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1. 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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2. 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
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  • [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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3. 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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4. 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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  • [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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5. Horny HP, Sotlar K, Valent P: Differential diagnoses of systemic mastocytosis in routinely processed bone marrow biopsy specimens: a review. Pathobiology; 2010;77(4):169-80
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  • Diagnosis of systemic mastocytosis (SM) is mainly based on the morphological demonstration of compact mast cell infiltrates in various tissue sites.
  • Reliable immunohistochemical markers for the diagnosis and grading of SM have been established, but various differential diagnoses including myeloproliferative neoplasms, basophilic and eosinophilic leukemias may be very difficult to delineate.
  • Even more challenging is the recognition of hematological neoplasms with signs of mast cell differentiation but not fulfilling diagnostic criteria for SM, especially the rare myelomastocytic leukemia.
  • This hypogranulation can be regarded as cellular atypia and may lead to the misdiagnosis aspect of monocytic leukemia or histiocytic neoplasm.
  • Therefore, such skin lesions are an important clue to the correct diagnosis in these patients.
  • However, in aggressive or leukemic SM skin lesions are usually absent and then the correct diagnosis relies on an appropriate investigation of bone marrow biopsy specimens using both SM-related immunohistochemical markers (tryptase, KIT, CD25, CD30) but also markers excluding potential differential diagnoses.
  • Investigation for presence of the activating KIT point mutation D816V is very helpful to establish a correct diagnosis of SM in all the difficult cases exhibiting a low degree of bone marrow infiltration or puzzling morphological findings.
  • [MeSH-major] Bone Marrow / pathology. Mastocytosis, Systemic / diagnosis
  • [MeSH-minor] Adult. Basophils / immunology. Basophils / pathology. Biopsy. Diagnosis, Differential. Humans. Mast Cells / immunology. Mast Cells / pathology. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics. Myeloproliferative Disorders / immunology. Point Mutation. Urticaria Pigmentosa / diagnosis. Urticaria Pigmentosa / genetics. Urticaria Pigmentosa / pathology

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  • (PMID = 20616612.001).
  • [ISSN] 1423-0291
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
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6. Yoshimi M, Nannya Y, Watanabe T, Asai T, Ichikawa M, Yamamoto G, Kumano K, Hangaishi A, Imai Y, Takahashi T, Chiba S, Kurokawa M: Acute eosinophilic pneumonia is a non-infectious lung complication after allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Mar;89(2):244-8
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  • [Title] Acute eosinophilic pneumonia is a non-infectious lung complication after allogeneic hematopoietic stem cell transplantation.
  • Acute eosinophilic pneumonia (AEP) is an acute febrile illness with respiratory impairment, diffuse pulmonary infiltrates, and eosinophilia in bronchoalveolar lavage (BAL) fluid.
  • The imaging test demonstrated interstitial infiltrates and BAL analysis revealed marked increase of eosinophils and no sign of infection.
  • We made a diagnosis of AEP and steroid was started.
  • [MeSH-minor] Graft vs Host Disease / pathology. Humans. Leukemia / complications. Leukemia / therapy. Male. Middle Aged. Pneumonia. Transplantation, Homologous

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  • (PMID = 19132457.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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7. 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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8. Fletcher S, Bain B: Diagnosis and treatment of hypereosinophilic syndromes. Curr Opin Hematol; 2007 Jan;14(1):37-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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9. 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 Oct 16;1:22
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  • [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] England
  • [Other-IDs] NLM/ PMC2572613
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10. 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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11. Bain BJ: Review: eosinophils and eosinophilic leukemia. Clin Adv Hematol Oncol; 2010 Dec;8(12):901-3
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  • [Title] Review: eosinophils and eosinophilic leukemia.
  • [MeSH-major] Eosinophils / physiology. Hypereosinophilic Syndrome / etiology
  • [MeSH-minor] Eosinophilia / diagnosis. Eosinophilia / etiology. Humans

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  • (PMID = 21326168.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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12. 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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  • [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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13. 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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  • [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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14. Wilk A, Urbańska K, Woolley DE, Korohoda W: Cell separation with horizontal cell electrophoresis under near-isopycnic conditions on a "density cushion". Cell Mol Biol Lett; 2008;13(3):366-74
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  • The experiments described show the differences between the electrophoretic mobilities of a human eosinophilic leukaemia cell line (Eol-1) and RBC, both with and without the modification of the cell surface properties.

