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1. Scheding S, Bergmannn M, Rathke G, Vogel W, Brugger W, Kanz L: Additional transplantation of ex vivo generated megakaryocytic cells after high-dose chemotherapy. Haematologica; 2004 May;89(5):630-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Additional transplantation of ex vivo generated megakaryocytic cells after high-dose chemotherapy.
  • The additional transplantation of ex vivo generated hematopoietic (post)-progenitor cells represents a possible approach to ameliorate high-dose chemotherapy induced cytopenia.
  • We investigated the feasibility of the large-scale expansion and transplantation of autologous megakaryocytic cells in four patients with advanced solid tumors.
  • [MeSH-minor] Antigens, CD34 / blood. Dose-Response Relationship, Drug. Hematopoietic Stem Cell Mobilization. Hematopoietic Stem Cell Transplantation. Pilot Projects. Transplantation, Autologous. Tumor Cells, Cultured

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  • (PMID = 15136238.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents
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2. Ge Y, Dombkowski AA, LaFiura KM, Tatman D, Yedidi RS, Stout ML, Buck SA, Massey G, Becton DL, Weinstein HJ, Ravindranath Y, Matherly LH, Taub JW: Differential gene expression, GATA1 target genes, and the chemotherapy sensitivity of Down syndrome megakaryocytic leukemia. Blood; 2006 Feb 15;107(4):1570-81
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  • [Title] Differential gene expression, GATA1 target genes, and the chemotherapy sensitivity of Down syndrome megakaryocytic leukemia.
  • Children with Down syndrome (DS) with acute megakaryocytic leukemia (AMkL) have very high survival rates compared with non-DS AMkL patients.
  • Transcripts for the bone marrow stromal-cell antigen 2 (BST2) gene, encoding a transmembrane glycoprotein potentially involved in interactions between leukemia cells and bone marrow stromal cells, were 7.3-fold higher (validated by real-time polymerase chain reaction) in the non-DS compared with the DS group.

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  • (PMID = 16249385.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA92308
  • [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 / DNA Primers; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 04079A1RDZ / Cytarabine; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC1895418
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3. Edwards H, Xie C, LaFiura KM, Dombkowski AA, Buck SA, Boerner JL, Taub JW, Matherly LH, Ge Y: RUNX1 regulates phosphoinositide 3-kinase/AKT pathway: role in chemotherapy sensitivity in acute megakaryocytic leukemia. Blood; 2009 Sep 24;114(13):2744-52
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  • [Title] RUNX1 regulates phosphoinositide 3-kinase/AKT pathway: role in chemotherapy sensitivity in acute megakaryocytic leukemia.
  • Translocations or down-regulation of RUNX1 have been linked to favorable clinical outcomes in acute leukemias, suggesting that RUNX1 may also play critical roles in chemotherapy responses in acute leukemias; however, the molecular mechanisms remain unclear.
  • The median level of RUNX1b transcripts in Down syndrome (DS) children with acute megakaryocytic leukemia (AMkL) were 4.4-fold (P < .001) lower than that in non-DS AMkL cases.
  • Our results suggest that RUNX1 may play a critical role in chemotherapy response in AMkL by regulating the PI3-kinase/Akt pathway.
  • Thus, the treatment of AMkL may be improved by integrating PI3-kinase or Akt inhibitors into the chemotherapy of this disease.

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  • (PMID = 19638627.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES006639; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NIEHS NIH HHS / ES / P30 ES06639
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / RNA, Small Interfering; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / Class I Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CD protein, human; EC 2.7.11.1 / Oncogene Protein v-akt
  • [Other-IDs] NLM/ PMC2756129
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4. Huang YC, Chao DK, Clifford Chao KS, Chen YJ: Oral small-molecule tyrosine kinase inhibitor midostaurin (PKC412) inhibits growth and induces megakaryocytic differentiation in human leukemia cells. Toxicol In Vitro; 2009 Sep;23(6):979-85
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  • [Title] Oral small-molecule tyrosine kinase inhibitor midostaurin (PKC412) inhibits growth and induces megakaryocytic differentiation in human leukemia cells.
  • Midostaurin (PKC412), a small-molecule multiple tyrosine kinase inhibitor, has been shown to suppress the growth of various tumor cells.
  • Since kinases inhibited by midostaurin are involved in megakaryocytic differentiation, we hypothesized that this novel target therapeutic might have a role in the treatment of human leukemia cells.
  • Midostaurin inhibited the growth of both K562 and HEL cells in dose- and time-dependent manner.
  • Midostaurin treatment enhanced the surface expression of the megakaryocytic marker CD61; in contrast, the erythroid marker glycophorin A expression was decreased.
  • At optimal conditions for inducing megakaryocytic differentiation, midostaurin upregulated the expression and signaling of c-Mpl, a thrombopoietin receptor-encoding gene, in HEL cells.
  • These results indicate that midostaurin can inhibit growth; induce megakaryocytic differentiation; and to a lesser extent, cause apoptosis in HEL cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Leukemia / drug therapy. Staurosporine / analogs & derivatives
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. K562 Cells. Megakaryocytes / metabolism. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / pharmacology. Receptors, Thrombopoietin / drug effects. Receptors, Thrombopoietin / metabolism. Signal Transduction / drug effects. Time Factors. Up-Regulation / drug effects

