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3. Saito SY, Maruyama Y, Kamiyama S, Nakahata N, Ohizumi Y: Ephedrae herba in Mao-Bushi-Saishin-To inhibits IgE-mediated histamine release and increases cAMP content in RBL-2H3 cells. J Pharmacol Sci; 2004 May;95(1):41-6
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  • Acute effect of Mao-Bushi-Saishin-To (Ma-Huang-Fu-Zi-Xi-Xin-Tang in Chinese: MBS) on histamine release was investigated.
  • Mao as well as MBS but not Saishin nor Bushi inhibited IgE-mediated histamine release from rat basophilic leukemia (RBL-2H3) cells.
  • [MeSH-major] Cyclic AMP / biosynthesis. Drugs, Chinese Herbal / pharmacology. Ephedra. Ephedrine / analogs & derivatives. Histamine Release / drug effects. Immunoglobulin E / physiology. Immunosuppressive Agents / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Leukemia, Basophilic, Acute / drug therapy. Leukemia, Basophilic, Acute / immunology. Male. Rats. Rats, Wistar

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  • (PMID = 15153649.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Immunosuppressive Agents; 0 / mao-bushi-saishin-to; 37341-29-0 / Immunoglobulin E; 60VH42A1KJ / N-methylephedrine; E0399OZS9N / Cyclic AMP; GN83C131XS / Ephedrine
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4. Moser AM, Manor E, Narkis G, Kapelushnik J: Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up. Cancer Genet Cytogenet; 2006 Oct 1;170(1):54-7
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  • [Title] Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up.
  • The case of an 11-year-old child with adult-type chronic myeloid leukemia, Philadelphia (BCR-ABL) positive, reverse transcription-polymerase chain reaction negative for the major, minor, and micro breakpoints is presented.
  • In the course of 3 years, the child failed to respond to treatment with hydroxyurea, refused all therapy for 6 months, was intolerant to alpha-interferon and progressed, while on imatinib, to acute basophilic leukemia.
  • A secondary cytogenetic clonal evolution, i(17q), developed during hydroxyurea treatment and a tertiary clonal evolution, +8, was detected during imatinib treatment.
  • It is not clear to what extent the several factors (undefined BCR-ABL breakpoint, treatment avoidance, and initial treatment choices, alone or in combination) played a role in the imatinib relapse and resistance and in the disease progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Genes, abl. Leukemia, Basophilic, Acute / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Bone Marrow Transplantation. Child. Disease Progression. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16965955.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [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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5. Yokohama A, Tsukamoto N, Hatsumi N, Suto M, Akiba T, Uchiumi H, Maehara T, Matsushima T, Karasawa M, Murakami H, Shinonome S, Saito H, Nojima Y: Acute basophilic leukemia lacking basophil-specific antigens: the importance of cytokine receptor expression in differential diagnosis. Int J Hematol; 2002 Apr;75(3):309-13
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  • [Title] Acute basophilic leukemia lacking basophil-specific antigens: the importance of cytokine receptor expression in differential diagnosis.
  • De novo acute basophilic leukemia (ABL) is a rare form of myeloid leukemia.
  • The low prevalence of ABL makes it difficult to define its clinical characteristics and to establish an effective therapeutic protocol.
  • The diagnosis of ABL depended on the following:.
  • The patient achieved complete remission with intensive chemotherapy composed of idarubicin and cytosine arabinoside and was disease free during the following 30 months.
  • [MeSH-major] Antigens, CD / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Basophilic, Acute / diagnosis. Mast Cells / immunology. Receptors, Cytokine / genetics
  • [MeSH-minor] Bone Marrow / pathology. Cytarabine / administration & dosage. Diagnosis, Differential. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Receptors, IgE / blood

