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

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  • Guide to Pharmacology. gene/protein/disease-specific - Aurora kinase (Aur) family - overview and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase A - data and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase B - data and references .
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  • (PMID = 17495131.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Organophosphates; 0 / Quinazolines; 0 / Tubulin Modulators; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; VC2W18DGKR / Thymidine; ZS7284E0ZP / Daunorubicin
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2. 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).
  • This occurred in parallel with the drug inhibiting FLT3 and its downstream signal pathways, as measured by fluorescence-activated cell sorting using the phospho-specific antibodies.
  • 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
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Humans. Mice. Mice, SCID. Transplantation, Heterologous. Treatment Outcome

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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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3. Verstovsek S, Tefferi A, Cortes J, O'Brien S, Garcia-Manero G, Pardanani A, Akin C, Faderl S, Manshouri T, Thomas D, Kantarjian H: Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis. Clin Cancer Res; 2008 Jun 15;14(12):3906-15
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  • [Title] Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis.
  • PURPOSE: Molecular characterization of Philadelphia chromosome-negative (Ph-) chronic myeloproliferative disorders, such as systemic mastocytosis (SM), has provided a clear rationale for investigating novel targeted therapies.
  • The tyrosine kinase (TK) inhibitor dasatinib is 325-fold more potent against Bcr-Abl TK than imatinib in vitro, significantly inhibiting wild-type KIT and platelet-derived growth factor receptor beta TKs, and is active against cells carrying the mutant KIT-D816V gene.
  • 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.
  • Both patients were negative for KIT-D816V mutation, had low tryptase levels, abnormal WBC counts, and anemia, and had failed prior therapy with erythropoietin.
  • Complete responses were achieved in two other patients (acute myeloid leukemia and hypereosinophilic syndrome).
  • CONCLUSION: These data show that dasatinib therapy may benefit a selected group of SM patients, primarily by improving their symptoms, but it does not eliminate the disease in the patients with KIT-D816V mutation.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Mastocytosis, Systemic / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Dasatinib. Female. Humans. Male. Middle Aged. Philadelphia Chromosome. Remission Induction. Treatment Outcome


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

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  • (PMID = 17535200.001).
  • [ISSN] 0004-8380
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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5. Tefferi A, Pardanani A: Imatinib therapy in clonal eosinophilic disorders, including systemic mastocytosis. Int J Hematol; 2004 Jun;79(5):441-7
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  • [Title] Imatinib therapy in clonal eosinophilic disorders, including systemic mastocytosis.
  • Clonal eosinophilia stipulates the presence of cytogenetic, molecular, or bone marrow histologic evidence of acute leukemia or a chronic myeloid disorder.
  • Idiopathic eosinophilia is a diagnosis of exclusion that is made after ruling out both "secondary" (reactive) and clonal eosinophilia.
  • A series of novel observations in the last 5 years have warranted a refined approach to the diagnosis as well as the treatment of clonal eosinophilic disorders, including systemic mastocytosis.
  • At the center of these new developments are mutations involving the platelet-derived growth factor receptor genes (PDGFRA and PDGFRB), which have been pathogenetically linked to clonal eosinophilia, and their presence predicts complete as well as durable treatment responses to imatinib mesylate.
  • The bone marrow histologic phenotype of these imatinib-sensitive eosinophilic disorders includes systemic mastocytosis, chronic eosinophilic leukemia, chronic myelomonocytic leukemia, and atypical chronic myeloproliferative disorder.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Eosinophilia / drug therapy. Eosinophilia / genetics. Mastocytosis, Systemic / drug therapy. Mastocytosis, Systemic / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use