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  • (PMID = 19573588.001).
  • [ISSN] 1879-3177
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Receptors, Thrombopoietin; 120685-11-2 / 4'-N-benzoylstaurosporine; 143641-95-6 / MPL protein, human; H88EPA0A3N / Staurosporine
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5. Cailleteau C, Micallef L, Lepage C, Cardot PJ, Beneytout JL, Liagre B, Battu S: Investigating the relationship between cell cycle stage and diosgenin-induced megakaryocytic differentiation of HEL cells using sedimentation field-flow fractionation. Anal Bioanal Chem; 2010 Oct;398(3):1273-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigating the relationship between cell cycle stage and diosgenin-induced megakaryocytic differentiation of HEL cells using sedimentation field-flow fractionation.
  • Differentiation therapy could be one strategy for stopping cancer cell proliferation.
  • A plant steroid, diosgenin, is known to induce megakaryocytic differentiation in human erythroleukemia (HEL) cells.
  • The specific goal of this study was to determine the relationship between cell cycle stage and sensitivity to megakaryocytic differentiation induction of HEL cells.
  • [MeSH-major] Cell Cycle / drug effects. Cell Differentiation / drug effects. Diosgenin / pharmacology. Fractionation, Field Flow / methods. Megakaryocytes / drug effects
  • [MeSH-minor] Cell Line, Tumor. Humans. Spectrophotometry, Ultraviolet

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  • (PMID = 20714892.001).
  • [ISSN] 1618-2650
  • [Journal-full-title] Analytical and bioanalytical chemistry
  • [ISO-abbreviation] Anal Bioanal Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] K49P2K8WLX / Diosgenin
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6. Fuchs R, Stelzer I, Haas HS, Leitinger G, Schauenstein K, Sadjak A: The alpha1-adrenergic receptor antagonists, benoxathian and prazosin, induce apoptosis and a switch towards megakaryocytic differentiation in human erythroleukemia cells. Ann Hematol; 2009 Oct;88(10):989-97
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  • [Title] The alpha1-adrenergic receptor antagonists, benoxathian and prazosin, induce apoptosis and a switch towards megakaryocytic differentiation in human erythroleukemia cells.
  • The erythroleukemia cell lines K562 and human erythroleukemia (HEL) are established models to study erythroid and megakaryocytic differentiation in vitro.
  • Furthermore, both tested substances induced the expression of the megakaryocytic marker CD41a, whereas the expression of the erythroid marker glycophorin-a was decreased or unchanged.
  • Even though the expression of differentiation markers was similar after benoxathian and prazosin treatment in both cell lines, endomitosis of erythroleukemia cells was observed only after prazosin treatment.
  • So far, benoxathian and prazosin are the first described extracellular ligands, which cause megakaryocytic differentiation in K562 and HEL cells.
  • In summary, these results indicate a possible role of alpha1-adrenergic receptor signaling in the regulation of erythroid and megakaryocytic differentiation, even though the receptor dependence of the observed effects needs further investigation.
  • [MeSH-major] Apoptosis / drug effects. Cell Differentiation / drug effects. Leukemia, Erythroblastic, Acute / drug therapy. Megakaryocytes / cytology. Oxathiins / pharmacology. Prazosin / pharmacology. Receptors, Adrenergic, alpha-1 / metabolism
  • [MeSH-minor] Adrenergic alpha-Antagonists / pharmacology. Cell Line, Tumor. Erythroid Cells. Humans. K562 Cells