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  • (PMID = 11999362.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Receptors, Cytokine; 0 / Receptors, IgE; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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6. Scolyer RA, Brun M, D'Rozario J, Webb M: Acute basophilic leukemia presenting with abnormal liver function tests and the absence of blast cells in the peripheral blood. Pathology; 2000 Feb;32(1):52-5
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  • [Title] Acute basophilic leukemia presenting with abnormal liver function tests and the absence of blast cells in the peripheral blood.
  • Acute basophilic leukemia is an uncommon form of acute leukemia, rarely occurring as a de novo disease.
  • We describe a case of de novo acute basophilic leukemia occurring in a 47-year-old man who presented with abnormal liver function tests in the absence of leukemic infiltration of the liver.
  • We postulate that this presentation occurred as a consequence of pathophysiological features of the malignant basophilic blast cells.
  • [MeSH-major] Leukemia, Basophilic, Acute / diagnosis. Leukemic Infiltration / pathology. Liver / pathology. Liver Function Tests. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Cytoplasmic Granules / ultrastructure. Diagnosis, Differential. Drug Therapy, Combination. Fatal Outcome. Humans. Idarubicin / therapeutic use. Immunophenotyping. Karyotyping. Male. Middle Aged

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  • (PMID = 10740808.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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7. Giagounidis AA, Hildebrandt B, Heinsch M, Germing U, Aivado M, Aul C: Acute basophilic leukemia. Eur J Haematol; 2001 Aug;67(2):72-6
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  • [Title] Acute basophilic leukemia.
  • Acute basophilic leukemia has recently been included into a revised classification of acute leukemias proposed by the WHO panel.
  • Due to the rarity of the disease, consistent diagnostic criteria are lacking.
  • We report on two cases of acute basophilic leukemia that occurred in our department during the last 10 yr.
  • Treatment of our patients consisted of supportive treatment in the one with normal karyotype and aggressive chemotherapy in the other patient.
  • Both patients died within one year after diagnosis due to progressive or recurrent leukemia.
  • [MeSH-major] Leukemia, Basophilic, Acute / diagnosis
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Coloring Agents. Cytarabine / administration & dosage. Cytoplasmic Granules / chemistry. Fatal Outcome. Humans. Idarubicin / administration & dosage. Immunophenotyping. Karyotyping. Leukocyte Count. Male. Middle Aged. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / pathology. Periodic Acid-Schiff Reaction. Peroxidase / analysis. Recurrence. Tolonium Chloride. Translocation, Genetic

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  • (PMID = 11722593.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Neoplasm Proteins; 04079A1RDZ / Cytarabine; 15XUH0X66N / Tolonium Chloride; EC 1.11.1.7 / Peroxidase; ZRP63D75JW / Idarubicin
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8. Qu X, Li Y, Liu J, Xu L, Zhang Y, Hu X, Hou K, Liu Y: Cbl-b promotes chemotherapy-induced apoptosis in rat basophilic leukemia cells by suppressing PI3K/Akt activation and enhancing MEK/ERK activation. Mol Cell Biochem; 2010 Jul;340(1-2):107-14
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  • [Title] Cbl-b promotes chemotherapy-induced apoptosis in rat basophilic leukemia cells by suppressing PI3K/Akt activation and enhancing MEK/ERK activation.
  • The ubiquitin ligase Cbl-b is a negative regulator of the PI3K/Akt pathway, the survival pathway implicated in chemotherapy resistance.
  • The consistent results were also showed in the process of Ara-c treatment.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Leukemia, Basophilic, Acute / enzymology. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-cbl / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Cytarabine / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Inhibitory Concentration 50. Mutation. Rats. Time Factors. Transfection