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  • (PMID = 18311546.001).
  • [ISSN] 1689-1392
  • [Journal-full-title] Cellular & molecular biology letters
  • [ISO-abbreviation] Cell. Mol. Biol. Lett.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Indicators and Reagents; 11103-72-3 / Ruthenium Red
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15. Suemori K, Fujiwara H, Watanabe S, Azuma T, Yasukawa M: A case of chronic myeloid leukemia with eosinophilic interstitial pneumonitis after administration of imatinib mesylate for 11 months. Int J Hematol; 2010 Dec;92(5):777-8
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  • [Title] A case of chronic myeloid leukemia with eosinophilic interstitial pneumonitis after administration of imatinib mesylate for 11 months.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lung Diseases, Interstitial / complications. Piperazines / therapeutic use. Pyrimidines / therapeutic use


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

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  • (PMID = 17041096.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / EIF4EBP1 protein, human; 0 / Indoles; 0 / Phosphoproteins; 0 / Pyrroles; 0 / sunitinib; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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18. 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


19. 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
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  • [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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20. 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
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  • [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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21. Nemoto T, Saito Y, Tokuhira M, Tomikawa A, Sagawa M, Haba Y, Hanzawa K, Sekiguchi Y, Watanabe R, Tamaru J, Itoyama S, Mori S, Kizaki M: [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy]. Rinsho Ketsueki; 2010 May;51(5):326-31
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  • [Title] [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy].
  • 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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22. 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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23. Zhang Y, He Q, Huang XJ, Jiang H, Yang SM, Lu J, Qing YZ, Shi Y, Dang H, Qiu JY, Lu DP: [Cytogenetic study on eosinophilia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):454-7
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  • The aim of study was to investigate the importance of chromosome aberration in differential diagnosis of eosinophilia and the chromosomal aberrations involved in patients with clonal eosinophilia.
  • Combining clinical, hematological and cytogenetical data, the 5 patients were diagnosed as acute myeloid leukemia with eosinophilia, chronic eosinophilic leukemia, 8p11 myeloproliferative syndrome, chronic myeloid leukemia in acute phase and acute myeloid leukemia-M(4Eo) respectively.
  • In conclusion, cytogenetical detection is very important in differential diagnosis of clonal eosinophilic disorders and chronic eosinophilic leukemia, which is suggested to be done routinely in clinic.

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  • (PMID = 17605843.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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24. Zhang Y, Yu MH, Xu SC, Yang L, Yu Y, Hao YS, Xiao ZJ: [Studying of clinical and laboratory features of chronic eosinophilic leukemias /hypereosinophilic syndrome]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jan;29(1):3-8
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  • [Title] [Studying of clinical and laboratory features of chronic eosinophilic leukemias /hypereosinophilic syndrome].
  • OBJECTIVE: To investigate the clinical and laboratory features of chronic eosinophilic leukemias (CEL) and hypereosinophilic syndrome (HES).
  • There was no significant difference in circulating absolute eosinophil, leukocyte, platelet counts, hemoglobin level and percentages of eosinophil and blast cell in bone marrow between CEL and HES.
  • The morphological abnormalities of eosinophils on bone marrow smear were easily found in CEL, including hypogranularity, and cytoplasmic vacuolization, increased basophilic granule.
  • Bone marrow morphology might be of a little help in diagnosis of CEL. (3) JAK2 V617F may be involved in the pathogenesis of HES. (4) Patients with CEL carried the FIP1L1-PDGFRA fusion gene and TCR gamma rearrangement concurrently, their relationship warrants further study.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis

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  • (PMID = 18512307.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [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; EC 2.7.10.2 / Janus Kinase 2
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25. Ando J, Sugimoto K, Tamayose K, Ando M, Kojima Y, Oshimi K: Cytokine-producing sarcoma mimics eosinophilic leukaemia. Eur J Haematol; 2007 Feb;78(2):169-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine-producing sarcoma mimics eosinophilic leukaemia.
  • [MeSH-major] Diagnostic Errors. Granulocyte-Macrophage Colony-Stimulating Factor / secretion. Histiocytoma, Malignant Fibrous / secretion. Hypereosinophilic Syndrome / diagnosis. Interleukin-6 / secretion. Neoplasm Proteins / secretion. Paraneoplastic Syndromes / diagnosis. Sarcoma / secretion

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  • (PMID = 17328718.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Neoplasm Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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26. 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
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  • [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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27. Sharifi H, Nassiri SM, Esmaelli H, Khoshnegah J: Eosinophilic leukaemia in a cat. J Feline Med Surg; 2007 Dec;9(6):514-7
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  • [Title] Eosinophilic leukaemia in a cat.
  • An enzyme-linked immunosorbent assay (ELISA) test for feline leukaemia virus was negative.
  • Blood film and bone marrow examination revealed a large number of immature eosinophils with variable sizes and numbers of faintly azurophilic granules.
  • As eosinophilic leukaemia is difficult to identify by light microscopy, well-defined diagnostic criteria and the use of flow cytometry and cytochemical staining can improve the ability to correctly diagnose this type of leukaemia in cats.
  • [MeSH-major] Cat Diseases / diagnosis. Hypereosinophilic Syndrome / veterinary
  • [MeSH-minor] Animals. Blood Cell Count / veterinary. Cats. Diagnosis, Differential. Female