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  • (PMID = 19241077.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenergic alpha-Antagonists; 0 / Oxathiins; 0 / Receptors, Adrenergic, alpha-1; 92642-94-9 / benoxathian; XM03YJ541D / Prazosin
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7. Ge Y, Jensen TL, Matherly LH, Taub JW: Transcriptional regulation of the cystathionine-beta -synthase gene in Down syndrome and non-Down syndrome megakaryocytic leukemia cell lines. Blood; 2003 Feb 15;101(4):1551-7
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  • [Title] Transcriptional regulation of the cystathionine-beta -synthase gene in Down syndrome and non-Down syndrome megakaryocytic leukemia cell lines.
  • In this study, we examined the transcriptional regulation of the CBS gene in the DS megakaryocytic leukemia (AMkL) cell line, CMK, characterized by significantly higher CBS transcripts compared with the non-DS AMkL cell line, CMS.
  • Decreased binding of Sp1/Sp3 in CMK nuclear extracts following treatment with calf alkaline phosphatase suggested a role for phosphorylation of Sp1/Sp3 in regulating CBS promoter activity and in the differential CBS expression between CMK and CMS cells.
  • The results of this study with clinically relevant cell line models suggest potential mechanisms for disparate patterns of CBS gene expression in DS and non-DS myeloblasts and may, in part, explain the greater sensitivity to chemotherapy shown by patients with DS AML.
  • [MeSH-minor] Cytarabine / metabolism. Cytarabine / pharmacology. DNA / metabolism. DNA-Binding Proteins / metabolism. Humans. Luciferases / genetics. Mutagenesis, Site-Directed. Phosphorylation. Promoter Regions, Genetic. Sp1 Transcription Factor / metabolism. Sp3 Transcription Factor. Transcription Factors / metabolism. Transcription, Genetic. Transfection. Tumor Cells, Cultured

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  • (PMID = 12393509.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / SP3 protein, human; 0 / Sp1 Transcription Factor; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; 148710-94-5 / Sp3 Transcription Factor; 9007-49-2 / DNA; EC 1.13.12.- / Luciferases; EC 4.2.1.22 / Cystathionine beta-Synthase
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8. Erickson-Miller CL, Chadderton A, Gibbard A, Kirchner J, Pillarisetti K, Baker K, Pandite L, El-Hariry I, Mostafa Kamel Y, Liu Y, Martin AM, Messam C: Thrombopoietin receptor levels in tumor cell lines and primary tumors. J Oncol; 2010;2010:135354
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  • [Title] Thrombopoietin receptor levels in tumor cell lines and primary tumors.
  • Thrombopoietin (TPO) receptor agonists represent a new approach for the treatment of thrombocytopenia, which may develop as a consequence of immune thrombocytopenia, chemotherapy treatment, chronic hepatitis C infection, or myelodysplastic syndromes.
  • There are concerns that use of certain growth factors can hasten disease progression in some types of hematologic malignancies and solid tumors.
  • In this study, expression of MPL (TPO-R) mRNA was examined in tumor cell lines, patient tumor samples (renal cell carcinoma, prostatic carcinoma, soft tissue and bony/cartilage sarcoma, colon cancer, and lymphoma), and normal tissues using microarray analysis and qRT-PCR.
  • These data suggest TPO-R agonists will likely preferentially stimulate proliferation and differentiation of cells of megakaryocytic lineage, potentially demonstrating their utility for correcting thrombocytopenia in clinical settings.

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  • (PMID = 21318160.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC3026977
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9. Hager ED, Dziambor H, Höhmann D, Winkler P, Strama H: Effects of lithium on thrombopoiesis in patients with low platelet cell counts following chemotherapy or radiotherapy. Biol Trace Elem Res; 2001 Nov;83(2):139-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of lithium on thrombopoiesis in patients with low platelet cell counts following chemotherapy or radiotherapy.
  • Therapy for neoplasma is limited by hematological side effects of tumor-destructive therapy and, in part, makes expensive supportive care necessary to overcome and treat leukopenia and thrombocytopenia and their consequences.
  • Thrombocytopenia is a major clinical problem caused by chemotherapy and radiotherapy.
  • Other cytokines, such as interleukin-1 (IL-1), IL-6, and tumor-necrosis factor-alpha (TNF-alpha), are also stimulated.
  • Apart from granulocyte-macrophage-CSF (GM-CSF), there have as yet been no reports of lithium salts inducing early activating factors for the megakaryocytic lineage, such as IL-3, IL-11, stem cell factor and flt-3 ligand, or maturation factors, such as thrombopoietin (TPO).
  • A statistically significant increase in the mean number of platelets for patients with cell counts below 150,000/microL on the commencement of treatment with lithium carbonate could be observed.
  • Patient tolerability of lithium carbonate therapy is very good.
  • Patients with persistent leukopenia and thrombocytopenia following chemotherapy or radiotherapy can be treated with this trace element very cost-effectively.
  • Unfortunately this treatment has not gained acceptance in clinical oncology in the face of extremely cost-intensive treatment with recombinant GM-CSF, IL-11 or, potentially, thrombopoietin.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Lithium / therapeutic use. Radiotherapy / adverse effects. Thrombocytopenia / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Leukocyte Count. Leukopenia / blood. Male. Middle Aged. Neoplasms / blood. Neoplasms / complications. Neoplasms / therapy. Platelet Count