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  • (PMID = 20177738.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 2.3.2.27 / Proto-Oncogene Proteins c-cbl; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 6.3.2.19 / Cblb protein, rat
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9. Kamiya S, Kawaguchi T, Hasebe S, Kamiya N, Saito Y, Miura S, Wada S, Yajima H, Katayama T, Fukai F: A fibronectin fragment induces tumor necrosis factor production of rat basophilic leukemia cells. Biochim Biophys Acta; 2004 Nov 18;1675(1-3):87-94
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  • [Title] A fibronectin fragment induces tumor necrosis factor production of rat basophilic leukemia cells.
  • Proteolytic digest of fibronectin (FN), but not intact FN, induced TNF-alpha secretion of rat basophilic leukemia (RBL-2H3) cells.
  • The TNF-alpha secretion was abrogated by treatment of RBL-2H3 cells with cycloheximide, indicating the de novo synthesis of TNF-alpha, but not with polymyxin B, excluding the possible TNF-alpha induction by some contaminated lipopolysaccharides.
  • [MeSH-major] Fibronectins / pharmacology. Leukemia, Basophilic, Acute / drug therapy. Peptide Fragments / pharmacology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Anti-Bacterial Agents / pharmacology. Antigens, CD29 / metabolism. Cell Adhesion / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Cycloheximide / pharmacology. Heparin / metabolism. Humans. Lipopolysaccharides / pharmacology. Polymyxin B / pharmacology. Protein Structure, Tertiary. Protein Synthesis Inhibitors / pharmacology. Rats. Tumor Cells, Cultured

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  • (PMID = 15535971.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, CD29; 0 / Fibronectins; 0 / Lipopolysaccharides; 0 / Peptide Fragments; 0 / Protein Synthesis Inhibitors; 0 / Tumor Necrosis Factor-alpha; 1404-26-8 / Polymyxin B; 9005-49-6 / Heparin; 98600C0908 / Cycloheximide
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10. Yang W, Chen J, Zhou L: Effects of shear stress on intracellular calcium change and histamine release in rat basophilic leukemia (RBL-2H3) cells. J Environ Pathol Toxicol Oncol; 2009;28(3):223-30
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  • [Title] Effects of shear stress on intracellular calcium change and histamine release in rat basophilic leukemia (RBL-2H3) cells.
  • Massage, one form of physical therapy, is widely used for a large number of musculoskeletal disorders, but its exact mechanism still remains to be elucidated.
  • One hypothesis is that the shear stress caused by massage may induce cutaneous mast cells to release histamine, thereby improving the local tissue microcirculation of blood.
  • In the present work, a mast cell line (rat basophilic leukemia cells, RBL-2H3) was used in vitro to study cellular responses to the stimulus of shear stress generated by a rotating rotor in a cell dish.
  • Because histamine is a well-known mediator of microvascular tissue dilation, these results may have an important impact on understanding the mechanism involved in massage therapy.
  • [MeSH-minor] Animals. Calcium Channels / drug effects. Calcium Channels / physiology. Calcium Signaling / drug effects. Calcium Signaling / physiology. Cell Line, Tumor. Cell Membrane / drug effects. Cell Membrane / metabolism. Indicators and Reagents / pharmacology. Leukemia, Basophilic, Acute. Microcirculation. Rats. Ruthenium Red / pharmacology. Stress, Mechanical. TRPV Cation Channels / antagonists & inhibitors. TRPV Cation Channels / metabolism

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  • (PMID = 19888909.001).
  • [ISSN] 2162-6537
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Indicators and Reagents; 0 / TRPV Cation Channels; 0 / Trpv4 protein, rat; 11103-72-3 / Ruthenium Red; 820484N8I3 / Histamine; SY7Q814VUP / Calcium
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11. Chan JH, Liao W, Lau HY, Wong WS: Gab2 antisense oligonucleotide blocks rat basophilic leukemic cell functions. Int Immunopharmacol; 2007 Jul;7(7):937-44
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  • [Title] Gab2 antisense oligonucleotide blocks rat basophilic leukemic cell functions.
  • The present study aimed to investigate the pharmacological effects of an antisense oligonucleotide (ASO) targeted at Gab2 on the immune responses of rat basophilic leukemic (RBL)-2H3 cells.
  • Gab2 mRNA and protein knockdown was confirmed by real-time RT-PCR and immunoblotting, respectively.
  • Our findings show that Gab2 knockdown in RBL-2H3 cells by ASO strategy can suppress many aspects of the mast cell functions and, therefore, a selective Gab2 ASO may have therapeutic potential for mast cell-dependent allergic disorders.
  • [MeSH-major] Basophils / immunology. Leukemia, Basophilic, Acute / drug therapy. Leukemia, Basophilic, Acute / immunology. Oligonucleotides, Antisense / pharmacology. Phosphoproteins / genetics. RNA, Messenger / metabolism. Signal Transduction / genetics