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  • (PMID = 17669677.001).
  • [ISSN] 1098-612X
  • [Journal-full-title] Journal of feline medicine and surgery
  • [ISO-abbreviation] J. Feline Med. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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28. 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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  • 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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29. Lavastre V, Chiasson S, Cavalli H, Girard D: Viscum album agglutinin-I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils. Br J Haematol; 2005 Aug;130(4):527-35
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  • [Title] Viscum album agglutinin-I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils.
  • Although there are several agents that induce neutrophil apoptosis, few are known as inducers of eosinophil apoptosis.
  • As eosinophils are potent effector cells contributing to allergic inflammation and asthma, we investigated whether the pro-apoptotic agent Viscum album agglutinin-I (VAA-I) could induce eosinophil apoptosis.
  • VAA-I was found to induce apoptosis in eosinophilic AML14.3D10 (3D10) cells and that these cells expressed caspases-1, -2, -3, -4, -7, -8, -9 and -10.
  • Treatment of purified human eosinophils with VAA-I was found to induce apoptosis, degradation of gelsolin and lamin B1, but unlike 3D10 cells, cleavage of lamin B1 and cell apoptosis was not reversed by z-VAD.
  • We conclude that VAA-I is a potent inducer of eosinophil apoptosis and that proteases other than those inhibited by z-VAD in 3D10 cells are involved in VAA-I-induced peripheral blood eosinophil apoptosis and lamin B1 cleavage.
  • Thus, VAA-I represents a potential candidate for the reduction of the number of eosinophils in diseases where they play important roles.
  • [MeSH-major] Caspases / metabolism. Cytoskeletal Proteins / metabolism. Leukemia, Myeloid / metabolism. Plant Preparations / pharmacology. Plant Proteins / pharmacology. Toxins, Biological / pharmacology
  • [MeSH-minor] Acute Disease. Apoptosis. Caspase 3. Caspase 8. Cell Line, Tumor. DNA Fragmentation. Eosinophils / metabolism. Gelsolin / analysis. Gelsolin / metabolism. Humans. Laminin / metabolism. Paxillin. Phosphoproteins / analysis. Phosphoproteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Ribosome Inactivating Proteins. Vimentin / analysis. Vimentin / metabolism

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  • (PMID = 16098066.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Gelsolin; 0 / LAMB1 protein, human; 0 / Laminin; 0 / PXN protein, human; 0 / Paxillin; 0 / Phosphoproteins; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Toxins, Biological; 0 / VAA-I protein, Viscum album; 0 / Vimentin; EC 3.2.2.22 / Ribosome Inactivating Proteins; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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30. Suzuki Y, Nakamura T, Tokoro M, Togano T, Ohsaka M, Kohri M, Hirata Y, Miyazaki K, Danbara M, Horie R, Miura I, Sunakawa K, Higashihara M: A case of giardiasis expressing severe systemic symptoms and marked hypereosinophilia. Parasitol Int; 2010 Sep;59(3):487-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Her peripheral blood count showed a white blood cell (WBC) count of 27.1x10(9)/L with 82.1% eosinophils.
  • At first, her eosinophil count was so high that we suspected she had an eosinophilic leukemia or hypereosinophilic syndrome.
  • Her WBC count decreased to 6.0x10(9)/L with 10% eosinophils, and her systemic symptoms improved.
  • Metronidazole was administered for two weeks, and her eosinophil count decreased. G. duodenalis is a protozoan parasite, and it is one of the most common waterborne transmission gastrointestinal parasites in the world. G. duodenalis rarely causes hypereosinophilia.
  • [MeSH-major] Eosinophilia / etiology. Giardia / isolation & purification. Giardiasis / complications. Giardiasis / diagnosis

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  • (PMID = 20601107.001).
  • [ISSN] 1873-0329
  • [Journal-full-title] Parasitology international
  • [ISO-abbreviation] Parasitol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-5
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31. 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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32. 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
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  • [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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33. Hess A, Korosoglou G, Rottbauer W, Katus HA, Mereles D: Successful treatment of cardiac manifestation of eosinophilic leukemia. Clin Res Cardiol; 2010 Jun;99(6):409-10
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  • [Title] Successful treatment of cardiac manifestation of eosinophilic leukemia.
  • [MeSH-major] Heart Diseases / diagnosis. Hypereosinophilic Syndrome / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Electrocardiography. Humans. Male. Treatment Outcome

