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1. Tajeddine N, Louis M, Vermylen C, Gala JL, Tombal B, Gailly P: Tumor associated antigen PRAME is a marker of favorable prognosis in childhood acute myeloid leukemia patients and modifies the expression of S100A4, Hsp 27, p21, IL-8 and IGFBP-2 in vitro and in vivo. Leuk Lymphoma; 2008 Jun;49(6):1123-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor associated antigen PRAME is a marker of favorable prognosis in childhood acute myeloid leukemia patients and modifies the expression of S100A4, Hsp 27, p21, IL-8 and IGFBP-2 in vitro and in vivo.
  • We also demonstrated that PRAME overexpression induced the repression of three genes (Hsp27, S100A4 and p21) associated with an unfavorable prognosis in leukemia.
  • We performed a gene profiling study by analysing PRAME shRNA-silenced leukemic cells on high-density micro-arrays (Affymetrix) and found that PRAME altered the expression of two additional genes potentially involved in cancerogenesis and cancer progression: IL-8 and IGFBP-2.
  • In a series of 28 acute myeloid leukemia pediatric patients, we observed that PRAME expression was associated with an increased leukemia-free survival.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Heat-Shock Proteins / metabolism. Insulin-Like Growth Factor Binding Protein 2 / metabolism. Interleukin-8 / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. S100 Proteins / metabolism

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  • (PMID = 18452107.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Interleukin-8; 0 / Neoplasm Proteins; 0 / PRAME protein, human; 0 / RNA, Small Interfering; 0 / S100 Proteins; 142662-27-9 / S100A4 protein, human
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2. Moreaux J, Veyrune JL, Reme T, De Vos J, Klein B: CD200: a putative therapeutic target in cancer. Biochem Biophys Res Commun; 2008 Feb 1;366(1):117-22
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  • CD200 was recently described as a new prognosis factor in multiple myeloma and acute myeloid leukemia.
  • We found significant overexpression of CD200 in renal carcinoma, head and neck carcinoma, testicular cancer, malignant mesothelioma, colon carcinoma, MGUS/smoldering myeloma, and in chronic lymphocytic leukemia compared to their normal cells or their tissue counterparts.
  • Moreover, we show that CD200 expression is associated with tumor progression in various cancers.

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  • (PMID = 18060862.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / antigens, CD200
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3. Barabé F, Kennedy JA, Hope KJ, Dick JE: Modeling the initiation and progression of human acute leukemia in mice. Science; 2007 Apr 27;316(5824):600-4
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  • [Title] Modeling the initiation and progression of human acute leukemia in mice.
  • Our understanding of leukemia development and progression has been hampered by the lack of in vivo models in which disease is initiated from primary human hematopoietic cells.
  • We showed that upon transplantation into immunodeficient mice, primitive human hematopoietic cells expressing a mixed-lineage leukemia (MLL) fusion gene generated myeloid or lymphoid acute leukemias, with features that recapitulated human diseases.
  • Analysis of serially transplanted mice revealed that the disease is sustained by leukemia-initiating cells (L-ICs) that have evolved over time from a primitive cell type with a germline immunoglobulin heavy chain (IgH) gene configuration to a cell type containing rearranged IgH genes.
  • The L-ICs retained both myeloid and lymphoid lineage potential and remained responsive to microenvironmental cues.
  • [MeSH-major] Disease Models, Animal. Leukemia, Lymphoid. Leukemia, Myeloid. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Animals. Bone Marrow Transplantation. Cell Transformation, Neoplastic. Disease Progression. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Genes, Immunoglobulin. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Immunoglobulin Heavy Chains / genetics. Mice. Transduction, Genetic. Tumor Cells, Cultured

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  • (PMID = 17463288.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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4. Struski S, Mauvieux L, Gervais C, Hélias C, Liu KL, Lessard M: ETV6/GOT1 fusion in a case of t(10;12)(q24;p13)-positive myelodysplastic syndrome. Haematologica; 2008 Mar;93(3):467-8
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  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / genetics. Aspartate Aminotransferase, Cytoplasmic / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 12 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Chromosome Breakage. Disease Progression. Fatal Outcome. Female. Humans. Karyotyping. Mastocytosis / complications

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  • (PMID = 18310541.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / ETV6-GOT1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; EC 2.6.1.- / Aspartate Aminotransferase, Cytoplasmic
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5. Sternsdorf T, Phan VT, Maunakea ML, Ocampo CB, Sohal J, Silletto A, Galimi F, Le Beau MM, Evans RM, Kogan SC: Forced retinoic acid receptor alpha homodimers prime mice for APL-like leukemia. Cancer Cell; 2006 Feb;9(2):81-94
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  • [Title] Forced retinoic acid receptor alpha homodimers prime mice for APL-like leukemia.
  • RARA becomes an acute promyelocytic leukemia (APL) oncogene by fusion with any of five translocation partners.
  • Although in vivo the artificial fusions alone are poor initiators of leukemia, p50-RARalpha readily cooperates with an activated mutant CDw131 to induce APL-like disease.
  • These results demonstrate that the dimerization interface of RARalpha fusion partners is a critical element in APL pathogenesis while pointing to other features of PML for enhancing penetrance and progression.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Receptors, Retinoic Acid / chemistry. Receptors, Retinoic Acid / metabolism
  • [MeSH-minor] Animals. Bone Marrow / pathology. Carcinogens / metabolism. Cell Line. DNA / metabolism. DNA-Binding Proteins / metabolism. Dimerization. Down-Regulation / genetics. Mice. Mice, Transgenic. Mutation / genetics. Myeloid Cells / metabolism. Myeloid Cells / pathology. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Protein Binding. Protein Structure, Quaternary. Receptors, Cytokine / metabolism. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Repressor Proteins / chemistry. Repressor Proteins / genetics. Repressor Proteins / metabolism. Retinoid X Receptors / metabolism. Transcription, Genetic / genetics


6. Wang H, Wang X, Xu X, Lin G: Cytogenetic features and prognosis analysis in Chinese patients with myelodysplastic syndrome: a multicenter study. Ann Hematol; 2010 Jun;89(6):535-44
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  • Of the 435 patients, 186 (42.8%) had died and 40 (9.2%) had progressed to acute myeloid leukemia.
  • Multivariate analysis identified older age, higher percent of marrow blasts, and poor-risk IPSS cytogenetics as characteristics associated with worse survival and higher risk of leukemia transformation.
  • For predicting leukemia evolution, the Spanish scoring system was most effective.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Chromosome Aberrations / statistics & numerical data. Cytogenetic Analysis. Disease Progression. Female. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis. World Health Organization. Young Adult


7. Zardo G, Fazi F, Travaglini L, Nervi C: Dynamic and reversibility of heterochromatic gene silencing in human disease. Cell Res; 2005 Sep;15(9):679-90
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  • The relevant contribution of epigenetic mechanisms to a proper cellular function is highlighted by the effects of their deregulation that cooperate with genetic alterations to the development of various diseases and to the establishment and progression of tumors.
  • [MeSH-minor] Chromatin / metabolism. DNA / metabolism. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation. Genetic Diseases, Inborn / genetics. Histones / metabolism. Humans. Leukemia, Myeloid, Acute / genetics. Models, Biological. Neoplasms / genetics. Nucleosomes / metabolism. Oligodeoxyribonucleotides. Protein Processing, Post-Translational. Protein Structure, Tertiary. RNA / chemistry. RNA Interference. Sequence Analysis, DNA. Transcription, Genetic. Tretinoin / metabolism

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  • (PMID = 16212874.001).
  • [ISSN] 1001-0602
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CPG-oligonucleotide; 0 / Chromatin; 0 / Heterochromatin; 0 / Histones; 0 / Nucleosomes; 0 / Oligodeoxyribonucleotides; 5688UTC01R / Tretinoin; 63231-63-0 / RNA; 9007-49-2 / DNA
  • [Number-of-references] 124
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8. Advani AS, Lim K, Gibson S, Shadman M, Jin T, Copelan E, Kalaycio M, Sekeres MA, Sobecks R, Hsi E: OCT-2 expression and OCT-2/BOB.1 co-expression predict prognosis in patients with newly diagnosed acute myeloid leukemia. Leuk Lymphoma; 2010 Apr;51(4):606-12
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  • [Title] OCT-2 expression and OCT-2/BOB.1 co-expression predict prognosis in patients with newly diagnosed acute myeloid leukemia.
  • OCT-2 and its co-activator, BOB.1, are B-cell associated transcription factors expressed in a subset of patients with acute myeloid leukemia (AML).
  • OCT-2 (per 10% increase) was associated with a decreased progression-free survival (HR 1.10, p = 0.036) and a trend toward a worse OS (HR 1.10, p = 0.063).
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Octamer Transcription Factor-2 / metabolism. Trans-Activators / metabolism

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  • (PMID = 20141429.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Octamer Transcription Factor-2; 0 / POU2AF1 protein, human; 0 / POU2F2 protein, human; 0 / Trans-Activators
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9. Oran B, Giralt S, Saliba R, Hosing C, Popat U, Khouri I, Couriel D, Qazilbash M, Anderlini P, Kebriaei P, Ghosh S, Carrasco-Yalan A, de Meis E, Anagnostopoulos A, Donato M, Champlin RE, de Lima M: Allogeneic hematopoietic stem cell transplantation for the treatment of high-risk acute myelogenous leukemia and myelodysplastic syndrome using reduced-intensity conditioning with fludarabine and melphalan. Biol Blood Marrow Transplant; 2007 Apr;13(4):454-62
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  • [Title] Allogeneic hematopoietic stem cell transplantation for the treatment of high-risk acute myelogenous leukemia and myelodysplastic syndrome using reduced-intensity conditioning with fludarabine and melphalan.
  • One hundred twelve acute myelogenous leukemia/myelodysplastic syndromes patients received fludarabine and melphalan (FM) conditioning with allogeneic HSCT.
  • In multivariate analysis, survival was negatively influenced by active disease at HSCT and development of grade II-IV acute GVHD.
  • Presence of circulating blasts at HSCT negatively influenced freedom from disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Aged. Disease Progression. Drug Therapy, Combination. Female. Humans. Kaplan-Meier Estimate. Male. Melphalan / administration & dosage. Middle Aged. Risk Factors. Survivors. Transplantation, Homologous. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives


10. Agrawal S, Koschmieder S, Bäumer N, Reddy NG, Berdel WE, Müller-Tidow C, Serve H: Pim2 complements Flt3 wild-type receptor in hematopoietic progenitor cell transformation. Leukemia; 2008 Jan;22(1):78-86
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  • Pim2 is a serine/threonine kinase expressed at high levels in several malignancies including acute leukemia.
  • Here we show that Pim2 can complement Flt3-Wt signaling and induce transformation similar to Flt3-ITD in myeloid cells.
  • This increase was associated with enhanced S-phase cell cycle progression.
  • The Flt3 point mutant D835Y, which is not able to support colony growth of myeloid cells, also induced clonogenic growth in the presence of Pim2.
  • Pim2 complements with Flt3-Wt signaling to induce proliferation by enhancing G(1)/S-phase progression of the cell cycle.
  • [MeSH-minor] Animals. Apoptosis / physiology. Blotting, Western. Cell Differentiation / physiology. Cell Proliferation. Cells, Cultured. Colony-Forming Units Assay. Gene Expression Regulation. Humans. Membrane Proteins / metabolism. Mice. Myeloid Cells / metabolism. RNA, Small Interfering / pharmacology. S Phase / physiology. STAT5 Transcription Factor / metabolism. Signal Transduction. Tandem Repeat Sequences / genetics

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  • (PMID = 17943165.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Pim2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / STAT5 Transcription Factor; 0 / flt3 ligand protein; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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11. Janus A, Linke A, Cebula B, Robak T, Smolewski P: Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine. Anticancer Drugs; 2009 Sep;20(8):693-701
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine.
  • Overexpression of the mTOR signaling pathway has been described in several tumor cells, including the majority of acute myeloid leukemia (AML) cases.
  • The study showed that RAPA in concentrations of 1-10 nmol/l arrested the cell cycle progression of Hl-60 cells in the G1 phase, without evident cytotoxic effect.
  • In conclusion, these data indicate that RAPA might be effective in the treatment of acute leukemia patients, especially in combination with Ara-C, the drug routinely used in AML treatment.