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  • (PMID = 17499196.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Fibronectins; 0 / Gab2 protein, rat; 0 / Oligonucleotides, Antisense; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Receptors, IgE; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
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12. Kobayashi S, Tanabe S: Evaluation of the anti-allergic activity of Citrus unshiu using rat basophilic leukemia RBL-2H3 cells as well as basophils of patients with seasonal allergic rhinitis to pollen. Int J Mol Med; 2006 Mar;17(3):511-5
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  • [Title] Evaluation of the anti-allergic activity of Citrus unshiu using rat basophilic leukemia RBL-2H3 cells as well as basophils of patients with seasonal allergic rhinitis to pollen.
  • To examine this anti-allergic mechanism in detail, we next used rat basophlilic leukemia RBL-2H3 cells.
  • [MeSH-major] Anti-Allergic Agents / therapeutic use. Basophils / drug effects. Citrus. Leukemia, Basophilic, Acute / immunology. Phytotherapy. Pollen / immunology. Rhinitis, Allergic, Seasonal / drug therapy
  • [MeSH-minor] Animals. Cell Degranulation / drug effects. Flavonoids / chemistry. Flavonoids / pharmacology. Flavonoids / therapeutic use. Histamine Release / drug effects. Humans. Immunoglobulin E / metabolism. Phosphatidylinositol 3-Kinases. Phosphorylation / drug effects. Plant Preparations / pharmacology. Plant Preparations / therapeutic use. Proto-Oncogene Proteins c-akt / metabolism. Rats. beta-N-Acetylhexosaminidases / secretion

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  • (PMID = 16465400.001).
  • [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 / Anti-Allergic Agents; 0 / Flavonoids; 0 / Plant Preparations; 37341-29-0 / Immunoglobulin E; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
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13. Abe M, Shibata K, Urata H, Sakata N, Katsuragi T: Induction of leukotriene C4 synthase after the differentiation of rat basophilic leukemia cells with retinoic acid and a low dose of actinomycin D and its suppression with methylprednisolone. J Cell Physiol; 2003 Jul;196(1):154-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of leukotriene C4 synthase after the differentiation of rat basophilic leukemia cells with retinoic acid and a low dose of actinomycin D and its suppression with methylprednisolone.
  • LTC(4) S activity in rat basophilic leukemia-1 (RBL-1) cells increased after culture in the presence of retinoic acid (RA) analogues, which was inhibited by cycloheximide or actinomycin D (ACD).
  • The suppression of LTC(4) S with MP showed a dependent manner on the time-point and duration of MP-treatment after RA-addition which was correlated with reduction in LTC(4) S mRNA and protein.
  • In consideration of RA-differentiation therapy, it may be of pathophysiological relevance that the antineoplastic agents potentiate RA-induced, steroid-sensitive, induction of LTC(4) S in RBL-1 cells.
  • [MeSH-major] Cell Differentiation / drug effects. Dactinomycin / antagonists & inhibitors. Dactinomycin / pharmacology. Glutathione Transferase / biosynthesis. Leukemia, Basophilic, Acute / enzymology. Methylprednisolone / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Calcimycin / pharmacology. Cell Line. Cell Size / drug effects. Chymases. Cycloheximide / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histamine / metabolism. Interleukin-4 / genetics. Lipoxygenase / metabolism. RNA Stability / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Serine Endopeptidases / metabolism. Solubility. Time Factors. Transcription, Genetic / drug effects