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  • (PMID = 11762531.001).
  • [ISSN] 0163-4984
  • [Journal-full-title] Biological trace element research
  • [ISO-abbreviation] Biol Trace Elem Res
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 9FN79X2M3F / Lithium
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10. Léger DY, Battu S, Liagre B, Beneytout JL, Cardot PJ: Megakaryocyte cell sorting from diosgenin-differentiated human erythroleukemia cells by sedimentation field-flow fractionation. Anal Biochem; 2006 Aug 1;355(1):19-28

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Anticancer differentiation therapy could be one strategy to stop cancer cell proliferation.
  • Human erythroleukemia (HEL) cell line, incubated with 10 microM diosgenin, underwent megakaryocytic differentiation.
  • Thus, the association diosgenin/HEL could be used as a model of chemically induced cellular differentiation and anticancer treatment.
  • The goal of this work was to determine the capacity of sedimentation field-flow fractionation (SdFFF) to sort megakaryocytic differentiated cells.
  • As demonstrated by cell size measurement methods, cellular morphology, ploidy, and phenotype, we obtained an enriched, sterile, viable, and functional fraction of megakaryocytic cells.
  • Thus, SdFFF is proposed as a routine method to prepare differentiated cells that will be further used to better understand the megakaryocytic differentiation process.
  • [MeSH-major] Cell Differentiation / drug effects. Cell Separation / methods. Diosgenin / pharmacology. Fractionation, Field Flow / methods. Megakaryocytes / cytology
  • [MeSH-minor] Cell Line, Tumor. Cell Size / drug effects. Humans. Leukemia, Erythroblastic, Acute / pathology. Leukemia, Erythroblastic, Acute / physiopathology. Platelet Membrane Glycoprotein IIb / analysis

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  • (PMID = 16806034.001).
  • [ISSN] 0003-2697
  • [Journal-full-title] Analytical biochemistry
  • [ISO-abbreviation] Anal. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet Membrane Glycoprotein IIb; K49P2K8WLX / Diosgenin
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11. Tímár J, Tóvári J, Rásó E, Mészáros L, Bereczky B, Lapis K: Platelet-mimicry of cancer cells: epiphenomenon with clinical significance. Oncology; 2005;69(3):185-201

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Stem cell mimicry of cancer cells has been known for a long time and is considered to be responsible for ectopic gene expressions.
  • The stem cell characteristics of tumor cells are shown to be involved in epithelial-mesenchymal transition and in the phenomenon of vascular mimicry.
  • Certain cancer types acquire a geno-phenotype closely resembling the platelets and express several megakaryocytic genes (adhesion receptors alpha IIb beta 3, thrombin receptor and PECAM/CD 31 and/or platelet-type 12-LOX) able to activate the coagulation cascade or the platelets themselves.
  • Data all support that platelet mimicry of certain cancer types is an important factor in their hematogenous dissemination and provides an attractive therapeutic target.
  • Besides the long-available preclinical data, clinical trials have only recently provided evidence that targeting platelet mimicry of cancers is an efficient way to prevent tumor progression.
  • The systematic discovery of the markers of platelet mimicry in various cancer types and their molecular targeting may provide new supportive therapeutic modalities for the management of the progressing disease.
  • [MeSH-minor] Animals. Blood Coagulation Disorders / drug therapy. Blood Coagulation Disorders / etiology. Gene Expression Regulation, Neoplastic. Genotype. Humans. Megakaryocytes / metabolism. Neoplasm Metastasis / genetics. Phenotype. Platelet Aggregation Inhibitors / therapeutic use