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  • (PMID = 19584709.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Cyclins; 0 / EIF4EBP1 protein, human; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Phosphoproteins; 04079A1RDZ / Cytarabine; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 3.4.22.- / Caspase 3; W36ZG6FT64 / Sirolimus
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12. Choi SW, Boxer LA, Pulsipher MA, Roulston D, Hutchinson RJ, Yanik GA, Cooke KR, Ferrara JL, Levine JE: Stem cell transplantation in patients with severe congenital neutropenia with evidence of leukemic transformation. Bone Marrow Transplant; 2005 Mar;35(5):473-7
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  • With appropriate treatment using recombinant human granulocyte-colony-stimulating factor (r-HuG-CSF), SCN patients are now surviving longer, but are at increased risk of developing myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML).
  • SCN patients should be monitored carefully for progression to MDS in order to be treated with HSCT as soon as they have progressed and before developing AML.
  • For SCN patients who progress to AML, HSCT should still be considered, even though the risks appear to be greater.
  • [MeSH-major] Cell Transformation, Neoplastic. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Neutropenia / complications
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow Examination. Child. Child, Preschool. Disease Progression. Female. Humans. Infant. Karyotyping. Male. Myelodysplastic Syndromes / etiology. Myelodysplastic Syndromes / therapy. Retrospective Studies. Survival Rate. Transplantation Conditioning. Treatment Outcome

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  • (PMID = 15640815.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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13. Centers for Disease Control and Prevention (CDC): Progressive vaccinia in a military smallpox vaccinee - United States, 2009. MMWR Morb Mortal Wkly Rep; 2009 May 22;58(19):532-6
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  • The service member had been newly diagnosed with acute mylegenous leukemia M0 (AML M0).
  • [MeSH-minor] Adult. Clostridium Infections. DNA, Viral / analysis. Disease Progression. Humans. Immunoglobulins, Intravenous / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Male. Military Personnel. Multiple Organ Failure. Pseudomonas Infections. United States

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  • (PMID = 19478722.001).
  • [ISSN] 1545-861X
  • [Journal-full-title] MMWR. Morbidity and mortality weekly report
  • [ISO-abbreviation] MMWR Morb. Mortal. Wkly. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Immunoglobulins, Intravenous; 0 / Smallpox Vaccine
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14. Chim CS, Wong KY, Qi Y, Loong F, Lam WL, Wong LG, Jin DY, Costello JF, Liang R: Epigenetic inactivation of the miR-34a in hematological malignancies. Carcinogenesis; 2010 Apr;31(4):745-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia [acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL)], chronic leukemia [chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML)], multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL).
  • In MM patients with paired samples, miR-34a methylation status remained unchanged at progression.

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  • [ErratumIn] Carcinogenesis. 2014 Nov;35(11):2631
  • (PMID = 20118199.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN34 microRNA, human; 0 / MicroRNAs
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15. Bessho F, Imashuku S, Hibi S, Tsuchida M, Nakahata T, Miyazaki S, Kojima S, Tsukimoto I, Hamajima N, Pediatric AA Follow-up Study Group in Japan: Serial morphologic observation of bone marrow in aplastic anemia in children. Int J Hematol; 2005 Jun;81(5):400-4
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  • Recent reports of myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) developing after treatment with immunosuppressants and granulocyte colony-stimulating factor (G-CSF) has raised the question of whether previously unrecognized myelodysplastic features had been present or whether actual transformation had occurred.
  • [MeSH-minor] Bone Marrow Examination. Child. Chromosome Aberrations. Disease Progression. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / diagnosis. Mast Cells / pathology. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / diagnosis

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  • [Cites] Hum Pathol. 1979 Mar;10(2):242-3 [422194.001]
  • [Cites] Br J Haematol. 1986 Aug;63(4):665-9 [3460627.001]
  • [Cites] Nature. 1990 Jul 19;346(6281):274-6 [2374592.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1985;405(4):503-9 [3920822.001]
  • [Cites] Blood. 1987 Dec;70(6):1718-21 [3676511.001]
  • [Cites] Haematologica. 2003 Nov;88(11):ECR31 [14607763.001]
  • [Cites] Br J Cancer. 1999 Feb;79(3-4):451-5 [10027312.001]
  • [Cites] Acta Haematol. 1980;64(3):131-5 [6778045.001]
  • [Cites] J Histochem Cytochem. 1997 Jul;45(7):935-45 [9212819.001]
  • [Cites] Hum Pathol. 1981 Jul;12(7):605-8 [7024100.001]
  • [Cites] Br J Haematol. 1991 Apr;77(4):509-14 [2025576.001]
  • [Cites] N Engl J Med. 2003 Apr 24;348(17):1709-11 [12711748.001]
  • [Cites] Blood. 2000 Jan 1;95(1):309-13 [10607717.001]
  • [Cites] Lancet. 2001 Jan 6;357(9249):43-4 [11197365.001]
  • [Cites] J Clin Pathol. 1974 Mar;27(3):231-41 [4832303.001]
  • [Cites] Clin Haematol. 1980 Oct;9(3):587-606 [6450011.001]
  • [Cites] Mol Biol Cell. 1998 Apr;9(4):875-84 [9529385.001]
  • [Cites] J Clin Pathol. 2004 Jan;57(1):108-9 [14693852.001]
  • [Cites] Leuk Res. 1989;13(2):173-8 [2927174.001]
  • [Cites] Br J Haematol. 1989 Jul;72(3):439-44 [2788455.001]
  • [Cites] Blood. 1997 Aug 1;90(3):1009-13 [9242530.001]
  • [Cites] J Immunol. 1993 Sep 15;151(6):3261-6 [8376778.001]
  • [Cites] Exp Hematol. 2000 Sep;28(9):993-1000 [11008011.001]
  • [Cites] Immunol Today. 1990 Dec;11(12):458-64 [2073318.001]
  • [Cites] Hematol Pathol. 1994;8(3):55-73 [7527020.001]
  • [Cites] Br J Haematol. 1994 Jul;87(3):503-8 [7527645.001]
  • [Cites] Hum Pathol. 1978 May;9(3):295-308 [26634.001]
  • [Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]
  • [Cites] Int J Hematol. 1994 Oct;60(3):185-9 [7532030.001]
  • [Cites] Leuk Res. 1999 Jun;23(6):579-84 [10374851.001]
  • [Cites] Br J Haematol. 1988 Jul;69(3):413-8 [3044440.001]
  • [Cites] Br J Haematol. 1975 Apr;29(4):545-52 [1191564.001]
  • [Cites] J Clin Pathol. 1985 Nov;38(11):1218-24 [4066981.001]
  • [Cites] Am J Dis Child. 1973 Sep;126(3):389-96 [4746551.001]
  • [Cites] Postgrad Med. 1974 May;55(5):267-8 [4824724.001]
  • [Cites] Br J Haematol. 1992 Mar;80(3):298-304 [1374626.001]
  • [Cites] Haematologica. 1997 Jan-Feb;82(1):21-4 [9107077.001]
  • [Cites] Lancet. 1971 Oct 30;2(7731):971-2 [4107917.001]
  • [Cites] Br J Cancer. 1999 Dec;81(8):1398-401 [10604739.001]
  • (PMID = 16158820.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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16. Yao DM, Qian J, Xu WR, Lin J, Jiang YW, Fei X, Han LX, Wang Y, Cen JN, Chen ZX: [Alteration of methylation status of fragile histidine triad gene promoter in patients with myelodysplastic syndrome]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Feb;25(1):36-9
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  • Although significant difference was not observed in the frequencies of FHIT gene hypermethylation among patients with refractory anemia/refractory anemia with ringed sideroblasts (RA/RAS) (1/6, 16.7%), refractory anemia/refractory anemia with ringed sideroblasts (RCMD) and refractory cytopenia with multilineage dysplasia with ringed blasts (RCMD-RS) (6/19, 31.6%), refractory anemia with excess blasts-1 (RAEB-1) (7/11, 63.6%), refractory anemia with excess blasts-2 (RAEB-2) (4/7, 57.1%) and refractory anemia with excess blasts in transformation/acute myeloid leukemia (RAEBt/AML) (8/11, 72.7%)(chi-square=8.417, P=0.077), it was observed in patients in early stages (RA/RAS and RCMD) (7/25, 28.0%), advanced stages (RAEB-1 and RAEB-2)(11/18, 61.1%) and RAEBt/AML (8/11, 72.7%) (chi-square=7.938, P=0.019).
  • CONCLUSION: FHIT gene hypermethylation might be one of the molecular events involved in the disease progression of MDS.

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  • (PMID = 18247301.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases
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17. Wang YY, Cen JN, He J, Shen HJ, Liu DD, Yao L, Qi XF, Chen ZX: Accelerated cellular senescence in myelodysplastic syndrome. Exp Hematol; 2009 Nov;37(11):1310-7
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  • OBJECTIVE: To investigate the contribution of cellular senescence to the progression and prognosis of myelodysplastic syndrome (MDS).
  • MATERIALS AND METHODS: We have analyzed the expression of p16INK4a in bone marrow mononuclear cells or CD34(+) cells from 53 patients with MDS, 12 acute myeloid leukemia (AML), and 11 healthy controls.
  • Additionally, We have assessed quantitatively senescence-associated beta-galactosidase (SA-beta-gal) staining on bone marrow mononuclear cells from MDS and AML patients, HL60 and SHI-1 leukemia cell lines, and healthy control cells.
  • CONCLUSIONS: These results of our present study suggested an accelerated cellular senescence occurred in MDS, and the cellular senescence may be involved in the progression and prognosis of MDS.
  • [MeSH-major] Cell Aging. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Anemia, Refractory / metabolism. Anemia, Refractory / pathology. Anemia, Refractory, with Excess of Blasts / metabolism. Anemia, Refractory, with Excess of Blasts / pathology. Biomarkers. Cell Line, Tumor / chemistry. Cell Line, Tumor / pathology. Cyclin-Dependent Kinase Inhibitor p16 / analysis. Female. Genes, p16. Humans. Male. Middle Aged. Neoplasm Proteins / analysis. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Severity of Illness Index. Young Adult. beta-Galactosidase / analysis

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  • (PMID = 19748549.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.2.1.23 / beta-Galactosidase
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18. Mesa RA, Powell H, Lasho T, Dewald G, McClure R, Tefferi A: JAK2(V617F) and leukemic transformation in myelofibrosis with myeloid metaplasia. Leuk Res; 2006 Nov;30(11):1457-60
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  • [Title] JAK2(V617F) and leukemic transformation in myelofibrosis with myeloid metaplasia.
  • Amongst 42 consecutive patients with leukemic transformation (LT) from myelofibrosis with myeloid metaplasia (MMM) 72% carried the JAK2(V617F) mutation.
  • The mutation was observed at expected frequencies in all subtypes of MMM and acute myeloid leukemia.
  • Additionally, both the lack of mutation status progression in serial analysis (available in nine patients) and the low frequency of patients with high mutated allele burden suggest that LT arising from MMM is probably not dependent on changes in JAK2(V617F) mutation status.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Myeloid / genetics. Primary Myelofibrosis / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Substitution / genetics. Cytogenetic Analysis / methods. DNA / genetics. Disease Progression. Female. Humans. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Survival Rate

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  • (PMID = 16563504.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 K23 CA96780-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9007-49-2 / DNA; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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19. Follo MY, Mongiorgi S, Finelli C, Clissa C, Ramazzotti G, Fiume R, Faenza I, Manzoli L, Martelli AM, Cocco L: Nuclear inositide signaling in myelodysplastic syndromes. J Cell Biochem; 2010 Apr 15;109(6):1065-71
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  • Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML).
  • Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions.
  • [MeSH-minor] Animals. Humans. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Phosphatidylinositols / metabolism. Phospholipase C beta / metabolism. Proto-Oncogene Proteins c-akt / metabolism


20. Braun T, Carvalho G, Coquelle A, Vozenin MC, Lepelley P, Hirsch F, Kiladjian JJ, Ribrag V, Fenaux P, Kroemer G: NF-kappaB constitutes a potential therapeutic target in high-risk myelodysplastic syndrome. Blood; 2006 Feb 1;107(3):1156-65
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  • Myelodysplastic syndrome (MDS) is a preneoplastic condition that frequently develops into overt acute myeloid leukemia (AML).
  • Purified hematopoietic stem cells (CD34+) and immature myeloid cells (CD33+) from high-risk MDS patients demonstrated the nuclear translocation of the p65 NF-kappaB subunit.
  • The frequency of cells with nuclear p65 correlated with blast counts, apoptosis suppression, and disease progression.
  • [MeSH-major] Apoptosis / drug effects. Cell Nucleus / metabolism. Myelodysplastic Syndromes / metabolism. Myeloid Progenitor Cells / metabolism. RNA, Small Interfering / pharmacology. Transcription Factor RelA / antagonists & inhibitors