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12767051.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 1CC1JFE158 / Dactinomycin; 207137-56-2 / Interleukin-4; 37H9VM9WZL / Calcimycin; 5688UTC01R / Tretinoin; 820484N8I3 / Histamine; 98600C0908 / Cycloheximide; EC 1.13.11.12 / Lipoxygenase; EC 2.5.1.18 / Glutathione Transferase; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.39 / Chymases; EC 4.4.1.20 / leukotriene-C4 synthase; X4W7ZR7023 / Methylprednisolone
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14. Angulo J, Haro R, González-Guerra E, Fariña MC, Martín L, Requena L: Leukemia cutis presenting as localized cutaneous hyperpigmentation. J Cutan Pathol; 2008 Jul;35(7):662-5
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  • [Title] Leukemia cutis presenting as localized cutaneous hyperpigmentation.
  • The usual clinical presentations of leukemia cutis include solitary infiltrated erythematous or violaceous plaques or nodules and multiple localized or generalized papules.
  • On the other hand, cutaneous hyperpigmentation is a frequent finding in patients with malignancies, most of the cases because of chemotherapy or other drugs that the patient is taking.
  • We present a case of cutaneous hyperpigmentation as the presenting sign of leukemia cutis.
  • A 61-year-old male presented with cutaneous hyperpigmentation, which had appeared during the last chemotherapy cycle for treatment for biphenotypic leukemia.
  • This infiltrate was composed of atypical basophilic cells with large hyperchromatic nuclei and scant cytoplasm.
  • A diagnosis of biphenotypic leukemia cutis was established.
  • In our review of the literature we have not found any report of cutaneous hyperpigmentation as the presenting manifestation of leukemia cutis.
  • [MeSH-major] Hyperpigmentation / etiology. Leukemia, Biphenotypic, Acute / pathology. Skin / pathology. Skin Neoplasms / pathology

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  • (PMID = 18422694.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD
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15. Tsai MH, Yang CP, Chung HT, Shih LY: Acute myeloid leukemia in a young girl presenting with mediastinal granulocytic sarcoma invading pericardium and causing superior vena cava syndrome. J Pediatr Hematol Oncol; 2009 Dec;31(12):980-2
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  • [Title] Acute myeloid leukemia in a young girl presenting with mediastinal granulocytic sarcoma invading pericardium and causing superior vena cava syndrome.
  • A 1-year-4-month-old girl who presented with pericardial effusion and superior vena cava (SVC) syndrome caused by a mediastinal mass was later proved to be a case of acute myeloid leukemia (AML) with mixed-lineage leukemia-gene translocation.
  • The unusual presentation and the giant blasts with basophilic vacuolated cytoplasm had led to initial misdiagnosis of mediastinal lymphoma.
  • She developed progressive SVC syndrome, unresolved pericardial effusion, and extensive leukemia cutis after initial induction therapy.
  • She died soon after second-course chemotherapy.
  • To our knowledge, this is the first reported case of childhood acute myeloid leukemia presenting with mediastinal granulocytic sarcoma causing pericardium invasion and SVC syndrome.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Mediastinal Neoplasms / diagnosis. Pericardium / pathology. Sarcoma, Myeloid / diagnosis. Superior Vena Cava Syndrome / diagnosis
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Fatal Outcome. Female. Humans. Infant. Pericardial Effusion / etiology


16. Brink DS: Transient leukemia (transient myeloproliferative disorder, transient abnormal myelopoiesis) of Down syndrome. Adv Anat Pathol; 2006 Sep;13(5):256-62
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  • [Title] Transient leukemia (transient myeloproliferative disorder, transient abnormal myelopoiesis) of Down syndrome.
  • Transient leukemia of Down syndrome (DS-TL), also known as transient myeloproliferative disorder of Down syndrome (DS) and transient abnormal myelopoiesis of DS, occurs in approximately 10% of DS neonates and in phenotypically normal neonates with trisomy 21 mosaicism.
  • Bone marrow characteristics of DS-TL are, likewise, variable, though (in contrast to other leukemias) the bone marrow blast differential can be lower than the peripheral blood blast differential.
  • DS-TL neonates have a approximately 15% risk of developing potentially fatal liver disease and show <10% incidence of hydrops fetalis.
  • Despite its typical transient nature, 20% to 30% of DS-TL patients develop overt (nontransient) acute leukemia, usually within 3 years and typically of the M7 phenotype (acute megakaryoblastic leukemia).
  • The pathogenesis of DS-TL (and of subsequent acute leukemia) involves mutation of GATA1 (on chromosome X), which normally encodes a transcription factor integral to normal development of erythroid, megakaryocytic, and basophilic/mast cell lines.
  • Though indications for chemotherapy in DS-TL have not been firmly established, the blasts of DS-TL are sensitive to low-dose cytosine arabinoside.
  • [MeSH-minor] GATA1 Transcription Factor / genetics. Humans. Hydrops Fetalis / etiology. Infant, Newborn. Leukemia / etiology. Liver Diseases / etiology. Mutation