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16138000.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Platelet Aggregation Inhibitors
  • [Number-of-references] 166
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12. Vasconcellos MC, Bezerra DP, Fonseca AM, Pereira MR, Lemos TL, Pessoa OD, Pessoa C, Moraes MO, Alves AP, Costa-Lotufo LV: Antitumor activity of biflorin, an o-naphthoquinone isolated from Capraria biflora. Biol Pharm Bull; 2007 Aug;30(8):1416-21
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  • Pharmacological studies with an aqueous extract obtained from leaves of Capraria biflora showed potent cytotoxic, analgesic, antimicrobial and anti-inflammatory activities.
  • It has been demonstrated that biflorin possesses an in vitro cytotoxic activity against tumor cells.
  • The results showed a decrease in Ki67 staining in tumor cells from treated-animals when compared with non-treated groups, which suggests an inhibition of tumor proliferation rate.
  • It was also demonstrated that biflorin acts as an immunoadjuvant agent, rising the production of ovalbumin-specific antibodies and inducing a discreet increase of the white pulp and nest of megakaryocytic in spleen of treated mice, which can be related to its antitumor properties.
  • [MeSH-minor] Adjuvants, Immunologic / pharmacology. Animals. Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / pathology. Female. Fluorouracil / therapeutic use. Immunohistochemistry. Indicators and Reagents. Ki-67 Antigen / metabolism. Mice. Neoplasm Transplantation. Ovalbumin / immunology. Sarcoma 180 / drug therapy. Sarcoma 180 / pathology

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  • (PMID = 17666796.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Indicators and Reagents; 0 / Ki-67 Antigen; 0 / Naphthoquinones; 0 / biflorin; 9006-59-1 / Ovalbumin; U3P01618RT / Fluorouracil
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13. Brugger W, Scheding S, Ziegler B, Bühring HJ, Kanz L: Ex vivo manipulation of hematopoietic stem and progenitor cells. Semin Hematol; 2000 Jan;37(1 Suppl 2):42-9
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  • These manipulations include the positive selection of CD34+ cells for tumor-cell reduction and/or T-cell depletion, the ex vivo expansion of hematopoietic progenitor and stem cells under appropriate cytokine-stimulated culture conditions, and the ex vivo generation of myeloid or megakaryocytic postprogenitor cells and Immune effector cells.
  • This article summarizes both the preclinical data on the ex vivo expansion of hematopoietic progenitor and stem cells from purified CD34+ cells and the Initial clinical studies with ex vivo-expanded stem and progenitor cells for hematopoietic support after high-dose chemotherapy.

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  • (PMID = 10718158.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Congresses; Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Number-of-references] 55
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14. Drexler HG, Matsuo Y, MacLeod RA: Malignant hematopoietic cell lines: in vitro models for the study of erythroleukemia. Leuk Res; 2004 Dec;28(12):1243-51

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  • It is striking that many cell lines though committed to either the erythroid or megakaryocytic lineage tend to co-express features of the other lineage, consistent with the concept of a common erythroid-megakaryocytic progenitor.
  • Several cell lines may be induced to differentiate along the erythroid, megakaryocytic or monocytic pathway by treatment with pharmacological or physiological reagents.
  • [MeSH-major] Cell Line, Tumor. Erythroid Cells / pathology. Leukemia, Erythroblastic, Acute / pathology

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  • (PMID = 15475063.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 67
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15. Hashimoto S, Toba K, Fuse I, Watanabe K, Takahashi H, Abe T, Yano T, Koike T, Takahashi M, Aizawa Y: Thrombopoietin activates the growth of megakaryoblasts in patients with chronic myeloproliferative disorders and myelodysplastic syndrome. Eur J Haematol; 2000 Apr;64(4):225-30
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  • However, TPO had no effect on the cells lacking megakaryocytic characteristics.
  • Some patients with CMPD and MDS develop acute transformation with blasts demonstrating megakaryocytic features, and some of these cells show growth in response to TPO.
  • [MeSH-major] Megakaryocytes / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Myeloproliferative Disorders / drug therapy. Myeloproliferative Disorders / pathology. Thrombopoietin / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Chronic Disease. Humans. Tumor Cells, Cultured


16. Mishima Y, Terui Y, Mishima Y, Taniyama A, Kuniyoshi R, Takizawa T, Kimura S, Ozawa K, Hatake K: Autophagy and autophagic cell death are next targets for elimination of the resistance to tyrosine kinase inhibitors. Cancer Sci; 2008 Nov;99(11):2200-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We observed the excessive autophagy in chronic myelogenous leukemia (CML) cell line, K562, associated with treatment of 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which can induce K562 cells to differentiate into megakaryocytic lineage.
  • Confocal microscopic analysis demonstrated that autophagic cells did not express a megakaryocyte marker, the CD41 molecule, indicating that the autophagy was independent of megakaryocytic differentiation.
  • Autophagy has not been considered during imatinib treatment; nonetheless, co-treatment with imatinib and chloroquine markedly enhanced imatinib-induced cell death, compared to K562 cells treated only with imatinib.
  • Furthermore, imatinib-resistant cell lines, BaF3/T315I and BaF3/E255K, also underwent cell death by co-treatment with imatinib and chloroquine.
  • The block of autophagy could be a new strategy in the treatment of CML.
  • [MeSH-major] Autophagy / drug effects. Drug Resistance, Neoplasm. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Cell Death. Cell Differentiation. Cell Line, Tumor. Humans. K562 Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Tetradecanoylphorbol Acetate / pharmacology. Tetradecanoylphorbol Acetate / therapeutic use