21. de Melo Campos P, Traina F, da Silva Santos Duarte A, Lorand-Metze I, Costa FF, Saad ST: Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome. Leuk Res; 2007 Jun;31(6):853-7
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  • Apoptosis is dysregulated in patients with myelodysplastic syndrome (MDS) and acute myelogenous leukaemia (AML).
  • Furthermore, FLIP(SHORT) mRNA expression was significantly lower in low risk MDS, compared to MDS-AML/AML de novo (P=0.0006), according to FAB classification.
  • Increased levels of FLIP(SHORT) in RAEB and AML may be related to apoptosis resistance in these diseases and to MDS progression.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. CASP8 and FADD-Like Apoptosis Regulating Protein / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism


22. Keen-Kim D, Nooraie F, Rao PN: Cytogenetic biomarkers for human cancer. Front Biosci; 2008;13:5928-49
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  • Here we describe many of the best-known chromosome rearrangements and variant rearrangements in hematologic disease and solid tumors, indicate the genes and underlying molecular mechanisms known to be involved in development and progression of disease, and describe the newer molecular cytogenetic technologies and how they are currently being used in cancer diagnostics.
  • [MeSH-minor] Bone Neoplasms / genetics. Breast Neoplasms / genetics. Female. Humans. Kidney Neoplasms / genetics. Leukemia, Myeloid, Acute / genetics. Lymphoma, B-Cell / genetics. Lymphoma, T-Cell / genetics. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / genetics. Urinary Bladder Neoplasms / genetics

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  • (PMID = 18508633.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM008243
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 157
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23. Stiefelhagen P: [Pancytopenia with unclear genesis -- bad surprise in differential blood picture]. MMW Fortschr Med; 2009 Jun 25;151(26-29):18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Pancytopenia / etiology
  • [MeSH-minor] Acute Disease. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Male. Middle Aged

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  • (PMID = 19739538.001).
  • [ISSN] 1438-3276
  • [Journal-full-title] MMW Fortschritte der Medizin
  • [ISO-abbreviation] MMW Fortschr Med
  • [Language] ger
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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24. Martelli AM, Nyåkern M, Tabellini G, Bortul R, Tazzari PL, Evangelisti C, Cocco L: Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia; 2006 Jun;20(6):911-28
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  • [Title] Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.
  • The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is crucial to many aspects of cell growth, survival and apoptosis, and its constitutive activation has been implicated in the both the pathogenesis and the progression of a wide variety of neoplasias.
  • Recent studies showed that PI3K/Akt signaling is frequently activated in acute myeloid leukemia (AML) patient blasts and strongly contributes to proliferation, survival and drug resistance of these cells.
  • [MeSH-major] Leukemia, Myeloid / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Acute Disease. Humans. Models, Biological. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 16642045.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Number-of-references] 250
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25. Walter MJ, Park JS, Ries RE, Lau SK, McLellan M, Jaeger S, Wilson RK, Mardis ER, Ley TJ: Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha. Proc Natl Acad Sci U S A; 2005 Aug 30;102(35):12513-8
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  • [Title] Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.
  • Recently, haploinsufficiency for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineage.
  • We have previously shown that transgenic mice expressing PML-RARalpha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a large (>20 Mb) interstitial deletion of chromosome 2 that includes PU.1.
  • To directly assess the relevance of levels of expression of PU.1 for leukemia progression, we bred hCG-PR mice with PU.1+/- mice and assessed their phenotype.
  • Young, nonleukemic hCG-PR x PU.1+/- mice developed splenomegaly because of the abnormal expansion of myeloid cells in their spleens. hCG-PR x PU.1+/- mice developed a typical APL syndrome after a long latent period, but the penetrance of disease was 84%, compared with 7% in hCG-PR x PU.1+/+ mice (P < 0.0001).
  • However, PR expression in U937 myelomonocytic cells and primary murine myeloid bone marrow cells caused a reduction in PU.1 mRNA levels.
  • Therefore, the loss of one copy of PU.1 through a deletional mechanism, plus down-regulation of the residual allele caused by PR expression, may synergize to expand the pool of myeloid progenitors that are susceptible to transformation, increasing the penetrance of APL.

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  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):15103-8 [10611345.001]
  • [Cites] Oncogene. 2005 May 19;24(22):3678-83 [15750630.001]
  • [Cites] J Exp Med. 2001 Feb 19;193(4):531-43 [11181704.001]
  • [Cites] Leuk Res. 2002 May;26(5):451-7 [11916518.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] Blood. 2002 Aug 1;100(3):998-1007 [12130514.001]
  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2570-4 [12468434.001]
  • [Cites] Blood. 2003 Aug 1;102(3):1072-4 [12689927.001]
  • [Cites] Nat Immunol. 2003 Oct;4(10):1029-36 [12958595.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3727-36 [12893766.001]
  • [Cites] Cell. 2003 Oct 31;115(3):305-18 [14636558.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14275-80 [14614138.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Cancer Res. 1983 Jan;43(1):367-73 [6571708.001]
  • [Cites] Br J Cancer. 1983 Feb;47(2):285-91 [6337614.001]
  • [Cites] Leukemia. 1988 Aug;2(8):545-50 [3166080.001]
  • [Cites] Leukemia. 1992 Jul;6(7):689-95 [1625487.001]
  • [Cites] Cell. 1993 Aug 27;74(4):679-91 [8395349.001]
  • [Cites] Science. 1994 Sep 9;265(5178):1573-7 [8079170.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8989-93 [8090757.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3385-91 [8631937.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5647-58 [8896458.001]
  • [Cites] Blood. 1997 Jan 15;89(2):376-87 [9002938.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2217-33 [9310473.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Feb;24(2):95-104 [9885975.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2143-8 [10090920.001]
  • [Cites] Blood Cells Mol Dis. 1999 Feb;25(1):38-45 [10349512.001]
  • [Cites] Mutat Res. 1999 Jul 16;428(1-2):33-9 [10517976.001]
  • [Cites] J Immunol. 1999 Nov 1;163(9):4917-23 [10528194.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3437-44 [15304397.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(24):10882-93 [15572690.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):23-33 [15601827.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1456-66 [15522959.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13306-11 [11087871.001]
  • (PMID = 16113082.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / R01 CA083962; United States / NCI NIH HHS / CA / CA101937; United States / NCI NIH HHS / CA / CA83962
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Trans-Activators; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC1188022
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26. Leone G, D'Alò F, Zardo G, Voso MT, Nervi C: Epigenetic treatment of myelodysplastic syndromes and acute myeloid leukemias. Curr Med Chem; 2008;15(13):1274-87
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  • [Title] Epigenetic treatment of myelodysplastic syndromes and acute myeloid leukemias.
  • In the medical field, an increasing body of evidence indicates that altered gene expression or de-regulated gene function lead to disease.
  • However, studies on leukemias have provided paradigmatic examples for the functional implications of the epigenetic alterations in cancer development and progression as well as their relevance for therapeutical targeting.
  • [MeSH-major] Epigenesis, Genetic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics

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  • [Cites] Clin Cancer Res. 2000 Mar;6(3):994-7 [10741726.001]
  • [Cites] Microbiol Mol Biol Rev. 2000 Jun;64(2):435-59 [10839822.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10014-9 [10954755.001]
  • [Cites] J Cancer Res Clin Oncol. 2000 Dec;126(12):693-8 [11153141.001]
  • [Cites] Invest New Drugs. 2001;19(1):1-11 [11291827.001]
  • [Cites] Oncogene. 2001 May 28;20(24):3156-65 [11420732.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2330-9 [11489809.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36734-41 [11473107.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):6969-78 [11742974.001]
  • [Cites] J Pathol. 2002 Jan;196(1):1-7 [11748635.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Annu Rev Biochem. 2001;70:81-120 [11395403.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):718-28 [11895901.001]
  • [Cites] Hematol J. 2000;1(1):53-66 [11920170.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):963-70 [11948101.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2441-52 [12011121.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] J Mass Spectrom. 2002 Jun;37(6):581-90 [12112740.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2142-8 [12114414.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5483-95 [12154409.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4916-21 [12208741.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3319-24 [12384433.001]
  • [Cites] Nat Genet. 2002 Nov;32(3):453-8 [12355068.001]
  • [Cites] Nat Genet. 2002 Nov;32(3):393-6 [12368916.001]
  • [Cites] Hematol Oncol. 2002 Dec;20(4):167-76 [12469326.001]
  • [Cites] Epilepsy Res. 2003 Feb;53(1-2):19-27 [12576164.001]
  • [Cites] Science. 2003 Apr 18;300(5618):489-92 [12702876.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3637-45 [12839953.001]
  • [Cites] EMBO J. 2003 Jul 1;22(13):3411-20 [12840003.001]
  • [Cites] Mol Cancer Ther. 2003 Aug;2(8):721-8 [12939461.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1762-4 [12970776.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1813-9 [12970781.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3578-88 [14506144.001]
  • [Cites] Mol Cell. 2003 Sep;12(3):723-34 [14527417.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6489-96 [14528273.001]
  • [Cites] J Med Chem. 2003 Nov 20;46(24):5097-116 [14613312.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Cancer Res. 1983 Feb;43(2):592-7 [6184151.001]
  • [Cites] Cancer Res. 1983 Feb;43(2):763-9 [6184156.001]
  • [Cites] Nature. 1983 Jan 6;301(5895):89-92 [6185846.001]
  • [Cites] Cell. 1995 Apr 21;81(2):197-205 [7537636.001]
  • [Cites] Cancer Res. 1995 Jul 15;55(14):3093-8 [7541710.001]
  • [Cites] J Cancer Res Clin Oncol. 1996;122(3):135-40 [8601560.001]
  • [Cites] Invest New Drugs. 1996;14(4):349-56 [9157069.001]
  • [Cites] Mutat Res. 1997 Sep 5;379(1):33-41 [9330620.001]
  • [Cites] Invest New Drugs. 1997;15(3):187-94 [9387041.001]
  • [Cites] Genes Dev. 1998 Mar 1;12(5):599-606 [9499396.001]
  • [Cites] Nat Genet. 1998 Jun;19(2):187-91 [9620779.001]
  • [Cites] Nature. 1998 May 28;393(6683):386-9 [9620804.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7 Suppl):1743s-1746s [10197590.001]
  • [Cites] Blood. 1999 Jul 15;94(2):417-28 [10397708.001]
  • [Cites] Mutat Res. 1999 Aug 11;429(1):37-44 [10434023.001]
  • [Cites] Genes Dev. 1999 Aug 1;13(15):1924-35 [10444591.001]
  • [Cites] Leukemia. 1999 Aug;13(8):1243-53 [10450753.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18030-5 [15596714.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):673-8 [15637150.001]
  • [Cites] Blood. 2005 Feb 1;105(3):959-67 [15466934.001]
  • [Cites] Leuk Res. 2005 Mar;29(3):325-9 [15661269.001]
  • [Cites] Anticancer Drugs. 2005 Mar;16(3):301-8 [15711182.001]
  • [Cites] Med Res Rev. 2005 May;25(3):261-309 [15717297.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3697-702 [15738394.001]
  • [Cites] Oncologist. 2005 Mar;10(3):176-82 [15793220.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 29;102(13):4842-7 [15778293.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):391-400 [15765097.001]
  • [Cites] Hum Mol Genet. 2005 Apr 15;14 Spec No 1:R65-76 [15809275.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(11):4727-41 [15899874.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3897-905 [15753459.001]
  • [Cites] Invest New Drugs. 2006 Mar;24(2):159-67 [16502349.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4628-35 [16899611.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3895-903 [16921040.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8903-11 [16951208.001]
  • [Cites] Cancer. 2006 Oct 15;107(8):1839-43 [16967444.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):540-5 [14695887.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 3;101(5):1241-6 [14734806.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):1079-86 [14871841.001]
  • [Cites] Nucleic Acids Res. 2004;32(3):959-76 [14960713.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1635-40 [14604977.001]
  • [Cites] Mol Cell. 2004 Mar 12;13(5):627-38 [15023334.001]
  • [Cites] J Clin Oncol. 2004 Apr 15;22(8):1373-81 [15007085.001]
  • [Cites] Nature. 2004 May 27;429(6990):457-63 [15164071.001]
  • [Cites] Cancer Immun. 2004 Aug 9;4:7 [15298487.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1266-9 [15155466.001]
  • [Cites] Blood. 1973 Sep;42(3):359-65 [4125239.001]
  • [Cites] Biochem Pharmacol. 1979 Apr 15;28(8):1443-4 [87202.001]
  • [Cites] Trends Biochem Sci. 2006 Feb;31(2):89-97 [16403636.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1794-803 [16532500.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1744-50 [16532502.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):88-91 [10615135.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):956-62 [10694544.001]
  • [Cites] Recent Results Cancer Res. 1983;84:202-11 [6189159.001]
  • [Cites] Biochem Pharmacol. 1983 Apr 1;32(7):1327-8 [6189497.001]
  • [Cites] Blood. 1984 Oct;64(4):922-9 [6206904.001]
  • [Cites] Carcinogenesis. 1984 Dec;5(12):1583-90 [6209028.001]
  • [Cites] Cancer Treat Rep. 1987 Oct;71(10):959-64 [2443243.001]
  • [Cites] Eur J Cancer Clin Oncol. 1987 Sep;23(9):1283-7 [3678322.001]
  • [Cites] Gene. 1988 Dec 25;74(1):9-12 [3248734.001]
  • [Cites] Mutat Res. 1989 Jul;226(3):185-90 [2473395.001]
  • [Cites] J Toxicol Environ Health. 1990;29(2):201-10 [1688953.001]
  • [Cites] J Biol Chem. 1990 Oct 5;265(28):17174-9 [2211619.001]
  • [Cites] N Engl J Med. 1992 Aug 20;327(8):569-70 [1378939.001]
  • [Cites] Mutat Res. 1993 Jan;285(1):61-7 [7678134.001]
  • [Cites] J Biol Chem. 1993 Oct 25;268(30):22429-35 [8226751.001]
  • [Cites] Int J Cancer. 1994 Mar 15;56(6):906-9 [8119779.001]
  • [Cites] Cancer. 1981 Apr 1;47(7):1739-42 [6164472.001]
  • [Cites] Leuk Res. 1981;5(6):453-62 [6173545.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3912-22 [15851766.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3971-93 [15897549.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1262-6 [15988529.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4912-22 [16000590.001]
  • [Cites] Semin Hematol. 2005 Jul;42(3 Suppl 2):S9-16 [16015507.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26729-34 [15937340.001]
  • [Cites] Mol Cancer Ther. 2005 Oct;4(10):1515-20 [16227400.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Mar;2(3):150-7 [16264908.001]
  • [Cites] Ann Hematol. 2005 Dec;84 Suppl 1:9-17 [16211386.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):23-32 [16343268.001]
  • [Cites] Cancer. 2006 Jan 1;106(1):112-9 [16323176.001]
  • [Cites] Mol Pharmacol. 2006 Jan;69(1):216-25 [16189296.001]
  • [Cites] Ann N Y Acad Sci. 2005 Nov;1058:246-54 [16394141.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526.001]
  • [Cites] Blood Rev. 2006 Jan;20(1):1-13 [16426940.001]
  • [Cites] Leukemia. 2006 Feb;20(2):212-7 [16357841.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Nat Cell Biol. 2007 Jan;9(1):2-6 [17199124.001]
  • [Cites] Nat Med. 2007 Jan;13(1):78-83 [17159988.001]
  • [Cites] Cancer. 2007 Jan 15;109(2):265-73 [17133405.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1370-7 [17283175.001]
  • [Cites] Cancer. 2007 Feb 15;109(4):713-7 [17219444.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Cancer. 2007 Mar 1;109(5):899-906 [17236224.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1114-24 [17315155.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1133-7 [17315156.001]
  • [Cites] Nat Rev Genet. 2007 Apr;8(4):286-98 [17339880.001]
  • [Cites] Nat Genet. 2007 Apr;39(4):457-66 [17334365.001]
  • [Cites] Cell Mol Life Sci. 2007 May;64(9):1043-62 [17347798.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2781-90 [17179232.001]
  • [Cites] Int J Cancer. 2007 Sep 1;121(5):1138-48 [17455259.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(7-8):1388-405 [17383217.001]
  • [Cites] Biochem Pharmacol. 2007 Sep 1;74(5):659-71 [17498667.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1937-44 [17611569.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3884-91 [17679729.001]
  • [Cites] J Clin Oncol. 2007 Sep 10;25(26):4051-6 [17827453.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]
  • [Cites] Cancer. 2007 Sep 1;110(5):943-54 [17647267.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):457-66 [17996649.001]
  • [Cites] Cell. 2007 Nov 16;131(4):822 [18022374.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1060-6 [17962510.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Apr;61(5):759-66 [17564707.001]
  • [Cites] Leuk Res. 2008 May;32(5):771-80 [18031811.001]
  • [Cites] Mol Cancer Ther. 2003 Feb;2(2):151-63 [12589032.001]
  • [Cites] Ann Oncol. 2003 May;14(5):766-74 [12702532.001]
  • [Cites] Science. 2003 Apr 18;300(5618):455 [12702868.001]
  • (PMID = 18537607.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 160
  • [Other-IDs] NLM/ PMC2764862
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27. Dingli D, Tefferi A: Hydroxyurea: The drug of choice for polycythemia vera and essential thrombocythemia. Curr Hematol Malig Rep; 2006 Jun;1(2):69-74
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  • However, many clinicians are reluctant to use it because of the perceived risk of progression to acute leukemia.
  • Relevant results from these studies are discussed, and the risk of leukemia is placed in perspective to demonstrate that hydroxyurea remains the drug of choice in patients with either of these disorders.
  • [MeSH-minor] Aged. Agranulocytosis / chemically induced. Alkylating Agents / therapeutic use. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Evidence-Based Medicine. Hemorrhage / etiology. Humans. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / prevention & control. Middle Aged. Phlebotomy. Phosphorus Radioisotopes / therapeutic use. Thrombophilia / etiology