6. Malagola M, Martinelli G, Rondoni M, Ottaviani E, Piccaluga PP, Ricci P, Visani G, Baccarani M: Soft tissue and skeletal involvement in FIP1L1-PDGFR-alpha positive chronic eosinophilic leukemia: imatinib mesylate may induce complete molecular and imaging remission. Haematologica; 2004 Aug;89(8):ECR25
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  • [Title] Soft tissue and skeletal involvement in FIP1L1-PDGFR-alpha positive chronic eosinophilic leukemia: imatinib mesylate may induce complete molecular and imaging remission.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hypereosinophilic Syndrome / blood. Hypereosinophilic Syndrome / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Receptor, Platelet-Derived Growth Factor alpha / blood. mRNA Cleavage and Polyadenylation Factors / blood
  • [MeSH-minor] Benzamides. Bone Marrow / pathology. Chronic Disease. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 15339694.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 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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7. Gérard J, Berdin B, Portier G, Godon A, Tessier-Marteau A, Geneviève F, Zandecki M: [Bone marrow necrosis in two patients with neoplastic disorders]. Ann Biol Clin (Paris); 2007 Nov-Dec;65(6):636-42
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  • Bone marrow necrosis is defined by extensive necrosis of the myeloid tissue and bone marrow stroma.
  • Diagnosis is done on characteristic cytological pattern of the bone marrow aspiration and/or biopsy.
  • An haematological malignancy was suspected after observation of a few peripheral blood blast cells, but necrosis was found on the bone marrow aspiration and could not lead to further haematological diagnosis.
  • Within next days, the white blood cell count and the number of blasts increased, leading to the diagnosis of acute monoblastic leukaemia.
  • A chemotherapy was started but the patient died 20 days after admission.
  • The second patient, aged 28, has been hospitalized for severe bleeding a few days after the diagnosis of a metastatic gastric tumour.
  • According to literature, bone marrow necrosis is in most instances secondary to either an haematological malignancy (60%) or to a solid tumour (30%), but only at times observed with a non-malignant disorder.
  • Bone pain, fever, cytopenias and elevated serum lactic dehydrogenase and alkaline phosphatase are frequently reported, but are mostly non specific of the diagnosis in these malignant conditions.
  • Examination of the bone marrow leads to the diagnosis: cells are pycnotic, scarcely recognizable in a background of amorphous extracellular eosinophilic proteinaceous material, and histology shows disappearance of fat spaces with preservation of the bone tissue.
  • Tissue hypoxemia due to microcirculation failure may be the main mechanism leading to the necrosis, whatever the related disorder.
  • Supportive care together with specific therapy of the causal disease must be started promptly.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Monocytic, Acute / pathology. Stomach Neoplasms / pathology

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  • (PMID = 18039608.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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8. Chu KH, Lee CC, Hsin SC, Cai BC, Wang JH, Chiang BL: Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma. Cell Mol Immunol; 2010 Sep;7(5):375-80
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  • The clinical hallmarks of asthma include elevated serum levels of immunoglobulin E (IgE), eosinophilic inflammation and airway hyper-responsiveness (AHR).
  • Today, As2O3 is used as one of the standard therapies for acute promyelocytic leukemia (APL).
  • As2O3 might therefore have therapeutic potential in treating allergic airway inflammatory diseases.
  • [MeSH-major] Arsenicals / therapeutic use. Asthma / drug therapy. Asthma / immunology. Bronchial Hyperreactivity / drug therapy. Bronchial Hyperreactivity / immunology. Eosinophils / drug effects. Eosinophils / immunology. Oxides / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bronchoalveolar Lavage Fluid / immunology. Cells, Cultured. Disease Models, Animal. Female. Immunoglobulin E / blood. Interleukin-5 / immunology. Mice. Mice, Inbred BALB C