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  • (PMID = 16998319.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 81
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17. Sato N, Nakazato T, Kizaki M, Ikeda Y, Okamoto S: Transformation of myelodysplastic syndrome to acute lymphoblastic leukemia: a case report and review of the literature. Int J Hematol; 2004 Feb;79(2):147-51
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  • [Title] Transformation of myelodysplastic syndrome to acute lymphoblastic leukemia: a case report and review of the literature.
  • Myelodysplastic syndrome (MDS) often transforms into acute leukemia, usually of a myeloid phenotype.
  • However, the transformation of MDS into acute lymphoblastic leukemia (ALL) is extremely rare.
  • Two months later, MDS progressed to erythroleukemia (French-American-British [FAB]classification, acute myeloid leukemia [AML]-M6), and in December, 2001, she was treated with combined chemotherapy containing aclarubicin, cytarabine, and granulocyte colony-stimulating factor, which improved her clinical symptoms.
  • However, 1 month after the chemotherapy, she developed ALL.
  • The blasts at that time had a markedly basophilic cytoplasm with multiple cytoplasmic vacuoles, and their morphology mimicked that of ALL-L3.
  • Southern-blot analysis revealed rearrangement of the immunoglobulin heavy chain, but no additional chromosomal abnormality characteristic of ALL-L3 was detected.
  • The patient was treated with chemotherapy, but she developed tumor lysis syndrome and died of multiple organ failure.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Myelodysplastic Syndromes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


18. Kawano-Yamamoto C, Muroi K, Nagatsuka Y, Higuchi M, Kikuchi S, Nagai T, Hakomori SI, Ozawa K: Establishment and characterization of a new erythroblastic leukemia cell line, EEB: phosphatidylglucoside-mediated erythroid differentiation and apoptosis. Leuk Res; 2006 Jul;30(7):829-39
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  • [Title] Establishment and characterization of a new erythroblastic leukemia cell line, EEB: phosphatidylglucoside-mediated erythroid differentiation and apoptosis.
  • A new erythroblastic leukemia cell line (EEB) was established from a patient with early erythroblastic leukemia.
  • The cells had features of immature erythroblasts, including an agranular basophilic cytoplasm and CD36, CD71, CD175s (sialyl-Tn) and CD235a (glycophorin A) expression without CD41 expression, myeloperoxidase activity and platelet-peroxidase activity.
  • An analysis of cell membrane lipids showed that EEB cells contain a type of glycerolipid, phosphatidylglucose (PhGlc), but not unbranched type 2 chains, i antigens.
  • [MeSH-major] Apoptosis / drug effects. Cell Line, Tumor. Erythroid Cells / drug effects. Glycerophospholipids / pharmacology. Immunoglobulin Fab Fragments / pharmacology. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Cytogenetic Analysis. Drug Screening Assays, Antitumor. Globins / drug effects. Globins / genetics. Humans. Immunophenotyping. Male. Middle Aged. Phosphorylation / drug effects. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Structure-Activity Relationship. Tyrosine / drug effects. Tyrosine / metabolism