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  • Hazardous Substances Data Bank. HYDROXYUREA .
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  • [Cites] Semin Oncol. 1992 Aug;19(4 Suppl 11):21-8 [1509278.001]
  • [Cites] Br J Cancer. 1981 Jul;44(1):75-80 [7020738.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]
  • [Cites] Neth J Med. 1999 Feb;54(2):46-62 [10079679.001]
  • [Cites] Blood Rev. 1997 Mar;11(1):1-7 [9218101.001]
  • [Cites] N Engl J Med. 1995 Apr 27;332(17):1132-6 [7700286.001]
  • [Cites] Ann Dermatol Venereol. 1994;121(6-7):499-500 [7702286.001]
  • [Cites] Leuk Lymphoma. 1996 Sep;22 Suppl 1:111-9 [8951781.001]
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17747-53 [10747958.001]
  • [Cites] Mayo Clin Proc. 1998 Dec;73(12):1177-84 [9868417.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3370-7 [9345019.001]
  • [Cites] Aust N Z J Med. 1998 Jun;28(3):347 [9673751.001]
  • [Cites] Curr Hematol Rep. 2003 May;2(3):237-41 [12901345.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):17-23 [9025158.001]
  • [Cites] Blood. 1951 Apr;6(4):372-5 [14820991.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):40-50 [9025161.001]
  • [Cites] N Engl J Med. 2004 Jan 8;350(2):114-24 [14711910.001]
  • [Cites] Mayo Clin Proc. 2003 Feb;78(2):174-94 [12583529.001]
  • [Cites] Semin Thromb Hemost. 1997;23(5):463-72 [9387205.001]
  • [Cites] Clin Pharmacokinet. 1998 May;34(5):347-58 [9592619.001]
  • [Cites] Clin Lab Haematol. 2000 Aug;22(4):229-32 [11012636.001]
  • [Cites] Cancer Chemother Rep. 1971 Apr;55(2):167-73 [5286990.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2319-27 [9116275.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):577-83 [10997967.001]
  • [Cites] Presse Med. 2000 Feb 12;29(5):242-5 [10701401.001]
  • [Cites] N Engl J Med. 1981 Feb 19;304(8):441-7 [7005681.001]
  • [Cites] Cancer. 1991 May 15;67(10):2658-63 [2015567.001]
  • [Cites] Clin Exp Dermatol. 2004 Nov;29(6):605-7 [15550132.001]
  • [Cites] Eur J Dermatol. 2002 Nov-Dec;12(6):586-8 [12459535.001]
  • [Cites] Blood. 1981 Nov;58(5):916-9 [7296002.001]
  • [Cites] Br J Haematol. 2002 Feb;116(2):243-54 [11841424.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):177-86 [12542474.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):174-95 [16029446.001]
  • [Cites] Semin Hematol. 2001 Jan;38(1 Suppl 2):1-4 [11242595.001]
  • [Cites] N Engl J Med. 2000 Apr 27;342(17):1255-65 [10781623.001]
  • [Cites] Blood. 1998 Jan 15;91(2):616-22 [9427717.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Ann Hematol. 2000 Jan;79(1):40-2 [10663620.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1186-7 [12764388.001]
  • [Cites] Br J Haematol. 2005 Sep;130(5):797-9 [16115143.001]
  • [Cites] Curr Hematol Rep. 2005 May;4(3):235-7 [15865878.001]
  • [Cites] Crit Rev Oncol Hematol. 1999 Feb;29(3):249-55 [10226728.001]
  • [Cites] Blood Rev. 2001 Sep;15(3):121-31 [11735160.001]
  • [Cites] Aust N Z J Med. 1998 Oct;28(5):657-9 [9847957.001]
  • [Cites] Leuk Lymphoma. 2000 Jan;36(3-4):239-53 [10674896.001]
  • [Cites] Semin Hematol. 1986 Jul;23(3):167-71 [3749925.001]
  • [Cites] Med Klin (Munich). 2003 Jul 15;98(7):394-7 [12937905.001]
  • [Cites] J Med Chem. 1963 Mar;6:201 [14188794.001]
  • [Cites] Am J Hematol. 1999 May;61(1):10-5 [10331505.001]
  • [Cites] Dermatology. 1998;196(2):274 [9568428.001]
  • [Cites] Crit Rev Oncol Hematol. 1996 Mar;22(2):89-126 [8679103.001]
  • [Cites] N Engl J Med. 2005 Jul 7;353(1):33-45 [16000354.001]
  • [Cites] Ann Hematol. 1999 Sep;78(9):389-92 [10525825.001]
  • [Cites] Am J Hematol. 2004 Dec;77(4):374-6 [15558807.001]
  • [Cites] Blood. 2003 May 1;101(9):3749 [12707224.001]
  • [Cites] J Clin Lab Anal. 1997;11(4):208-13 [9219062.001]
  • [Cites] Ann Dermatol Venereol. 2001 Sep;128(8-9):919-21 [11590345.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2664-70 [15585653.001]
  • [Cites] Haematologica. 2004 Feb;89(2):215-32 [15003898.001]
  • [Cites] Mayo Clin Proc. 2005 Jul;80(7):947-58 [16007902.001]
  • [Cites] Biochem Cell Biol. 1990 Dec;68(12):1364-71 [2085432.001]
  • [Cites] Leuk Lymphoma. 2005 May;46(5):641-50 [16019501.001]
  • (PMID = 20425334.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Phosphorus Radioisotopes; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 66
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28. Henrich S, Crossett B, Christopherson RI: Differentially expressed nuclear proteins in human CCRF-CEM, HL-60, MEC-1 and Raji cells correlate with cellular properties. Proteomics Clin Appl; 2007 Oct;1(10):1252-65
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  • The human cell lines CCRF-CEM (T-cell acute lymphocytic leukemia), HL-60 (acute myeloid leukemia), MEC-1 (B-cell chronic lymphocytic leukemia) and Raji (Burkitt's B-cell lymphoma) have been analysed for differences in their nuclear proteomes.
  • Proteins uniquely over-expressed between myeloid and lymphoid cell lines include those that may have use as markers for diagnosis, disease progression and B-cell maturation and differentiation.
  • Expression of various proliferation-associated nuclear proteins correlated with relative growth rates of the cell lines, giving these proteins potential diagnostic applications for distinction of chronic versus acute subtypes of haematological malignancies.
  • The nuclear expression profiles should enable classification of subtypes of leukemia, and identify potential nuclear protein targets for development of diagnostic and therapeutic strategies.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136623.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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29. Deininger MW, Cortes J, Paquette R, Park B, Hochhaus A, Baccarani M, Stone R, Fischer T, Kantarjian H, Niederwieser D, Gambacorti-Passerini C, So C, Gathmann I, Goldman JM, Smith D, Druker BJ, Guilhot F: The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells. Cancer; 2007 Oct 1;110(7):1509-19
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  • [Title] The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells.
  • BACKGROUND: Clonal cytogenetic abnormalities (CCA) were detected in Philadelphia chromosome (Ph)-negative cells in some patients with chronic myeloid leukemia (CML) who attained a cytogenetic response to imatinib mesylate.
  • In some patients, CCA/Ph-negative status was associated with myelodysplasia or acute myeloid leukemia.
  • METHODS: The authors compared the pretherapeutic risk factors (Kruskall-Wallis test), exposure to cytotoxic drugs (chi-square test), and overall and progression-free survival (Kaplan-Meyer and logistic regression analysis, respectively) of 515 patients with mostly chronic-phase CML who were treated with imatinib mesylate after failure of interferon-alpha according to whether they attained a major cytogenetic response (MCR) (n = 324 patients), an MCR with CCA/Ph-negative status (n = 30 patients), or no MCR (n = 161 patients).
  • No significant differences in pretherapeutic risk factors were detected between patients who attained an MCR with and without CCA/Ph-negative cells, except that exposure to alkylating agents was more frequent in patients with CCA/Ph-negative cells, and overall and progression-free survival were identical.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Chromosome Aberrations. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use