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  • (PMID = 20495578.001).
  • [ISSN] 2042-0226
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Interleukin-5; 0 / Oxides; 37341-29-0 / Immunoglobulin E; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4002675
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9. Rajesh G, Sadasivan S, Hiran KR, Nandakumar R, Balakrishnan V: Acute myeloid leukemia presenting as obstructive jaundice. Indian J Gastroenterol; 2006 Mar-Apr;25(2):93-4
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  • [Title] Acute myeloid leukemia presenting as obstructive jaundice.
  • We report a 32-year-old man with acute myeloid leukemia presenting as obstructive jaundice.
  • On evaluation he was found to have the eosinophilic variant of M4 subtype acute myeloid leukemia.
  • He expired before chemotherapy could be instituted.
  • [MeSH-minor] Adult. Common Bile Duct Diseases / complications. Humans. Leukemia, Myeloid, Acute / complications. Male

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  • (PMID = 16763341.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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10. Trojan A, Meier R, Licht A, Taverna C: Eosinophilic pneumonia after administration of fludarabine for the treatment of non-Hodgkin's lymphoma. Ann Hematol; 2002 Sep;81(9):535-7
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  • [Title] Eosinophilic pneumonia after administration of fludarabine for the treatment of non-Hodgkin's lymphoma.
  • Fludarabine is a purine analogue which is effective in the treatment of patients with low-grade non-Hodgkin's lymphoma, including chronic lymphocytic leukemia.
  • While pulmonary toxicity due to cytotoxic drugs is increasingly diagnosed, only few cases of interstitial pneumonitis have been described following fludarabine administration.
  • Here we report the first case in the literature of an acute eosinophilic pneumonia associated with peripheral blood eosinophilia after the administration of fludarabine monotherapy for stage IV follicular lymphoma.
  • [MeSH-major] Lymphoma, Non-Hodgkin / drug therapy. Pulmonary Eosinophilia / chemically induced. Vidarabine / adverse effects. Vidarabine / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Aortic Valve Stenosis / complications. Female. Heart Failure / complications. Humans. Lymphoma, Follicular / complications. Lymphoma, Follicular / drug therapy. Middle Aged

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  • (PMID = 12373357.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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11. Tashiro H, Shirasaki R, Noguchi M, Gotoh M, Kawasugi K, Shirafuji N: Molecular analysis of chronic eosinophilic leukemia with t(4;10) showing good response to imatinib mesylate. Int J Hematol; 2006 Jun;83(5):433-8
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  • [Title] Molecular analysis of chronic eosinophilic leukemia with t(4;10) showing good response to imatinib mesylate.
  • A 38-year-old Japanese man was referred to our hospital in June 2003 for treatment of acute respiratory failure with severe eosinophilia.
  • However, karyotypic examination of bone marrow cells revealed that chromosomal translocation with t(4;10)(q12;p11) had occurred in 2000, and chronic eosinophilic leukemia was diagnosed.
  • Despite treatment with steroid pulse therapy and cytarabine, the blood eosinophil count did not decrease, and the patient's respiratory condition worsened.
  • [MeSH-major] Hypereosinophilic Syndrome / drug therapy. Hypereosinophilic Syndrome / enzymology. Oncogene Proteins, Fusion / antagonists & inhibitors. Piperazines / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors. mRNA Cleavage and Polyadenylation Factors / antagonists & inhibitors
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. Benzamides. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 4 / genetics. Chronic Disease. Enzyme Activation / drug effects. Eosinophilia / drug therapy. Eosinophilia / enzymology. Eosinophilia / genetics. Follow-Up Studies. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Imatinib Mesylate. Leukocyte Count. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Time Factors. Translocation, Genetic / genetics

