, Luciano L, Aventin A, Sambani C, Testoni N, Foppoli M, Invernizzi R, Marynen P, Martelli MF, Mecucci C: The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases. Haematologica; 2005 May;90(5):596-601
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Increased bone marrow blasts (>5%) or cytogenetic/genetic markers indicate chronic eosinophilic leukemia (CEL).
  • INTERPRETATION AND CONCLUSIONS: FISH is a reliable diagnostic test for differentiating 4q-/CEL from other forms of HES, allowing an early diagnosis of good responders to imatinib mesylate therapy.

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  • (PMID = 15921374.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Benzamides; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 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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97. Zimmermann N, McBride ML, Yamada Y, Hudson SA, Jones C, Cromie KD, Crocker PR, Rothenberg ME, Bochner BS: Siglec-F antibody administration to mice selectively reduces blood and tissue eosinophils. Allergy; 2008 Sep;63(9):1156-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Siglec-F antibody administration to mice selectively reduces blood and tissue eosinophils.
  • We have recently identified Siglec-8 as an eosinophil-prominent Siglec, and cross-linking of Siglec-8 on human eosinophils induces apoptosis.
  • We therefore hypothesized that Siglec-F engagement would affect levels and viability of eosinophils in vivo.
  • METHODS: Wild type and hypereosinophilic mice were administered Siglec-F antibody and levels of eosinophils in peripheral blood and tissue were measured.
  • Eosinophil apoptosis (in vivo and in vitro) was determined by binding of Annexin-V.
  • RESULTS: Studies in IL-5 transgenic mice, displaying hypereosinophilia, show that administration of a single dose of Siglec-F antibody results in rapid reductions in quantum of eosinophils in the blood.
  • This decrease was accompanied by reductions in tissue eosinophils.
  • Quantum of eosinophils in blood was decreased using two separate antibodies, as well as in other mouse models (wild type mice and in a mouse model of chronic eosinophilic leukemia).
  • Mechanistic studies demonstrated that Siglec-F antibody administration induced apoptosis of eosinophils in vivo and in vitro.
  • CONCLUSION: These data demonstrate that activation of innate immune receptors, like Siglec-F, can significantly reduce mouse eosinophil viability.
  • As such, targeting Siglec-8/F may be a therapeutic approach for eosinophilic disorders.

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  • (PMID = 18699932.001).
  • [ISSN] 1398-9995
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 081882; United States / NIAID NIH HHS / AI / R01 AI041472; United States / NIAID NIH HHS / AI / R21 AI041472; United States / NIAID NIH HHS / AI / AI072265-01A1; United States / NIAID NIH HHS / AI / R01 AI041472-02; United States / NIAID NIH HHS / AI / AI041472-02; United States / NIAID NIH HHS / AI / AI072265-02; United States / NIAID NIH HHS / AI / AI41472; United States / NIAID NIH HHS / AI / R01 AI072265-02; United States / NIAID NIH HHS / AI / R01 AI072265; United States / NIAID NIH HHS / AI / R01 AI072265-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Siglec5 protein, mouse
  • [Other-IDs] NLM/ NIHMS124187; NLM/ PMC2726770
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98. Yamada Y, Sanchez-Aguilera A, Brandt EB, McBride M, Al-Moamen NJ, Finkelman FD, Williams DA, Cancelas JA, Rothenberg ME: FIP1L1/PDGFRalpha synergizes with SCF to induce systemic mastocytosis in a murine model of chronic eosinophilic leukemia/hypereosinophilic syndrome. Blood; 2008 Sep 15;112(6):2500-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] FIP1L1/PDGFRalpha synergizes with SCF to induce systemic mastocytosis in a murine model of chronic eosinophilic leukemia/hypereosinophilic syndrome.
  • Expression of the fusion gene FIP1-like 1/platelet-derived growth factor receptor alpha (FIP1L1/PDGFRalpha, F/P) and dysregulated c-kit tyrosine kinase activity are associated with systemic mastocytosis (SM) and chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES).

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  • [CommentIn] Blood. 2008 Sep 15;112(6):2179 [18779400.001]
  • (PMID = 18539901.001).
  • [ISSN] 1528-0020
  • [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] 0 / FIP1L1 protein, human; 0 / Recombinant Fusion Proteins; 0 / Stem Cell Factor; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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99. Kaushansky K: Hematopoietic growth factors, signaling and the chronic myeloproliferative disorders. Cytokine Growth Factor Rev; 2006 Dec;17(6):423-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In 1951, Dameshek argued that these disorders, along with chronic myelogenous leukemia (CML) display many similar clinical and laboratory features [Dameshek W.
  • In 2002, the World Health Organization expanded the definition of CMDs to also include chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia/hypereosinophilic syndrome (CEL/HES) and systemic mast cell disorder (SMCD) [Vardiman JW, Harris NL, Brunning RD.
  • Biology of chronic myelogenous leukemia-signaling pathways of initiation and transformation.
  • The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management.

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  • (PMID = 17055768.001).
  • [ISSN] 1359-6101
  • [Journal-full-title] Cytokine & growth factor reviews
  • [ISO-abbreviation] Cytokine Growth Factor Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA031615; United States / NIDDK NIH HHS / DK / DK049855-13; United States / NCI NIH HHS / CA / CA031615-25; United States / NCI NIH HHS / CA / R01 CA031615-25; United States / NIDDK NIH HHS / DK / R01 DK049855-13; United States / NIDDK NIH HHS / DK / R01 DK049855
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Hematopoietic Cell Growth Factors
  • [Number-of-references] 78
  • [Other-IDs] NLM/ NIHMS14809; NLM/ PMC1913942
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100. 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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  • 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).
  • [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

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  • (PMID = 18559612.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS814210; NLM/ PMC5018899
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