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  • (PMID = 18823378.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
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17. Maurer AM, Zhou B, Han ZC: Roles of platelet factor 4 in hematopoiesis and angiogenesis. Growth Factors; 2006 Dec;24(4):242-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Structure-function studies have shown that the DLQ determinant in position 54-56 is necessary for megakaryocytic inhibition whereas mutations of these residues into ELR sequence and more importantly, into DLR sequence, induce a stronger inhibitory activity of peptide p47-70 on angiogenesis.
  • In vivo, PF4 and its related peptides can protect hematopoiesis from chemotherapy by enhancing cell viability and suppress tumor growth through anti-angiogenic pathway.
  • Several PF4 fragments and modified molecules exhibit antiangiogenesis properties and may become an alternative for further therapeutic angiogenesis.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Hematopoiesis. Neovascularization, Pathologic / metabolism. Neovascularization, Physiologic. Platelet Factor 4 / physiology

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  • (PMID = 17381065.001).
  • [ISSN] 0897-7194
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Glycosaminoglycans; 0 / Peptides; 37270-94-3 / Platelet Factor 4
  • [Number-of-references] 95
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18. Wolber EM, Haase B, Jelkmann W: Thrombopoietin production in human hepatic cell cultures (HepG2) is resistant to IFN-alpha, IFN-beta, and IFN-gamma treatment. J Interferon Cytokine Res; 2002 Dec;22(12):1185-9

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  • [Title] Thrombopoietin production in human hepatic cell cultures (HepG2) is resistant to IFN-alpha, IFN-beta, and IFN-gamma treatment.
  • Thrombocytopenia is an important complication of interferon (IFN) therapy for chronic viral hepatitis.
  • Neither was the rate of secretion of immunoreactive TPO reduced on IFN treatment.
  • These findings support the concept that IFNs primarily mediate effects on megakaryocytic cells and platelets rather than on TPO-producing hepatocytes.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. Interferon-alpha / pharmacology. Interferon-beta / pharmacology. Interferon-gamma / pharmacology. Thrombopoietin / genetics
  • [MeSH-minor] Carcinoma, Hepatocellular. Dose-Response Relationship, Drug. Humans. Kinetics. Liver Neoplasms. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Tumor Cells, Cultured

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  • (PMID = 12581491.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / RNA, Messenger; 77238-31-4 / Interferon-beta; 82115-62-6 / Interferon-gamma; 9014-42-0 / Thrombopoietin
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19. Orsolić N, Basić I: Antitumor, hematostimulative and radioprotective action of water-soluble derivative of propolis (WSDP). Biomed Pharmacother; 2005 Dec;59(10):561-70
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  • Several studies suggest that dietary supplementation with antioxidant can influence the response to chemotherapy as well as the development of adverse side effects caused by treatment with chemotherapeutic agents.
  • Using CBA mouse model, we investigated a clinically potential use of a water-soluble derivative of propolis (WSDP) in the treatment of various cytopenias induced by radiation and/or chemotherapy.
  • Tumor was a transplantable mammary carcinoma (MCa) of CBA mouse.
  • Metastases in the lung were generated by injecting viable tumor cells intravenously (iv).
  • WSDP (50 or 150 mg/kg) exerted a significant antimetastatic effect (P < 0.001) when given either before or after tumor cell inoculation.
  • In combined treatment WSDP and Epirubicin profoundly inhibited metastasis formation; this synergistic effect is maximal when Epirubicin and WSDP were administrated after tumor cell inoculation.
  • Positive outcome of combined treatment with WSDP and Epirubicin was also found regarding the number of red and white blood cells in peripheral blood while in mice treated with Epirubicin alone the significant drop in all hematological parameters was noticed on day 13 after tumor cell inoculation.
  • WSDP given either for 20 or 40 days increased cellularity of hematopoietic tissue and the number of leucocytes in peripheral blood; prolonged treatment with WSDP also elevated myeloid and megakaryocytic types of CFUs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hematopoiesis / drug effects. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mammary Neoplasms, Experimental / drug therapy. Propolis / pharmacology. Radiation-Protective Agents / pharmacology
  • [MeSH-minor] Administration, Oral. Animals. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / adverse effects. Blood Cell Count. Cells, Cultured. Disease Models, Animal. Drug Therapy, Combination. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Gamma Rays. Injections, Intraperitoneal. Leukopenia / etiology. Leukopenia / prevention & control. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / metabolism. Male. Mice. Mice, Inbred CBA. Neoplasm Transplantation. Solubility. Time Factors