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  • (PMID = 16332389.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GL-7 Fab fragment; 0 / Glycerophospholipids; 0 / Immunoglobulin Fab Fragments; 0 / phosphatidylglucose; 42HK56048U / Tyrosine; 9004-22-2 / Globins
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19. Indig GL, Anderson GS, Nichols MG, Bartlett JA, Mellon WS, Sieber F: Effect of molecular structure on the performance of triarylmethane dyes as therapeutic agents for photochemical purging of autologous bone marrow grafts from residual tumor cells. J Pharm Sci; 2000 Jan;89(1):88-99
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  • [Title] Effect of molecular structure on the performance of triarylmethane dyes as therapeutic agents for photochemical purging of autologous bone marrow grafts from residual tumor cells.
  • Because a variety of tumor cells also retain pertinent cationic structures for longer periods of time compared with normal cells, mitochondrial targeting has been proposed as a selective therapeutic strategy of relevance for both chemotherapy and photochemotherapy of neoplastic diseases.
  • Crystal violet exhibits pronounced phototoxicity toward L1210 leukemia cells but comparatively small toxic effects toward normal hematopoietic cells (murine granulocyte-macrophage progenitors, CFU-GM).
  • [MeSH-minor] Animals. Gentian Violet / pharmacokinetics. Gentian Violet / toxicity. Hematopoietic Stem Cells / drug effects. Leukemia L1210. Leukemia, Basophilic, Acute. Mice. Mitochondria / drug effects. Mitochondria / metabolism. Neoplasm, Residual. Quaternary Ammonium Compounds / pharmacokinetics. Quaternary Ammonium Compounds / toxicity. Rats. Rosaniline Dyes / pharmacokinetics. Rosaniline Dyes / toxicity. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc. and the American Pharmaceutical Association J Pharm Sci 89: 88-99, 2000
  • (PMID = 10664541.001).
  • [ISSN] 0022-3549
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5F32 CA72225-03; United States / NCRR NIH HHS / RR / P412RR04224-11
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Photosensitizing Agents; 0 / Quaternary Ammonium Compounds; 0 / Rosaniline Dyes; 2390-60-5 / Victoria blue BO; 94UZ9RD7TJ / ethyl violet; J4Z741D6O5 / Gentian Violet
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20. Zhu J, Wang O, Ruan L, Hou X, Cui Y, Wang JM, Le Y: The green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR. Int Immunopharmacol; 2009 Aug;9(9):1126-30
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  • Pretreatment of human monocytic cells or FPR-transfected rat basophilic leukemia cells (ETFR cells) with EGCG significantly inhibited fMLF-induced chemotaxis.
  • [MeSH-minor] Animals. Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors. Camellia sinensis / immunology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / immunology. Flavonoids / pharmacology. Humans. Inflammation. Injections, Intraperitoneal. Leukemia, Basophilic, Acute / blood. Leukemia, Basophilic, Acute / drug therapy. Leukemia, Basophilic, Acute / immunology. Mice. Rats. Receptors, Formyl Peptide / genetics. Receptors, Formyl Peptide / immunology. Receptors, Formyl Peptide / metabolism. Signal Transduction / drug effects. Signal Transduction / immunology. Transfection. Transgenes

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  • (PMID = 19426837.001).
  • [ISSN] 1878-1705
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antioxidants; 0 / Flavonoids; 0 / Receptors, Formyl Peptide; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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21. Wender PA, Baryza JL, Brenner SE, Clarke MO, Craske ML, Horan JC, Meyer T: Function oriented synthesis: the design, synthesis, PKC binding and translocation activity of a new bryostatin analog. Curr Drug Discov Technol; 2004 Jan;1(1):1-11
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  • Bryostatin 1 represents a novel and potent therapeutic lead with a unique activity profile.
  • Function oriented synthesis provides a means to address this supply problem through the design of synthetically more accessible simplified structures that at the same time incorporate improved functional activity.
  • [MeSH-major] Drug Design. Macrolides / chemical synthesis. Macrolides / pharmacology. Protein Kinase C / metabolism
  • [MeSH-minor] Animals. Bryostatins. Cell Line, Tumor. Image Processing, Computer-Assisted. Indicators and Reagents. Isoenzymes / chemistry. Isoenzymes / metabolism. Leukemia, Basophilic, Acute / drug therapy. Leukemia, Basophilic, Acute / metabolism. Microscopy, Fluorescence. Models, Molecular. Protein Binding. Rats