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  • (PMID = 16787876.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 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 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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12. Walz C, Curtis C, Schnittger S, Schultheis B, Metzgeroth G, Schoch C, Lengfelder E, Erben P, Müller MC, Haferlach T, Hochhaus A, Hehlmann R, Cross NC, Reiter A: Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene. Genes Chromosomes Cancer; 2006 Oct;45(10):950-6
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  • [Title] Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene.
  • Chronic myeloproliferative disorders with rearrangements of the platelet-derived growth factor receptor A (PDGFRA) gene at chromosome band 4q12 have shown excellent responses to targeted therapy with imatinib.
  • Here we report a female patient who presented with advanced phase of a chronic eosinophilic leukemia.
  • Despite achieving complete cytogenetic and molecular remission on imatinib, the patient relapsed with imatinib-resistant acute myeloid leukemia that was characterized by a normal karyotype, absence of detectable CDK5RAP2-PDGFRA mRNA, and a newly acquired G12D NRAS mutation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 9 / genetics. Hypereosinophilic Syndrome / drug therapy. Hypereosinophilic Syndrome / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Aged. Amino Acid Sequence. Base Sequence. Benzamides. Chronic Disease. DNA Mutational Analysis. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Intracellular Signaling Peptides and Proteins / genetics. Molecular Sequence Data. Nerve Tissue Proteins / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor alpha / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16845659.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CDK5RAP2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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13. Nemoto T, Saito Y, Tokuhira M, Tomikawa A, Sagawa M, Haba Y, Hanzawa K, Sekiguchi Y, Watanabe R, Tamaru J, Itoyama S, Mori S, Kizaki M: [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy]. Rinsho Ketsueki; 2010 May;51(5):326-31
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  • [Title] [Acute-onset eosinophilic leukemia associated with tumor lysis syndrome after imatinib and steroid pulse therapy].
  • As plural effusion due to the underlying disease progressively worsened, she was given prednisolone and hydroxyurea, but the effect was limited.
  • Steroid pulse therapy and imatinib (100 mg/day) were administrated.
  • The WBC count rapidly decreased, but tumor lysis syndrome led to acute renal failure and disseminated intravasucular coagulation appeared.
  • Supportive therapies such as artificial dialysis and transfusions were conducted, but unfortunately she died because of alveolar hemorrhage.
  • [MeSH-major] Leukemia, Eosinophilic, Acute / complications. Leukemia, Eosinophilic, Acute / drug therapy. Methylprednisolone / adverse effects. Piperazines / adverse effects. Pyrimidines / adverse effects. Tumor Lysis Syndrome / etiology
  • [MeSH-minor] Acute Kidney Injury / etiology. Aged, 80 and over. Benzamides. Disseminated Intravascular Coagulation / etiology. Drug Synergism. Fatal Outcome. Female. Humans. Hypereosinophilic Syndrome / complications. Imatinib Mesylate. Pleural Effusion / etiology. Pulse Therapy, Drug

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  • (PMID = 20534953.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X4W7ZR7023 / Methylprednisolone
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14. Moralidis E, Papakonstantinou E, Arsos G, Boussios N, Koliouskas D, Karakatsanis C: Tc-99m HMPAO labeled white blood cell imaging in a child with eosinophilic lung disease. Clin Nucl Med; 2008 Jan;33(1):38-40
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  • [Title] Tc-99m HMPAO labeled white blood cell imaging in a child with eosinophilic lung disease.
  • In radiolabeled leukocyte imaging, Tc-99m HMPAO has a significantly higher selectivity for eosinophils than neutrophils, but this may be clinically meaningful in disorders with eosinophilic infiltration.
  • We present the case of a 2-year-old boy with infection who also developed drug-induced eosinophilic lung disease, as established later by bronchoalveolar lavage and discontinuation of the responsible antistaphylococcal agent.
  • These findings were consistent with eosinophilic lung infiltration and underline the importance of clinical and laboratory data in the comprehensive interpretation of Tc-99m HMPAO labeled leukocytes scans.
  • [MeSH-minor] Acetamides / adverse effects. Anti-Infective Agents / adverse effects. Child, Preschool. Humans. Leukemia, Myeloid, Acute / complications. Leukocytes. Linezolid. Magnetic Resonance Imaging. Male. Oxazolidinones / adverse effects. Staphylococcal Infections / drug therapy