30. Hovén E, Anclair M, Samuelsson U, Kogner P, Boman KK: The influence of pediatric cancer diagnosis and illness complication factors on parental distress. J Pediatr Hematol Oncol; 2008 Nov;30(11):807-14
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  • This category included central nervous system tumors, acute myeloid leukemia, and bone tumors.
  • Parental distress in that category (n=144) was compared with distress after acute lymphoblastic leukemia (n=177) in the child.
  • RESULTS: Parents in the complicated cancer category showed significantly heightened disease-related fear, anxiety, depression, loss of control, late effects-related uncertainty, and poorer self-esteem compared with parents of children with acute lymphoblastic leukemia.
  • [MeSH-minor] Adolescent. Adult. Anxiety / diagnosis. Anxiety / etiology. Child. Child, Preschool. Cranial Irradiation. Depression / diagnosis. Depression / etiology. Disease Progression. Female. Humans. Infant. Infant, Newborn. Internal-External Control. Male. Surveys and Questionnaires. Time Factors

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  • (PMID = 18989157.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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31. Pons A, Nomdedeu B, Navarro A, Gaya A, Gel B, Diaz T, Valera S, Rozman M, Belkaid M, Montserrat E, Monzo M: Hematopoiesis-related microRNA expression in myelodysplastic syndromes. Leuk Lymphoma; 2009 Nov;50(11):1854-9
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  • The present study sought to link hematopoiesis-relevant miRNAs with myelodysplastic syndromes (MDS) and MDS progression to acute myeloid leukemia (AML).
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Bone Marrow / metabolism. Bone Marrow / pathology. Disease Progression. Female. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Leuk Lymphoma. 2009 Nov;50(11):1735-6 [19883302.001]
  • (PMID = 19883312.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN15 microRNA, human; 0 / MIRN16 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
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32. Ryningen A, Stapnes C, Paulsen K, Lassalle P, Gjertsen BT, Bruserud O: In vivo biological effects of ATRA in the treatment of AML. Expert Opin Investig Drugs; 2008 Nov;17(11):1623-33
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  • BACKGROUND: All-trans retinoic acid (ATRA) is mandatory in the treatment of acute promyelocytic leukaemia (APL).
  • Experimental studies suggest that ATRA can induce differentiation and apoptosis in leukaemia cells also for other acute myelogenous leukaemia (AML) subtypes, but the clinical observations are conflicting.
  • Serum/plasma samples were collected before and after 2 days of ATRA, peripheral blood AML cells were collected from all 12 patients with circulating leukaemia cells (ClinicalTrials.gov NCT00175812; EudraCT no. 2004-001663-22).
  • Circulating leukaemia cells derived during therapy had increased intracellular levels of P21 (mean increase in mean fluorescence intensity (MFI) being 18.2%, p = 0.017), and decreased levels of Gata-2 (mean decrease in MFI 19%, p = 0.026), NF-kappaB p65 (mean decrease in MFI 15.4%, p = 0.033) and Bcl-2 (mean decrease in MFI 7.2%, p = 0.005).
  • CONCLUSIONS: In vivo ATRA treatment in AML affects leukaemic cell morphology, regulation of cell cycle progression and apoptosis, and possibly also microvascular endothelial cell functions.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 18922099.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00175812
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases
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33. Schneider F, Bohlander SK, Schneider S, Papadaki C, Kakadyia P, Dufour A, Vempati S, Unterhalt M, Feuring-Buske M, Buske C, Braess J, Wandt H, Hiddemann W, Spiekermann K: AML1-ETO meets JAK2: clinical evidence for the two hit model of leukemogenesis from a myeloproliferative syndrome progressing to acute myeloid leukemia. Leukemia; 2007 Oct;21(10):2199-201
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  • [Title] AML1-ETO meets JAK2: clinical evidence for the two hit model of leukemogenesis from a myeloproliferative syndrome progressing to acute myeloid leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Leukemic. Janus Kinase 2 / physiology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Myeloproliferative Disorders / pathology. Proto-Oncogene Proteins / physiology. Transcription Factors / physiology
  • [MeSH-minor] Cytoplasm / metabolism. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Middle Aged. Models, Genetic. Mutation

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  • (PMID = 17625612.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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34. Malinge S, Izraeli S, Crispino JD: Insights into the manifestations, outcomes, and mechanisms of leukemogenesis in Down syndrome. Blood; 2009 Mar 19;113(12):2619-28
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  • Moreover, hematologists have also noted that these children commonly show macrocytosis, abnormal platelet counts, and an increased incidence of transient myeloproliferative disease (TMD), acute megakaryocytic leukemia (AMKL), and acute lymphoid leukemia (ALL).
  • In this review, we summarize the clinical manifestations and characteristics of these leukemias, provide an update on therapeutic strategies and patient outcomes, and discuss the most recent advances in DS-leukemia research.
  • With the increased knowledge of the way in which trisomy 21 affects hematopoiesis and the specific genetic mutations that are found in DS-associated leukemias, we are well on our way toward designing improved strategies for treating both myeloid and lymphoid malignancies in this high-risk population.

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  • [Cites] Nat Cell Biol. 2007 Mar;9(3):339-46 [17277770.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Br J Haematol. 2007 May;137(4):337-41 [17456055.001]
  • [Cites] Immunity. 2007 Apr;26(4):421-31 [17442597.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1584-7 [17443226.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1077-9 [17644747.001]
  • [Cites] Mamm Genome. 2007 Jul;18(6-7):431-43 [17653795.001]
  • [Cites] Blood. 2007 Sep 15;110(6):2128-31 [17576817.001]
  • [Cites] Bone Marrow Transplant. 2007 Nov;40(10):945-9 [17768387.001]
  • [Cites] Nature. 2008 Jan 3;451(7174):73-5 [18172498.001]
  • [Cites] Blood. 2008 Jan 15;111(2):767-75 [17901249.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1575-83 [17971484.001]
  • [Cites] Br J Haematol. 2008 Mar;140(5):552-61 [18275433.001]
  • [Cites] Blood. 2008 Mar 15;111(6):2991-8 [18182574.001]
  • [Cites] Leukemia. 2008 Mar;22(3):521-9 [18094719.001]
  • [Cites] J Exp Med. 2008 Mar 17;205(3):585-94 [18299402.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jun 6;370(3):473-7 [18387358.001]
  • [Cites] Br J Haematol. 2008 May;141(5):681-8 [18397343.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Nat Immunol. 2008 Jul;9(7):810-9 [18500345.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1428-30 [18059480.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):515-21 [18521927.001]
  • [Cites] Br J Haematol. 2008 Aug;142(4):610-5 [18510680.001]
  • [Cites] Br J Haematol. 2008 Sep;142(6):934-45 [18557744.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1484-92 [18805579.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4220-6 [18755984.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4507-11 [18689547.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4503-6 [18812473.001]
  • [Cites] Blood. 2009 Jan 15;113(3):646-8 [18927438.001]
  • [Cites] Blood. 2009 Feb 26;113(9):1929-37 [19109561.001]
  • [Cites] Leukemia. 1998 May;12(5):645-51 [9593260.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6256-61 [9600952.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1817-24 [10068652.001]
  • [Cites] Clin Immunol. 1999 Apr;91(1):50-60 [10219254.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):21-8 [15368546.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):8-12 [15390275.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):1-7 [15486953.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):226-31 [15687366.001]
  • [Cites] Eur J Hum Genet. 2009 Apr;17(4):454-66 [19002211.001]
  • [Cites] Genome Res. 1999 Dec;9(12):1214-22 [10613844.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jan 1;116(1):1-5 [10616523.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):512-24 [10997960.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2862-9 [11023523.001]
  • [Cites] Genet Med. 2001 Mar-Apr;3(2):91-101 [11280955.001]
  • [Cites] Arch Dis Child. 2001 Oct;85(4):321-5 [11567943.001]
  • [Cites] Blood. 2002 Jan 1;99(1):245-51 [11756178.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):429-36 [11905737.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2002 Jul 15;100(2):618-26 [12091356.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] Hum Mol Genet. 2003 Feb 1;12(3):247-55 [12554679.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):930-8 [12648061.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4298-300 [12560215.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4333-41 [12576332.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4301-4 [12586620.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2960-8 [12816863.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2250-2 [12931214.001]
  • [Cites] Gene. 2003 Oct 30;318:137-47 [14585506.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4211-9 [15156175.001]
  • [Cites] Br J Haematol. 2004 Jul;126(1):3-10 [15198727.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1588-9 [15317736.001]
  • [Cites] Science. 2004 Oct 22;306(5696):687-90 [15499018.001]
  • [Cites] Nat Rev Genet. 2004 Oct;5(10):725-38 [15510164.001]
  • [Cites] J Exp Med. 1985 Aug 1;162(2):695-712 [3160808.001]
  • [Cites] Dev Genet. 1991;12(6):415-22 [1688019.001]
  • [Cites] J Clin Oncol. 1993 Jul;11(7):1361-7 [8315434.001]
  • [Cites] Am J Med Genet. 1993 Jun 15;46(5):510-2 [8322810.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2865-8 [8187069.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 May 24;91(11):4997-5001 [8197171.001]
  • [Cites] Eur J Hum Genet. 1993;1(2):114-24 [8055322.001]
  • [Cites] Nat Genet. 1995 Oct;11(2):177-84 [7550346.001]
  • [Cites] Leuk Lymphoma. 1996 May;21(5-6):359-68 [9172800.001]
  • [Cites] Leukemia. 1997 Jun;11(6):820-1 [9177434.001]
  • [Cites] Genes Dev. 1998 May 1;12(9):1315-26 [9573048.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):797-804 [15755283.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4500-5 [15755806.001]
  • [Cites] Klin Padiatr. 2005 May-Jun;217(3):126-34 [15858703.001]
  • [Cites] Pediatr Hematol Oncol. 2005 Apr-May;22(3):229-34 [16020107.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1355-60 [15920490.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7596-602 [16140924.001]
  • [Cites] Science. 2005 Sep 23;309(5743):2033-7 [16179473.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4043-9 [16109782.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Br J Haematol. 2006 Mar;132(5):576-83 [16445830.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1570-81 [16249385.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [Cites] Br J Haematol. 2006 Jun;133(6):646-8 [16704441.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4606-13 [16469874.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):807-12 [16783379.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] Leuk Res. 2006 Sep;30(9):1085-9 [16533526.001]
  • [Cites] C R Biol. 2006 Sep;329(9):726-32 [16945839.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2198-206 [16757682.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4714-20 [16954520.001]
  • [Cites] Mamm Genome. 2006 Oct;17(10):1005-12 [17019652.001]
  • [Cites] Br J Haematol. 2006 Dec;135(5):595-602 [17054672.001]
  • [Cites] Curr Opin Pediatr. 2007 Feb;19(1):9-14 [17224656.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2202-4 [17068151.001]
  • [Cites] Leukemia. 2007 Mar;21(3):574-6 [17252020.001]
  • (PMID = 19139078.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 2R01CA101774; United States / NCI NIH HHS / CA / 1R01CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA101774-07; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / CA101774-07; United States / NCI NIH HHS / CA / R01 CA120772
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; EC 2.7.10.2 / Janus Kinases
  • [Number-of-references] 105
  • [Other-IDs] NLM/ PMC2661853
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35. Vigil CE, Martin-Santos T, Garcia-Manero G: Safety and efficacy of azacitidine in myelodysplastic syndromes. Drug Des Devel Ther; 2010;4:221-9
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  • SUMMARY: Azacitidine is the first drug FDA-approved for the treatment of myelodysplastic syndromes that has demonstrated improvements in overall survival and delaying time to progression to acute myelogenous leukemia.
  • [MeSH-minor] Disease Progression. Drug Administration Schedule. Humans. Leukemia, Myeloid, Acute / prevention & control. Survival