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34. 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
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  • [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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35. 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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36. Latif N, Zaiden R, Pham D, Rana F: Soft tissue sarcoma mimicking eosinophilic leukemia. Clin Adv Hematol Oncol; 2010 Dec;8(12):899-903
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  • [Title] Soft tissue sarcoma mimicking eosinophilic leukemia.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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  • (PMID = 21326167.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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37. Fletcher S, Bain B: Eosinophilic leukaemia. Br Med Bull; 2007;81-82:115-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eosinophilic leukaemia.
  • The last few years have seen much progress in our understanding of, and treatments for, eosinophilic leukaemia.
  • In this article, we review the differential diagnosis and sub-classification of eosinophilic leukaemia, and go on to discuss clinical features, investigation and treatment of these disorders.
  • The successful treatment of certain of these patients with imatinib, followed by a greater understanding of the mechanism of this treatment, has revolutionized the outlook for many patients with eosinophilic leukaemia.
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Gene Fusion. Gene Rearrangement. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 17442690.001).
  • [ISSN] 0007-1420
  • [Journal-full-title] British medical bulletin
  • [ISO-abbreviation] Br. Med. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 32
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38. 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
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  • [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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39. 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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40. Baatout S, Derradji H, Jacquet P, Mergeay M: Increased radiation sensitivity of an eosinophilic cell line following treatment with epigallocatechin-gallate, resveratrol and curcuma. Int J Mol Med; 2005 Feb;15(2):337-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased radiation sensitivity of an eosinophilic cell line following treatment with epigallocatechin-gallate, resveratrol and curcuma.
  • Since the need to find new substances that would enhance the radiation-induced apoptosis in cancerous cells is great, we studied the effect of epigallocatechin-gallate (EGCG, a tea component), resveratrol (a wine component) and curcuma on cell proliferation and radiation-induced apoptosis in the human leukaemic cell line, EOL-1, derived from a patient with eosinophilic leukaemia.
  • [MeSH-major] Catechin / analogs & derivatives. Catechin / pharmacology. Curcuma / metabolism. Eosinophils / radiation effects. Leukemia / therapy. Plant Extracts / therapeutic use. Stilbenes / pharmacology

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  • (PMID = 15647852.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Plant Extracts; 0 / Stilbenes; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; Q369O8926L / resveratrol
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41. 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
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  • [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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42. Malfuson JV, Fagot T, Konopacki J, Mangouka L, Souleau B, de Revel T: [Hematological disorders and hypereosinophilias]. Rev Med Interne; 2009 Apr;30(4):322-30
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  • Clonal eosinophilia is related either to various myeloid malignancies or to a genuine myeloproliferative disorder from the eosinophile lineage, the so-called chronic eosinophilic leukaemia.
  • Chronic eosinophilic leukaemia can be associated with recurrent genes rearrangements involving PDGFRA, PDGFRB and FGFR1 or with clonal abnormalities not yet categorized.
  • Idiopathic hypereosinophilic syndrome remains an exclusive diagnosis in presence of moderate or severe unexplained eosinophilia with target organ damage.
  • Imatinib mesylate dramatically improves chronic eosinophilic leukaemias associated with PDGFR abnormalities, while corticosteroids are still the main treatment for the other patients.

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  • (PMID = 19201511.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Glucocorticoids; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 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
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43. Bogucka-Kocka A, Smolarz HD, Kocki J: Apoptotic activities of ethanol extracts from some Apiaceae on human leukaemia cell lines. Fitoterapia; 2008 Dec;79(7-8):487-97
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  • [Title] Apoptotic activities of ethanol extracts from some Apiaceae on human leukaemia cell lines.
  • The apoptotic activities of seven ethanol extracts from fruits of seven species of Apiaceae, Eryngium planum, Archangelica officinalis, Pastinaca sativa, Heracleum sibiricum, Carum carvi, Foeniculum vulgare, Levisticum officinale against ML-1--human acute myeloblastic leukaemia, J-45.01--human acute T cell leukaemia, EOL--human eosinophilic leukaemia, HL-60--human Caucasian promyelocytic leukaemia, 1301--human T cell leukaemia lymphoblast, C-8166--human T cell leukaemia, U-266B1--human myeloma, WICL--human Caucasian normal B cell, and H-9--human T cell, were investigated.
  • [MeSH-major] Apiaceae / chemistry. Apoptosis / drug effects. Leukemia / drug therapy. Phytotherapy. Plant Extracts / pharmacology

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  • (PMID = 18672039.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Plant Extracts
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44. 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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  • [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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45. 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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46. Simon D, Salemi S, Yousefi S, Simon HU: Primary resistance to imatinib in Fip1-like 1-platelet-derived growth factor receptor alpha-positive eosinophilic leukemia. J Allergy Clin Immunol; 2008 Apr;121(4):1054-6
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  • [Title] Primary resistance to imatinib in Fip1-like 1-platelet-derived growth factor receptor alpha-positive eosinophilic leukemia.

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  • (PMID = 18234315.001).
  • [ISSN] 1097-6825
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / mepolizumab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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47. 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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48. 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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49. 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.


50. 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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  • [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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51. 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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  • [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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