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  • (PMID = 16202559.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Radiation-Protective Agents; 3Z8479ZZ5X / Epirubicin; 9009-62-5 / Propolis
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20. Zhao S, Konopleva M, Cabreira-Hansen M, Xie Z, Hu W, Milella M, Estrov Z, Mills GB, Andreeff M: Inhibition of phosphatidylinositol 3-kinase dephosphorylates BAD and promotes apoptosis in myeloid leukemias. Leukemia; 2004 Feb;18(2):267-75
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  • We investigated the effects of LY294002 in megakaryocytic leukemia-derived MO7E cells, primary AML and normal bone marrow progenitor cells.
  • In conclusion, the data suggest that the inhibition of the PI3K/AKT signaling pathway restores apoptosis in AML and may be explored as a novel target for molecular therapeutics in AML.
  • [MeSH-minor] Cell Line, Tumor. Chromones / pharmacology. Drug Interactions. Humans. MAP Kinase Signaling System / drug effects. Morpholines / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Tretinoin / pharmacology. bcl-Associated Death Protein

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  • (PMID = 14628071.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAD protein, human; 0 / Carrier Proteins; 0 / Chromones; 0 / Morpholines; 0 / Proto-Oncogene Proteins; 0 / bcl-Associated Death Protein; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 5688UTC01R / Tretinoin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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21. Liu HC, Chen SH, Wang LY, Yeh TC, Chai IJ, Liang DC: In vitro cell growth stimulated by recombinant human cytokines can help to diagnose transient leukemia in neonates. J Formos Med Assoc; 2007 May;106(5):365-71
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  • Cytospin smears of liquid suspension cultures all showed good myeloid or megakaryocytic maturation consistent with TL rather than AML.
  • Among four patients followed long-term, one developed myelodysplastic syndrome at 21 months.
  • This child was given tailored chemotherapy and had a disease-free survival>20 months.

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  • (PMID = 17561471.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-3; 0 / Recombinant Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 9014-42-0 / Thrombopoietin
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22. Albella B, Faircloth G, López-Lázaro L, Guzmán C, Jimeno J, Bueren JA: In vitro toxicity of ET-743 and aplidine, two marine-derived antineoplastics, on human bone marrow haematopoietic progenitors. comparison with the clinical results. Eur J Cancer; 2002 Jul;38(10):1395-404
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  • With the aim of evaluating whether in vitro haematopoietic studies can predict the toxicity of these two drugs in patients, human bone marrow (BM) samples were incubated with these drugs under conditions which mimicked the administration exposures used in the clinics.
  • As it was observed in different cancer cell lines, ET-743 was more toxic on an equimolar basis in human hematopoietic progenitors (inhibitory concentration reducing the viability to 50% after 24 h exposures; IC50(24h): 10-50 nM) compared with doxorubicin (IC50(24h) values: 280-460 nM), used as a control anticancer drug.
  • For both ET-743 and aplidine, the megakaryocytic progenitor was the most sensitive, compared with the other haematopoietic progenitors (IC50 values were 3- to 5-fold lower in the CFU-Megs compared with the CFU-GMs).
  • The observation that the Cmax observed in patients treated with the aplidine maximum tolerated dose (MTD) (7.1 nM) was 21-75 fold lower than the IC50(24h) value observed for the different haematopoietic progenitors is highly consistent with the lack of haematotoxicity observed in patients treated with this drug.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Bone Marrow Diseases / chemically induced. Depsipeptides. Dioxoles / adverse effects. Hematopoietic Stem Cells / drug effects. Isoquinolines / adverse effects. Neoplasms / drug therapy
  • [MeSH-minor] Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Doxorubicin / adverse effects. Drug Screening Assays, Antitumor. Humans. Inhibitory Concentration 50. Peptides, Cyclic / adverse effects. Tetrahydroisoquinolines. Tumor Cells, Cultured