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  • (PMID = 18097257.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetamides; 0 / Anti-Infective Agents; 0 / Oxazolidinones; 0 / Radiopharmaceuticals; 3B744AG22N / Technetium Tc 99m Exametazime; ISQ9I6J12J / Linezolid
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15. Pamuk GE, Turgut B, Vural O, Demir M, Hatipoğlu O, Unlü E, Altaner S, Gerenli M, Cakir B: Pulmonary alveolar proteinosis in a patient with acute lymphoid leukemia regression after G-CSF therapy. Leuk Lymphoma; 2003 May;44(5):871-4
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  • [Title] Pulmonary alveolar proteinosis in a patient with acute lymphoid leukemia regression after G-CSF therapy.
  • Here, we present a patient with acute lymphoid leukemia (ALL) in first remission that developed fever and diffuse pulmonary infiltrates during the neutropenic stage of consolidation chemotherapy.
  • The histopathologic examination of bronchoalveolar lavage (BAL) fluid and transbronchial biopsy specimen demonstrated the presence of PAS-positive eosinophilic material.
  • After the correction of neutropenia with G-CSF, the patient's fever disappeared, acute phase reactants decreased, pulmonary infiltrates resolved.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Pulmonary Alveolar Proteinosis / drug therapy
  • [MeSH-minor] Female. Humans. Leukemic Infiltration. Middle Aged. Neutropenia / drug therapy. Remission Induction

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  • (PMID = 12802928.001).
  • [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] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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16. Nishioka C, Ikezoe T, Yang J, Yokoyama A: Long-term exposure of leukemia cells to multi-targeted tyrosine kinase inhibitor induces activations of AKT, ERK and STAT5 signaling via epigenetic silencing of the PTEN gene. Leukemia; 2010 Sep;24(9):1631-40
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  • [Title] Long-term exposure of leukemia cells to multi-targeted tyrosine kinase inhibitor induces activations of AKT, ERK and STAT5 signaling via epigenetic silencing of the PTEN gene.
  • Imatinib induces complete molecular response in patients with chronic myeloid leukemia (CML) and chronic eosinophilic leukemia (CEL).
  • However, development of resistance to imatinib has emerged as an important clinical problem for molecular-targeted therapy in CML and 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.
  • Anti-epigenetic agents may be useful for overcoming drug resistance in such a case.
  • [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
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Chromatin Immunoprecipitation. DNA Primers. Enzyme Activation. Flow Cytometry. Humans. Reverse Transcriptase Polymerase Chain Reaction

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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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17. O'Shea AM, Wilson GJ, Ling SC, Minassian BA, Turnbull J, Cutz E: Lafora-like ground-glass inclusions in hepatocytes of pediatric patients: a report of two cases. Pediatr Dev Pathol; 2007 Sep-Oct;10(5):351-7
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  • Case 1 had alpha-thalassaemia major and was receiving iron chelation therapy, whereas case 2 had trisomy 21 with a history of bone marrow transplantation for acute myeloid leukemia.
  • The liver sections in both cases showed eosinophilic, periodic acid-Schiff diastase-positive intracytoplasmic inclusions that were negative for hepatitis B surface antigen.
  • Ultrastructural changes in both cases differed from classical Lafora inclusions and ruled out hepatitis B surface antigen, glycogenosis type IV, and fibrinogen storage disease.
  • Genetic analysis of the Lafora's disease genes performed in case 2 revealed no mutations.
  • The development of hepatocyte cytoplasmic inclusions in both our cases could be related to medication effects, because similar inclusions were reported in patients using cyanamide.
  • Drug-induced inclusions, mimicking Lafora's disease, should be included in the differential diagnosis of hepatocyte ground-glass inclusions.
  • [MeSH-major] Chelation Therapy / adverse effects. Deferoxamine / adverse effects. Hepatocytes / drug effects. Hepatocytes / ultrastructure. Inclusion Bodies / ultrastructure
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Transplantation. Child, Preschool. Diagnosis, Differential. Down Syndrome. Humans. Immunohistochemistry. Iron. Lafora Disease / pathology. Leukemia, Myeloid, Acute / therapy. Male. Microscopy, Electron, Transmission. alpha-Thalassemia / drug therapy