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  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Cancer. 2010 Aug 15;116(16):3830-4 [20564137.001]
  • [Cites] Blood. 2004 Jul 15;104(2):579-85 [15039286.001]
  • [Cites] Cancer Chemother Rep. 1973 Sep-Oct;57(3):319-23 [4127393.001]
  • [Cites] Cancer Chemother Rep. 1974 Mar-Apr;58(2):217-22 [4133839.001]
  • [Cites] Blood. 1976 Sep;48(3):331-7 [60156.001]
  • [Cites] Blood. 1981 Jan;57(1):182-5 [6160887.001]
  • [Cites] Cancer. 1981 Apr 1;47(7):1739-42 [6164472.001]
  • [Cites] Lancet. 1984 Oct 13;2(8407):867-8 [6207398.001]
  • [Cites] Cancer Treat Rep. 1987 Oct;71(10):959-64 [2443243.001]
  • [Cites] Am J Hematol. 1993 Aug;43(4):286-90 [7690519.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] J Immunother. 1999 Jan;22(1):16-24 [9924695.001]
  • [Cites] Nat Rev Drug Discov. 2005 Apr;4(4):275-6 [15861567.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3895-903 [16921040.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] J Exp Med. 2007 Jul 9;204(7):1543-51 [17591856.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1937-44 [17611569.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]
  • [Cites] Leukemia. 2008 Mar;22(3):538-43 [18079733.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jun 13;370(4):578-83 [18395517.001]
  • [Cites] Blood. 2008 Aug 15;112(4):981-9 [18495956.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1680-4 [18548103.001]
  • [Cites] Cancer. 2008 Oct 1;113(7):1596-604 [18720364.001]
  • [Cites] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772.001]
  • [Cites] J Clin Oncol. 2009 Apr 10;27(11):1850-6 [19255328.001]
  • [Cites] Cancer. 2009 May 1;115(9):1899-905 [19235255.001]
  • [Cites] Expert Rev Anticancer Ther. 2009 Jul;9(7):875-84 [19589026.001]
  • [Cites] Clin Cancer Res. 2009 Aug 1;15(15):5002-7 [19638460.001]
  • [Cites] Cancer. 2009 Dec 15;115(24):5746-51 [19795507.001]
  • [Cites] Blood. 2010 Jan 7;115(1):107-21 [19887673.001]
  • [Cites] Cancer. 2010 Mar 15;116(6):1485-94 [20151429.001]
  • [Cites] Eur J Haematol. 2010 Aug;85(2):130-8 [20394651.001]
  • [Cites] Haematologica. 2002 Dec;87(12):1324-41 [12495905.001]
  • (PMID = 20957213.001).
  • [ISSN] 1177-8881
  • [Journal-full-title] Drug design, development and therapy
  • [ISO-abbreviation] Drug Des Devel Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2948932
  • [Keywords] NOTNLM ; Azacitidine / MDS / hypomethylating agents
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36. Galbizo E, Williams LA: Chronic graft-versus-host disease. Oncol Nurs Forum; 2006 Sep;33(5):881-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Chronic Disease. Disease Progression. Humans. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Prognosis. Risk Factors. Stem Cell Transplantation. Tacrolimus / therapeutic use

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  • (PMID = 16986223.001).
  • [ISSN] 1538-0688
  • [Journal-full-title] Oncology nursing forum
  • [ISO-abbreviation] Oncol Nurs Forum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents; WM0HAQ4WNM / Tacrolimus
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37. Heilig CE, Löffler H, Mahlknecht U, Janssen JW, Ho AD, Jauch A, Krämer A: Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group. J Cell Mol Med; 2010 Apr;14(4):895-902
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  • As for aneuploidy itself, the role of CIN in the evolution and progression of malignancy is a matter still open to debate.
  • Thereby, CIN was measured in 65 patients with myelodysplastic syndromes (MDS), acute myeloid leukaemia (AML) and control subjects.
  • In conclusion, elevated CIN levels may be valuable as an early indicator of poor prognosis in MDS, hence corroborating the concept of CIN as a driving force in tumour progression.
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Risk Factors. Treatment Outcome. Tumor Cells, Cultured


38. Stentoft J, Hokland P, Ostergaard M, Hasle H, Nyvold CG: Minimal residual core binding factor AMLs by real time quantitative PCR--initial response to chemotherapy predicts event free survival and close monitoring of peripheral blood unravels the kinetics of relapse. Leuk Res; 2006 Apr;30(4):389-95
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  • Molecular progression rate in relapsing CBFbeta/MYH11 was surprisingly slow with a time lag to hematological relapse approaching 1 year.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Disease-Free Survival. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology. Polymerase Chain Reaction / methods

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  • [CommentIn] Leuk Res. 2006 Jun;30(6):657-8 [16386301.001]
  • (PMID = 16243396.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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39. Duval A, Olaru D, Campos L, Flandrin P, Nadal N, Guyotat D: Expression and prognostic significance of heat-shock proteins in myelodysplastic syndromes. Haematologica; 2006 May;91(5):713-4
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  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Apoptosis. Disease Progression. Female. Flow Cytometry. Gene Expression Regulation. Genes, bcl-2. Glycoproteins / biosynthesis. Glycoproteins / genetics. Hematopoiesis. Humans. Leukemia, Myeloid / epidemiology. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Severity of Illness Index. Survival Analysis. bcl-X Protein / biosynthesis. bcl-X Protein / genetics


40. Nand S, Godwin J, Smith S, Barton K, Michaelis L, Alkan S, Veerappan R, Rychlik K, Germano E, Stiff P: Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3 acute myeloid leukemia and high-risk myelodysplastic syndromes in the elderly: results from a pilot trial. Leuk Lymphoma; 2008 Nov;49(11):2141-7
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  • [Title] Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3 acute myeloid leukemia and high-risk myelodysplastic syndromes in the elderly: results from a pilot trial.
  • Elderly patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndromes (MDS) have a poor prognosis due to low response rates (26-46%) to standard chemotherapy and high treatment-related mortality (11-31%).
  • Overall toxicity was acceptable with only one (5%) early death due to disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


41. Melo JV, Barnes DJ: Chronic myeloid leukaemia as a model of disease evolution in human cancer. Nat Rev Cancer; 2007 Jun;7(6):441-53
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  • [Title] Chronic myeloid leukaemia as a model of disease evolution in human cancer.
  • Chronic myeloid leukaemia (CML) can be considered as a paradigm for neoplasias that evolve through a multi-step process.
  • If not cured at this stage, CML invariably progresses and transforms into an acute-type leukaemia undergoing a 'blast crisis'.
  • What mechanisms underlie this progression, and are they shared by other common cancers?
  • [MeSH-major] Blast Crisis. Disease Progression. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Models, Biological

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  • (PMID = 17522713.001).
  • [ISSN] 1474-175X
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 153
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42. Netinatsunthorn W, Hanprasertpong J, Dechsukhum C, Leetanaporn R, Geater A: WT1 gene expression as a prognostic marker in advanced serous epithelial ovarian carcinoma: an immunohistochemical study. BMC Cancer; 2006;6:90
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  • Recent studies have shown that WT1 plays an important role in the progression of disease and indicates a poorer prognosis of human malignancies such as acute myeloid leukemia and breast cancer.

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  • [Cites] Blood. 1997 Aug 1;90(3):1217-25 [9242555.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8132-7 [9223327.001]
  • [Cites] Cancer Lett. 1997 Dec 23;121(2):169-75 [9570355.001]
  • [Cites] Jpn J Cancer Res. 1999 Feb;90(2):194-204 [10189890.001]
  • [Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]
  • [Cites] Anticancer Res. 1999 May-Jun;19(3B):2387-9 [10472362.001]
  • [Cites] J Obstet Gynaecol Res. 2005 Jun;31(3):268-76 [15916666.001]
  • [Cites] Gynecol Oncol. 2006 Apr;101(1):12-7 [16263157.001]
  • [Cites] Int J Gynecol Pathol. 2003 Apr;22(2):168-74 [12649672.001]
  • [Cites] Br J Haematol. 2003 Oct;123(1):49-59 [14510942.001]
  • [Cites] Int J Gynecol Cancer. 2003 Nov-Dec;13(6):776-84 [14675314.001]
  • [Cites] FEBS Lett. 2004 Feb 27;560(1-3):183-91 [14988020.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2004 Jun;12(2):122-6 [15354736.001]
  • [Cites] Cancer. 1985 Dec 1;56(11):2727-32 [4052947.001]
  • [Cites] Nature. 1990 Jul 12;346(6280):194-7 [2164159.001]
  • [Cites] Mol Cell Biol. 1991 Mar;11(3):1707-12 [1671709.001]
  • [Cites] J Clin Oncol. 1991 Jul;9(7):1138-50 [1904477.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3071-9 [7949179.001]
  • [Cites] Genes Dev. 1995 Sep 1;9(17):2143-56 [7657166.001]
  • [Cites] EMBO J. 1996 Aug 15;15(16):4297-306 [8861958.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 1995 Dec;63(2):115-24 [8903765.001]
  • [Cites] Mol Cell Biol. 1996 Dec;16(12):6945-56 [8943350.001]
  • [Cites] J Biol Chem. 1997 Jan 31;272(5):2901-13 [9006935.001]
  • [Cites] Oncogene. 1997 Jun 5;14(22):2689-700 [9178767.001]
  • [Cites] Gynecol Oncol. 2000 Mar;76(3):369-72 [10684712.001]
  • [Cites] Int J Gynecol Pathol. 2000 Apr;19(2):158-63 [10782413.001]
  • [Cites] Clin Cancer Res. 2000 Nov;6(11):4265-71 [11106242.001]
  • [Cites] Am J Clin Pathol. 2001 Aug;116(2):246-52 [11488072.001]
  • [Cites] Gene. 2001 Aug 8;273(2):141-61 [11595161.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):1167-71 [12006533.001]
  • [Cites] J Biol Chem. 1997 Dec 5;272(49):30678-87 [9388203.001]
  • (PMID = 16606472.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC1479357
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43. Manzoli L, Martelli AM, Billi AM, Faenza I, Fiume R, Cocco L: Nuclear phospholipase C: involvement in signal transduction. Prog Lipid Res; 2005 Jul;44(4):185-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The recent discovery of a possible involvement of the deletion of PI-PLCbeta1 gene in the progression of myelodysplastic syndrome (MDS) to acute myeloid leukemia (AML) in humans strengthens the contention that nuclear PI-PLC signaling is essential for physiological processes such as cell growth and differentiation.


44. Gyan E, Foussard C, Bertrand P, Michenet P, Le Gouill S, Berthou C, Maisonneuve H, Delwail V, Gressin R, Quittet P, Vilque JP, Desablens B, Jaubert J, Ramée JF, Arakelyan N, Thyss A, Moluçon-Chabrot C, Delépine R, Milpied N, Colombat P, Deconinck E, Groupe Ouest-Est des Leucémies et des Autres Maladies du Sang (GOELAMS): High-dose therapy followed by autologous purged stem cell transplantation and doxorubicin-based chemotherapy in patients with advanced follicular lymphoma: a randomized multicenter study by the GOELAMS with final results after a median follow-up of 9 years. Blood; 2009 Jan 29;113(5):995-1001
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  • The 9-year progression-free survival (PFS) was higher in the ASCT than the chemotherapy group (64% vs 39%; P = .004).
  • Secondary malignancies were more frequent in the HDT than in the chemotherapy group (6 secondary myelodysplastic syndrome/acute myeloid leukemia and 6 second solid tumor cancers vs 1 acute myeloid leukemia, P = .01).