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  • (PMID = 16472215.001).
  • [ISSN] 1570-1638
  • [Journal-full-title] Current drug discovery technologies
  • [ISO-abbreviation] Curr Drug Discov Technol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA31845; United States / NIMH NIH HHS / MH / MH064801
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Bryostatins; 0 / Indicators and Reagents; 0 / Isoenzymes; 0 / Macrolides; 37O2X55Y9E / bryostatin 1; EC 2.7.11.13 / Protein Kinase C
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22. Maruo T, Namikawa K, Kunihiro A, Lynch J, Shida T, Kishikawa S: Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog. J S Afr Vet Assoc; 2009 Dec;80(4):261-3

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  • [Title] Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog.
  • Seventy-two per cent (81360/ml) of the lymphocytes were found to be 12-17 microm in diameter, containing nuclei with mature clumped chromatin and abundant lightly basophilic cytoplasm with a variable number of fine azurophilic granules.
  • Based on these findings this case was diagnosed as LGL leukaemia.
  • As a result of multiple-agent chemotherapy, the markedly elevated levels of lymphocytes gradually decreased to 7500/ml on day 122 and the patient maintained a good quality of life for the following 3 months.
  • Shortly after diagnosis, the dog developed sudden onset of central nervous system signs and died on day 270.
  • A common outcome of canine LGL is the development of acute blast crisis or lymphoma.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Histiocytic Sarcoma / veterinary. Leukemia, Large Granular Lymphocytic / veterinary
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Dog Diseases. Dogs. Fatal Outcome. Male

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  • (PMID = 20458870.001).
  • [ISSN] 1019-9128
  • [Journal-full-title] Journal of the South African Veterinary Association
  • [ISO-abbreviation] J S Afr Vet Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] South Africa
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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23. Hartl A, Weiss R, Hochreiter R, Scheiblhofer S, Thalhamer J: DNA vaccines for allergy treatment. Methods; 2004 Mar;32(3):328-39
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  • [Title] DNA vaccines for allergy treatment.
  • This vaccination approach covers a broad range of possible applications, including the induction of protective immunity against viral, bacterial, and parasitic infections, and it opens new perspectives for treatment of cancer.
  • Surprisingly, DNA immunization also turned out as a promising novel type of immunotherapy against allergy.
  • Beyond, we offer a palette of recently developed modulations to optimize DNA vaccines for allergy treatment by increasing their immunogenicity and minimizing their anaphylactic potential.
  • [MeSH-major] Allergens / immunology. Hypersensitivity / drug therapy. Recombinant Proteins / immunology. Vaccines, DNA / immunology
  • [MeSH-minor] Animals. Humans. Leukemia, Basophilic, Acute / immunology. Leukemia, Basophilic, Acute / metabolism. Rats. beta-N-Acetylhexosaminidases / metabolism

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  • (PMID = 14962768.001).
  • [ISSN] 1046-2023
  • [Journal-full-title] Methods (San Diego, Calif.)
  • [ISO-abbreviation] Methods
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Allergens; 0 / Recombinant Proteins; 0 / Vaccines, DNA; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
  • [Number-of-references] 48
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24. Masamoto Y, Nannya Y, Arai S, Koike Y, Hangaishi A, Yatomi Y, Kurokawa M: Evidence for basophilic differentiation of acute promyelocytic leukaemia cells during arsenic trioxide therapy. Br J Haematol; 2009 Mar;144(5):798-9
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  • [Title] Evidence for basophilic differentiation of acute promyelocytic leukaemia cells during arsenic trioxide therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Basophils / pathology. Leukemia, Promyelocytic, Acute / pathology. Oxides / therapeutic use
  • [MeSH-minor] Cell Differentiation / drug effects. Humans. Male. Middle Aged

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  • (PMID = 19036092.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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