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  • (PMID = 17929993.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; E1UOL152H7 / Iron; J06Y7MXW4D / Deferoxamine
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18. Rossini MS, de Souza EM, Cintra ML, Pagnano KB, Chiari AC, Lorand-Metze I: Cutaneous adverse reaction to 2-chlorodeoxyadenosine with histological flame figures in patients with chronic lymphocytic leukaemia. J Eur Acad Dermatol Venereol; 2004 Sep;18(5):538-42
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  • [Title] Cutaneous adverse reaction to 2-chlorodeoxyadenosine with histological flame figures in patients with chronic lymphocytic leukaemia.
  • INTRODUCTION: 2-Chlorodeoxyadenosine (cladribine or 2-CdA) is a purine analogue that has been used successfully in hairy cell leukaemia (HCL).
  • Moreover, it has been increasingly used to treat chronic lymphoproliferative syndromes and paediatric acute myeloid leukaemia.
  • Cutaneous side-effects associated with this drug have seldom been described in cases of HCL.
  • PATIENTS AND METHODS: We describe three patients with chronic lymphocytic leukaemia that presented generalized skin eruptions after treatment with 2-CdA.
  • RESULTS: All patients had advanced disease, receiving 2-CdA as a second or third line chemotherapy.
  • Skin lesions were severe and chemotherapy had to be discontinued.
  • Histological examination of skin biopsies showed an eosinophil-rich infiltrate with flame figures, similar to what is observed in Wells' syndrome (eosinophilic cellulitis).
  • CONCLUSIONS: Cutaneous adverse reactions associated with 2-CdA have seldom been observed in the treatment of HCL.
  • The pathophysiology of these lesions is unclear, but it is probably related to drug-induced change in T-cell imbalance in severely immunosuppressed patients.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cladribine / adverse effects. Drug Eruptions / diagnosis. Exanthema / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Middle Aged

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  • [Copyright] Copyright 2004 European Academy of Dermatology and Venereology
  • (PMID = 15324388.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 47M74X9YT5 / Cladribine
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19. Panigrahi I, Naithani R: Imatinib mesylate: A designer drug. J Assoc Physicians India; 2006 Mar;54:203-6
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  • [Title] Imatinib mesylate: A designer drug.
  • Molecularly targeted therapy is a novel approach in cancer treatment.
  • Imatinib, a specific tyrosine kinase inhibitor, since its inception in 1990s, has become the first-line drug in management of chronic myelogenous leukemia (CML) chronic phase.
  • It has also shown promising results in treatment of gastro-intestinal stromal tumors, clonal eosinophilic disorders and Philadelphia chromosome positive acute lymphatic leukemia.
  • The efficacy of imatinib has geared up further research into development of designer drugs with molecular targets.
  • [MeSH-minor] Benzamides. Eosinophilia / drug therapy. Gastrointestinal Stromal Tumors / drug therapy. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16800347.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 31
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20. Agnew KL, Ruchlemer R, Catovsky D, Matutes E, Bunker CB: Cutaneous findings in chronic lymphocytic leukaemia. Br J Dermatol; 2004 Jun;150(6):1129-35
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  • [Title] Cutaneous findings in chronic lymphocytic leukaemia.
  • BACKGROUND: Chronic lymphocytic leukaemia (CLL) is a malignancy characterized by clonal expansion of B lymphocytes with distinct morphology and immunophenotype.
  • In 21 of these 41 complications there had been no prior immunosuppressive therapy.
  • Other cutaneous findings included varicella zoster (n = 6), leukaemia cutis (n = 3), acute graft-versus-host disease (n = 5), cutaneous drug eruptions (n = 9), multiple warts (n = 3), herpes simplex (n = 3), cutaneous T-cell lymphoma (n = 2), eosinophilic folliculitis (n = 2), malignant melanoma (n = 2) and Merkel cell tumour (n = 2).
  • The atypia was independent of prior chemotherapy.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Skin Diseases / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Carcinoma, Basal Cell / complications. Carcinoma, Merkel Cell / complications. Carcinoma, Squamous Cell / complications. Chickenpox / complications. Drug Eruptions / complications. Female. Folliculitis / complications. Graft vs Host Disease. Herpes Simplex / complications. Humans. Lymphoma, T-Cell, Cutaneous / complications. Male. Melanoma / complications. Middle Aged. Retrospective Studies. Skin Neoplasms / complications. Warts / complications