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  • (PMID = 18955565.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00696735
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists; 8N3DW7272P / Cyclophosphamide
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45. Follo MY, Finelli C, Clissa C, Mongiorgi S, Bosi C, Martinelli G, Baccarani M, Manzoli L, Martelli AM, Cocco L: Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia. J Clin Oncol; 2009 Feb 10;27(5):782-90
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  • [Title] Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia.
  • Kaplan-Meier analysis revealed a significant association (P < .0001) between the PI-PLCbeta1 mono-allelic deletion and a higher risk of evolution into acute myeloid leukemia (AML), since 23 of 35 MDS patients (65.7%) bearing the PI-PLCbeta1 mono-allelic deletion evolved into AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / genetics. Phospholipase C beta / genetics. Phospholipase C gamma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Deletion. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction


46. Mehta PA, Harris RE, Davies SM, Kim MO, Mueller R, Lampkin B, Mo J, Myers K, Smolarek TA: Numerical chromosomal changes and risk of development of myelodysplastic syndrome--acute myeloid leukemia in patients with Fanconi anemia. Cancer Genet Cytogenet; 2010 Dec;203(2):180-6
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  • [Title] Numerical chromosomal changes and risk of development of myelodysplastic syndrome--acute myeloid leukemia in patients with Fanconi anemia.
  • Fanconi Anemia (FA) is an inherited bone marrow failure syndrome characterized by congenital abnormalities, progressive marrow failure and predisposition to myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and solid tumors.
  • A few reports also suggest that gains of 3q are associated with progression to MDS-AML and overall poor prognosis.
  • In conclusion, children with FA should be followed closely with FISH analyses, because some of the clonal chromosomal abnormalities may be early indicators of progression toward MDS-AML and thus also of the need for hematopoietic stem cell transplantation.
  • [MeSH-major] Chromosome Deletion. Chromosome Mapping. Fanconi Anemia / complications. Fanconi Anemia / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / genetics


47. Shen M, Yen A: Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells. Oncology; 2009;76(2):91-100
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  • [Title] Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells.
  • Nicotinamide, the amide derivative of vitamin B(3), cooperates with retinoic acid (RA), a form of vitamin A, and 1,25-dihydroxyvitamin D(3) (D3), to regulate cell differentiation and proliferation of human myeloblastic leukemia cells.
  • In human myeloblastic leukemia cells, RA or D3 are known to cause MAPK signaling leading to myeloid or monocytic differentiation and G0 cell cycle arrest.
  • Nicotinamide thus regulated RA- or D3-induced differentiation and G0 arrest, causing a transient delay in certain early aspects of the progression to terminal differentiation but ultimately accelerating the occurrence of terminally, functionally differentiated G0 cells.
  • [MeSH-major] Calcitriol / metabolism. Leukemia, Myelomonocytic, Acute / drug therapy. Niacinamide / administration & dosage. Tretinoin / administration & dosage

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  • [Cites] Exp Cell Res. 1987 Jan;168(1):247-54 [3023118.001]
  • [Cites] Blood. 1983 Oct;62(4):709-21 [6192859.001]
  • [Cites] Diabetologia. 1989 May;32(5):316-21 [2526769.001]
  • [Cites] Science. 1990 Sep 21;249(4975):1429-31 [2402637.001]
  • [Cites] Science. 1993 Nov 12;262(5136):1056-9 [8235624.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Nov 15;196(3):1459-65 [8250903.001]
  • [Cites] Prog Clin Biol Res. 1995;392:369-73 [8524944.001]
  • [Cites] Blood. 1996 Jan 1;87(1):227-37 [8547646.001]
  • [Cites] Immunogenetics. 1996;45(1):35-43 [8881035.001]
  • [Cites] FEBS Lett. 1997 Aug 11;413(1):99-103 [9287124.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):3163-72 [9679985.001]
  • [Cites] Biosci Biotechnol Biochem. 1998 Dec;62(12):2351-6 [9972261.001]
  • [Cites] Immunogenetics. 1999 Jul;49(7-8):597-604 [10369916.001]
  • [Cites] Mol Cell. 2005 Apr 1;18(1):83-96 [15808511.001]
  • [Cites] J Cell Physiol. 2005 Sep;204(3):964-74 [15799027.001]
  • [Cites] Horm Metab Res. 2006 Jan;38(1):12-5 [16477534.001]
  • [Cites] J Cell Biochem. 2006 Apr 15;97(6):1328-38 [16329108.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982.001]
  • [Cites] Autoimmunity. 2006 Jun;39(4):333-40 [16891222.001]
  • [Cites] Biochem Pharmacol. 2007 Mar 15;73(6):831-42 [17188249.001]
  • [Cites] Ann N Y Acad Sci. 2006 Dec;1091:356-67 [17341628.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):334-41 [17380201.001]
  • [Cites] Eur Respir J. 2007 Aug;30(2):199-204 [17504797.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8624-32 [17875702.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):4375-86 [18006504.001]
  • [Cites] Diabetologia. 2000 Nov;43(11):1337-45 [11126400.001]
  • [Cites] J Virol. 2001 Jun;75(11):5302-14 [11333911.001]
  • [Cites] J Biol Chem. 2002 Jan 4;277(1):13-22 [11689561.001]
  • [Cites] Exp Biol Med (Maywood). 2002 Oct;227(9):753-62 [12324654.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49453-8 [12386160.001]
  • [Cites] Clin Exp Immunol. 2003 Jan;131(1):48-52 [12519385.001]
  • [Cites] Curr Med Chem. 2003 Feb;10(4):321-40 [12570705.001]
  • [Cites] Biosci Biotechnol Biochem. 2003 May;67(5):1132-5 [12834294.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2146-55 [12763926.001]
  • [Cites] Transplant Proc. 2003 Aug;35(5):2021-3 [12962883.001]
  • [Cites] Proc Soc Exp Biol Med. 1969 Mar;130(3):992-4 [4304354.001]
  • [Cites] Leuk Res. 1987;11(2):191-6 [3469486.001]
  • (PMID = 19127080.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD14; 25X51I8RD4 / Niacinamide; 5688UTC01R / Tretinoin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.2.2.5 / Antigens, CD38; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2826433
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48. Scrideli CA, de Oliveira FM, Brassesco MS, de Paula Queiroz R, Bernardes JE, Valera ET, Tone LG: Is p190 bcr-abl rearrangement necessary for acute transformation in some p210 CML of childhood? Leuk Res; 2009 Mar;33(3):495-9
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  • [Title] Is p190 bcr-abl rearrangement necessary for acute transformation in some p210 CML of childhood?
  • Chronic myeloid leukemia (CML) is a rare disease in childhood which is almost exclusively associated with bcr-abl p210 (M-bcr) rearrangements.
  • It has been suggested that co-expression of p190 and p210 may be a pathway of CML progression in adult patients.
  • We report two cases of pediatric patients with a diagnosis of CML who presented co-expression of the p210 and p190 transcripts during progression to the blastic phase.
  • The present data suggest that p190 may be a secondary event in at least some cases of childhood CML, suggesting an association with progression to a blastic crisis in these patients.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Fusion Proteins, bcr-abl / genetics. Gene Rearrangement. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Blast Crisis. Child, Preschool. Disease Progression. Female. Humans. Male. RNA, Neoplasm / analysis

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  • (PMID = 18495245.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Neoplasm; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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49. Raanani P, Shpilberg O, Ben-Bassat I: Extramedullary disease and targeted therapies for hematological malignancies--is the association real? Ann Oncol; 2007 Jan;18(1):7-12
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  • Extramedullary involvement is a rare manifestation of acute and chronic leukemias and of multiple myeloma.
  • We reviewed the reports on this phenomenon in patients treated with all-trans-retinoic acid and arsenic trioxide for acute promyelocytic leukemia, thalidomide and bortezomib for multiple myeloma and imatinib for chronic myeloid leukemia.
  • The pathogenetic mechanisms suggested are: life prolongation by these treatments allowing for disease progression arising from dormant cells; poor penetration of the drugs to sanctuary sites like the central nervous system; the requirement of some of these drugs, especially thalidomide, for the marrow microenvironment to exert their action; and finally, a possible active role for some of the drugs, like all-trans-retinoic acid.

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  • (PMID = 16790518.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 62
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50. Barbui T, Finazzi G: Evidence-based management of polycythemia vera. Best Pract Res Clin Haematol; 2006;19(3):483-93
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  • The clinical course of polycythemia vera is marked by significant thrombotic complications and a variable risk of the disease turning either into myeloid metaplasia with myelofibrosis or into acute myeloid leukemia.
  • However, there is concern that certain myelosuppressive drugs accelerate the disease progression to acute leukemia.
  • Thus, the objective of management is two-fold: first, to minimize the risk of thrombotic complications; second, to prevent progression to myelofibrotic or leukemic transformation.
  • This chapter provides updated estimates of the risk of thrombosis and disease progression and evaluates the various randomized and observational studies in polycythemia vera, according to an evidence-based approach.

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  • (PMID = 16781485.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Platelet Aggregation Inhibitors; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 27
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51. Xu JH, Wang T, Wang XG, Wu XP, Zhao ZZ, Zhu CG, Qiu HL, Xue L, Shao HJ, Guo MX, Li WX: PU.1 can regulate the ZNF300 promoter in APL-derived promyelocytes HL-60. Leuk Res; 2010 Dec;34(12):1636-46
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  • Our data showed that expression of ZNF300 changed significantly in various leukemia blasts in the bone marrow aspirates of newly diagnosed leukemia patients.
  • To investigate the potential relationship between expression of ZNF300 and the progression of leukemia development and hematopoietic differentiation, we cloned and characterized the putative human ZNF300 gene promoter and identified its transcription start sites (TSSs).
  • Deletion and mutagenesis analysis demonstrated that a myeloid-specific transcription factor PU.1 binding site was responsible for myeloid-specific regulation of ZNF300 promoter activity.
  • Overexpression of PU.1 elevated ZNF300 promoter activity, whereas silencing of PU.1 expression significantly reduced the activity in myeloid-derived HL-60 cell but not in T-cell Jurkat.
  • These results demonstrated that ZNF300 was activated by PU.1 and suggested that the regulation may be involved in the progression of leukemia development and hematopoietic differentiation.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Promyelocytic, Acute / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / biosynthesis. Response Elements. Trans-Activators / metabolism. Up-Regulation

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20471086.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Cryoprotective Agents; 0 / ITGAM protein, human; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / ZNF300 protein, human; 0 / proto-oncogene protein Spi-1; YOW8V9698H / Dimethyl Sulfoxide
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52. Kalff A, Shortt J, Farr J, McLennan R, Lui A, Scott J, Spencer A: Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia. Haematologica; 2008 Jan;93(1):e16-7
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  • [Title] Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Tumor Lysis Syndrome / etiology
  • [MeSH-minor] Disease Progression. Electrolytes / metabolism. Fatal Outcome. Humans. Indoles. Male. Middle Aged

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  • (PMID = 18166770.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Electrolytes; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Indoles; 9647FM7Y3Z / panobinostat
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53. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 8. Clone Cells. Disease Progression. Humans. Male. Mutation. Neoplasms, Second Primary. Trisomy

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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54. Falini B, Tiacci E, Martelli MP, Ascani S, Pileri SA: New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues. Discov Med; 2010 Oct;10(53):281-92
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  • [Title] New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues.
  • Here, we focus on changes that, as compared to the 2001 edition, were introduced into the 2008 WHO classification of acute myeloid leukemia (AML) and related precursor neoplasms.
  • Finally, we describe the unique characteristics of myeloid proliferations associated with Down syndrome and blastic plasmacytoid dendritic cell neoplasm.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / pathology. Lymphoproliferative Disorders / classification. Lymphoproliferative Disorders / pathology. Medical Oncology / trends. Neoplasms / classification. Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Down Syndrome / complications. Down Syndrome / pathology. Humans. Precancerous Conditions / classification. Precancerous Conditions / genetics. Precancerous Conditions / pathology. World Health Organization

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  • (PMID = 21034669.001).
  • [ISSN] 1944-7930
  • [Journal-full-title] Discovery medicine
  • [ISO-abbreviation] Discov Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
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55. Milligan DW, Fernandes S, Dasgupta R, Davies FE, Matutes E, Fegan CD, McConkey C, Child JA, Cunningham D, Morgan GJ, Catovsky D, National Cancer Research Institute Haematological Studies Group: Results of the MRC pilot study show autografting for younger patients with chronic lymphocytic leukemia is safe and achieves a high percentage of molecular responses. Blood; 2005 Jan 01;105(1):397-404
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  • [Title] Results of the MRC pilot study show autografting for younger patients with chronic lymphocytic leukemia is safe and achieves a high percentage of molecular responses.
  • We have assessed autologous stem cell transplantation after treatment with fludarabine in previously untreated patients with chronic lymphocytic leukemia (CLL).
  • It is of concern that 5 of 65 (8%) patients developed posttransplant acute myeloid leukemia/myelodysplastic syndrome.
  • [MeSH-major] Aging / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Transplantation, Autologous / immunology
  • [MeSH-minor] Adult. Disease Progression. Female. Follow-Up Studies. Hematopoietic Stem Cell Mobilization. Humans. Male. Middle Aged. Myelodysplastic Syndromes / complications. Neoplasm, Residual / pathology. Pilot Projects. Survival Rate

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  • (PMID = 15117764.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0001160
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
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56. Antonsson A, Persson JL: Induction of apoptosis by staurosporine involves the inhibition of expression of the major cell cycle proteins at the G(2)/m checkpoint accompanied by alterations in Erk and Akt kinase activities. Anticancer Res; 2009 Aug;29(8):2893-8
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  • Our previous studies in clinical settings have suggested that certain subpopulations of patients with acute myeloid leukemia (AML) had poor response to chemotherapy.
  • We also show that the effects of stauroporine on cell cycle progression and apoptosis in U-937 cells are closely linked.