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  • [CommentIn] Eur J Cancer. 2002 Jul;38(10):1297 [12091058.001]
  • (PMID = 12091072.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Depsipeptides; 0 / Dioxoles; 0 / Isoquinolines; 0 / Peptides, Cyclic; 0 / Tetrahydroisoquinolines; 114899-77-3 / trabectedin; 80168379AG / Doxorubicin; Y76ID234HW / aplidine
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23. Rassidakis GZ, Georgakis GV, Oyarzo M, Younes A, Medeiros LJ: Lack of c-kit (CD117) expression in CD30+ lymphomas and lymphomatoid papulosis. Mod Pathol; 2004 Aug;17(8):946-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • c-Kit receptor (CD117) is expressed by erythroid, megakaryocytic, and myeloid precursors and mature mast cells and has been reported to be expressed in CD30+ lymphomas such as Hodgkin's disease and anaplastic large-cell lymphoma.
  • Imatinib mesylate, a well-established inhibitor of bcr-abl tyrosine kinase, and currently used for the treatment of patients with chronic myeloid leukemia, also inhibits c-kit receptor kinase activity.
  • In view of the possible use of imatinib as experimental therapy for patients with c-kit-positive tumors, we assessed c-kit expression in CD30+ cell lines and lymphomas.
  • Furthermore, treatment with imatinib did not inhibit proliferation of cell lines in vitro.
  • Our data demonstrate that expression of c-kit receptor is exceedingly rare among CD30+ lymphomas and lymphomatoid papulosis, suggesting that c-kit receptor is unlikely to be an appropriate target for therapeutic options such as imatinib in patients with these tumors.
  • [MeSH-minor] Antigens, CD30 / analysis. Antineoplastic Agents / pharmacology. Benzamides. Cell Division / drug effects. Cell Line, Tumor. Flow Cytometry. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Hodgkin Disease / pathology. Humans. Imatinib Mesylate. Immunohistochemistry. Piperazines / pharmacology. Pyrimidines / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15105813.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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24. Ge Y, Jensen TL, Stout ML, Flatley RM, Grohar PJ, Ravindranath Y, Matherly LH, Taub JW: The role of cytidine deaminase and GATA1 mutations in the increased cytosine arabinoside sensitivity of Down syndrome myeloblasts and leukemia cell lines. Cancer Res; 2004 Jan 15;64(2):728-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The presence of several GATA1 binding sites in the CDAsf promoter and the uniform detection of GATA1 mutations in DS megakaryocytic leukemia suggested the potential role of GATA1 in regulating CDA transcription and the CDAsf promoter acting as an enhancer.
  • Additional identification of the mechanisms of differential expression of genes encoding enzymes involved in ara-C metabolism between DS and non-DS myeloblasts may lead to improvements in AML therapy.
  • [MeSH-minor] Base Sequence. Cell Death / drug effects. Cell Line, Tumor. Cells, Cultured. DNA Primers. Erythroid-Specific DNA-Binding Factors. Exons / genetics. GATA1 Transcription Factor. Humans. Introns / genetics. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 14744791.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; EC 3.5.4.1 / Cytosine Deaminase
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25. Gomez JA, Sun W, Gama V, Hajkova D, Yoshida T, Wu Z, Miyagi M, Pink JJ, Jackson MW, Danielpour D, Matsuyama S: The C-terminus of interferon gamma receptor beta chain (IFNgammaR2) has antiapoptotic activity as a Bax inhibitor. Cancer Biol Ther; 2009 Sep;8(18):1771-86
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  • Overexpression of IFNgammaR2 (wild type and IFNgammaR2(296-337)) rescued cells from etoposide and staurosporine, which are known to induce Bax-mediated cell death.
  • We found that the C-terminal fragment (cytoplasmic domain) of IFNgammaR2 is expressed in human cancer cell lines of megakaryocytic cancer (DAMI), breast cancer (MDA-MD-468), and prostate cancer (PC3 cells).

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  • (PMID = 19657228.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01AG031903; United States / NCI NIH HHS / CA / P30CA43703; United States / NCI NIH HHS / CA / PC0CA1037; United States / NIA NIH HHS / AG / R01 AG031903; United States / NCI NIH HHS / CA / P30 CA043703; United States / NIA NIH HHS / AG / R01 AG031903-02; United States / NCI NIH HHS / CA / P30 CA43703; United States / NIA NIH HHS / AG / AG031903-02
  • [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 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / IFNGR2 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Interferon; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ NIHMS220341; NLM/ PMC2927208
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