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  • (PMID = 15214899.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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21. Crook TW, Rogers BB, McFarland RD, Kroft SH, Muretto P, Hernandez JA, Latimer MJ, McKenna RW: Unusual bone marrow manifestations of parvovirus B19 infection in immunocompromised patients. Hum Pathol; 2000 Feb;31(2):161-8
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  • Parvovirus B19 is responsible for a spectrum of disease in humans.
  • The usual bone marrow findings in acute parvovirus infections are marked erythroid hypoplasia and occasional giant erythroblasts.
  • Intranuclear inclusions in developing erythroid precursors are rarely described in children or adults with parvovirus infection, although abundant intranuclear inclusions are commonly observed in the placenta and other tissues in infected fetuses.
  • Six of the 8 patients had documented immunodeficiencies; 4 had acquired immune deficiency syndrome (AIDS), and 2 were on chemotherapy.
  • Unlike the typical pattern in parvovirus infection, the bone marrow was hypercellular in most of the patients, and erythroid precursors were usually increased with the entire spectrum of normoblast maturation represented; abundant intranuclear inclusions were observed similar to the finding in fetuses.
  • The inclusions were variably eosinophilic and compressed the chromatin against the nuclear membrane.
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / virology. Adult. Anemia / virology. Antineoplastic Agents / adverse effects. Biopsy. Cell Nucleus / pathology. Child. DNA, Viral / analysis. Erythrocytes / ultrastructure. Erythroid Precursor Cells / ultrastructure. Female. Humans. Inclusion Bodies / ultrastructure. Leukemia, Lymphoid / drug therapy. Male. Microscopy, Electron. Middle Aged

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  • (PMID = 10685629.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Viral
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22. 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
  • [MeSH-minor] Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Fruit. Humans

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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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23. Zouboulis CC: Retinoids--which dermatological indications will benefit in the near future? Skin Pharmacol Appl Skin Physiol; 2001 Sep-Oct;14(5):303-15
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Psoriasis and related disorders, congenital disorders of keratinization, acne, photoaging and hypovitaminosis A are classical approved indications of retinoid treatment, whereas cutaneous T-cell lymphoma, AIDS-associated Kaposi's sarcoma, acute promyelocytic leukemia and actinic lentigines were currently confirmed.
  • In addition, retinoids have been successfully used in several other dermatoses, e.g. epithelial precanceroses and tumors, seborrhea, rosacea and acneiform dermatoses, lichen planus, eosinophilic folliculitis, condylomata accuminata, lichen sclerosus and atrophicus.
  • New, more effective and less toxic retinoids, alone or in combination with other drugs and new delivery systems may provide therapeutic solutions for benign and malignant proliferative skin diseases, such as psoriasis and non-melanoma tumors, cancer chemoprevention and differentiation therapy.
  • [MeSH-major] Retinoids / therapeutic use. Skin Diseases / drug therapy

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11586072.001).
  • [ISSN] 1422-2868
  • [Journal-full-title] Skin pharmacology and applied skin physiology
  • [ISO-abbreviation] Skin Pharmacol. Appl. Skin Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Retinoids
  • [Number-of-references] 90
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24. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.
  • Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes.
  • Treatment of hypereosinophilic patients depends on the variant of disease, presence of end organ damage, molecular targets, and the overall situation in each case.
  • In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.
  • [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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