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  • (PMID = 19661292.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; H88EPA0A3N / Staurosporine
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57. Wallen H, Gooley TA, Deeg HJ, Pagel JM, Press OW, Appelbaum FR, Storb R, Gopal AK: Ablative allogeneic hematopoietic cell transplantation in adults 60 years of age and older. J Clin Oncol; 2005 May 20;23(15):3439-46
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  • Diagnoses included myelodysplastic syndrome (MDS; n = 35), chronic myeloid leukemia (CML; n = 8), acute myeloid leukemia (AML; n = 6), and other (n = 3).
  • Median overall survival (OS) and progression-free survival were 300 and 218 days, respectively.
  • Grade 3 to 4 acute graft-versus-host disease (GVHD) occurred in 20% of patients, and chronic extensive GVHD was described in 53% of patients.

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  • (PMID = 15824415.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA78902; United States / NHLBI NIH HHS / HL / HL 36444; United States / NCI NIH HHS / CA / T32 CA009515-20; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / T32 CA009515; United States / NCI NIH HHS / CA / P01 CA1802; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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
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58. Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H: Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis. Cancer Genomics Proteomics; 2010 Jul-Aug;7(4):173-80
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  • We analyzed 70 bone marrow (BM) samples from acute myeloid leukemia (AML) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
  • Patients with more than 10% NG2(+) cells showed a tendency to have a shorter progression-free survival (mean: 7 months) than patients with fewer than 10% NG2(+) cells (mean survival: 17 months; p=0.08).
  • [MeSH-major] Antigens / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Proteoglycans / analysis

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  • (PMID = 20656983.001).
  • [ISSN] 1790-6245
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
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59. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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  • [Title] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • Compared with animals transplanted with only CBFbeta-SMMHC-expressing cells, FLT3-ITD further restricted early myeloid differentiation and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.
  • FLT3-ITD also accelerated disease progression in all CBFbeta-SMMHC/FLT3-ITD-reconstituted animals, which died of a highly aggressive and transplantable AML within 3 to 5 months.
  • [MeSH-major] Chromosome Inversion / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Oncogene Proteins, Fusion / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Animals. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Disease Progression. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Lymphopoiesis. Mice. Mutation / genetics. Myelopoiesis. Smooth Muscle Myosins / genetics. Smooth Muscle Myosins / metabolism. Survival Rate

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  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Cancer Cell. 2006 Jan;9(1):57-68 [16413472.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12822-7 [10536006.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2232-5 [11956074.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Nat Struct Biol. 2002 Sep;9(9):674-9 [12172539.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4154-61 [12393674.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):607-19 [12509458.001]
  • [Cites] Curr Opin Genet Dev. 2003 Feb;13(1):48-54 [12573435.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4342-6 [12560221.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 27;94(11):5697-702 [9159135.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11863-8 [9751756.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7432-43 [9819429.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7 Suppl):1789s-1793s [10197598.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] Br J Haematol. 2005 Jan;128(1):18-34 [15606546.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):523-38 [12899708.001]
  • [Cites] Haematologica. 2004 Jan;89(1):106 [14754614.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4924-9 [15044690.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3200-7 [15070703.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4297-307 [15156186.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1213-25 [1827140.001]
  • [Cites] Virology. 1993 May;194(1):314-31 [8386878.001]
  • [Cites] Mol Cell Biol. 1993 Jun;13(6):3324-39 [8497254.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Blood. 1995 May 1;85(9):2289-302 [7727763.001]
  • [Cites] J Exp Med. 1996 Jan 1;183(1):187-94 [8551222.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1630-5 [8643682.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12359-63 [8901586.001]
  • [Cites] Cell. 1996 Nov 15;87(4):687-96 [8929537.001]
  • [Cites] J Biol Chem. 2005 Dec 2;280(48):40097-103 [16199529.001]
  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
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60. Eklund EA, Platanias LC: Screening for microRNAs in myelodysplastic syndromes. Leuk Lymphoma; 2009 Nov;50(11):1735-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Acute Disease. Bone Marrow / metabolism. Bone Marrow / pathology. Disease Progression. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • [CommentOn] Leuk Lymphoma. 2009 Nov;50(11):1854-9 [19883312.001]
  • (PMID = 19883302.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / BLRD VA / BX / I01 BX002067; United States / NCI NIH HHS / CA / R01 CA195642
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN15 microRNA, human; 0 / MIRN16 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
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61. Jankowska AM, Szpurka H, Tiu RV, Makishima H, Afable M, Huh J, O'Keefe CL, Ganetzky R, McDevitt MA, Maciejewski JP: Loss of heterozygosity 4q24 and TET2 mutations associated with myelodysplastic/myeloproliferative neoplasms. Blood; 2009 Jun 18;113(25):6403-10
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  • Chromosomal abnormalities are frequent in myeloid malignancies, but in most cases of myelodysplasia (MDS) and myeloproliferative neoplasms (MPN), underlying pathogenic molecular lesions are unknown.
  • We identified recurrent areas of somatic copy number-neutral loss of heterozygosity (LOH) and deletions of chromosome 4q24 in a large cohort of patients with myeloid malignancies including MDS and related mixed MDS/MPN syndromes using single nucleotide polymorphism arrays.
  • The frequency of mutations in this candidate myeloid regulatory gene suggests an important role in the pathogenesis of poor prognosis MDS/MPN and sAML and may act as a disease gene marker for these often cytogenetically normal disorders.

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  • [Cites] Bioessays. 2000 May;22(5):452-9 [10797485.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1315-25 [18832655.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):187-200 [12542475.001]
  • [Cites] Leukemia. 2003 Mar;17(3):637-41 [12646957.001]
  • [Cites] Int J Oncol. 2004 Oct;25(4):1193-9 [15375572.001]
  • [Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1411-5 [15920487.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2355-8 [16239911.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1648-57 [17554386.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2382-4 [17554374.001]
  • [Cites] PLoS One. 2007;2(11):e1225 [18030353.001]
  • [Cites] PLoS Comput Biol. 2007 Nov;3(11):e244 [18052545.001]
  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] Leukemia. 2009 May;23(5):905-11 [19262601.001]
  • [Cites] Blood. 2009 Jul 2;114(1):144-7 [19420352.001]
  • [Cites] Leukemia. 2008 Jan;22(1):14-22 [17882280.001]
  • [Cites] Nature. 2008 Jan 17;451(7176):335-9 [18202658.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Blood. 2008 Aug 15;112(4):965-74 [18505780.001]
  • [Cites] Exp Hematol. 2008 Nov;36(11):1480-6 [18723264.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Exp Hematol. 2002 Mar;30(3):229-36 [11882360.001]
  • (PMID = 19372255.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC2710933
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62. Jädersten M, Hellström-Lindberg E: Myelodysplastic syndromes: biology and treatment. J Intern Med; 2009 Mar;265(3):307-28
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  • This review focuses on low-risk MDS, for which chronic anaemia and eventual progression to acute myeloid leukaemia are the main concerns.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Blood Transfusion. Chromosomes, Human, Pair 5 / genetics. Disease Progression. Erythropoietin / therapeutic use. Female. Humans. Immunosuppressive Agents / therapeutic use. Iron Chelating Agents / therapeutic use. Male. Recombinant Proteins. Sequence Deletion. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. World Health Organization


63. Sallmyr A, Fan J, Rassool FV: Genomic instability in myeloid malignancies: increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair. Cancer Lett; 2008 Oct 18;270(1):1-9
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  • [Title] Genomic instability in myeloid malignancies: increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair.
  • Disease progression in myeloid malignancies results from the accumulation of "mutations" in genes that control cellular growth and differentiation.
  • Many types of genetic alterations have been identified in myeloid diseases.
  • Increasing evidence suggests that the genetic changes in myeloid malignancies lead to increased production of endogenous sources of DNA damage, such as, reactive oxygen species (ROS).
  • The fusion gene BCR-ABL in chronic myeloid leukemia (CML), FLT3/ITD in acute myeloid leukemia (AML), and RAS mutations in myelodysplastic syndromes (MDS)/myeloproliferative diseases (MPD) result in ROS production.
  • This article will review evidence for activation of RAS/PI3K/STAT pathways, that lead to increased ROS, DNA damage and defective repair in myeloid diseases, a mechanism for acquisition of additional mutations that can drive disease progression.
  • [MeSH-major] DNA Breaks, Double-Stranded. DNA Repair. Genomic Instability. Leukemia, Myeloid / genetics. Reactive Oxygen Species / metabolism

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  • (PMID = 18467025.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / STAT Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 61
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64. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN: Clinico-hematological profile in biphenotypic acute leukemia. Indian J Cancer; 2009 Apr-Jun;46(2):160-8
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  • [Title] Clinico-hematological profile in biphenotypic acute leukemia.
  • BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).
  • We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.
  • B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.
  • Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).
  • BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.
  • [MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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  • (PMID = 19346652.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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65. Wong KF, Wong WS, Siu LL, Lau TC: JAK2 V617F mutation in myeloid neoplasms with 3q21 and 3q26 abnormalities in Chinese patients. Leuk Lymphoma; 2009 Aug;50(8):1386-8
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  • [Title] JAK2 V617F mutation in myeloid neoplasms with 3q21 and 3q26 abnormalities in Chinese patients.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 3 / ultrastructure. Janus Kinase 2 / genetics. Leukemia, Myeloid / genetics. Mutation, Missense. Myelodysplastic Syndromes / genetics. Point Mutation. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Anemia, Refractory, with Excess of Blasts / genetics. Chromosomes, Human, Pair 7. Disease Progression. Female. Hong Kong / epidemiology. Humans. Male. Middle Aged. Monosomy. Syndrome. Thrombocytosis / etiology

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  • (PMID = 19562620.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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66. Li JM, Shen Y, Wu DP, Liang H, Jin J, Chen FY, Song YP, Song EY, Qiu XF, Hou M, Qiu ZC, Shen ZX: Aclarubicin and low-dose Cytosine arabinoside in combination with granulocyte colony-stimulating factor in treating acute myeloid leukemia patients with relapsed or refractory disease and myelodysplastic syndrome: a multicenter study of 112 Chinese patients. Int J Hematol; 2005 Jul;82(1):48-54
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  • [Title] Aclarubicin and low-dose Cytosine arabinoside in combination with granulocyte colony-stimulating factor in treating acute myeloid leukemia patients with relapsed or refractory disease and myelodysplastic syndrome: a multicenter study of 112 Chinese patients.
  • One hundred twelve patients with geriatric acute myeloid leukemia (AML), refractory or relapsed AML, or myelodysplastic syndrome and refractory anemia with excess of blasts in transformation (MDS-RAEBt) were entered into this study to receive CAG (aclarubicin and low-dose cytosine arabinoside [Ara-C]in combination with granulocyte colony-stimulating factor [G-CSF]) with the objective of evaluating the efficacy and tolerance of this regimen.
  • Of the 52 patients followed up, the 12-month progression-free survival (PFS) and overall survival (OS) rates estimated by the Kaplan-Meier method were 40.73% 3 8.15% and 42.85% 3 8.23%, respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Aclarubicin / administration & dosage. Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Dose-Response Relationship, Drug. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Injections, Subcutaneous. Male. Middle Aged. Neutropenia / chemically induced. Survival Analysis. Thrombocytopenia / chemically induced. Treatment Outcome


67. Jabbour E, Cortes J, Kantarjian H, Giralt S, Andersson BS, Giles F, Shpall E, Kebriaei P, Champlin R, de Lima M: Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity. Cancer; 2007 Jul 15;110(2):340-4
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  • [Title] Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity.
  • BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for chronic myeloid leukemia (CML) are increasingly likely to have received a novel tyrosine kinase inhibitor (NTKI) after failing imatinib mesylate.
  • Acute and chronic graft-versus-host disease (GVHD) was observed in 7 and 6 patients, respectively.
  • Three patients had disease progression by Day 30 after HSCT.
  • After a median follow-up of 10 months, 7 patients were alive in molecular response and 5 patients had died, 4 of disease progression and 1 of extensive chronic GVHD.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


68. Rosenberg PS, Alter BP, Ebell W: Cancer risks in Fanconi anemia: findings from the German Fanconi Anemia Registry. Haematologica; 2008 Apr;93(4):511-7
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  • BACKGROUND: Fanconi anemia is an inherited genomic instability syndrome associated with progressive bone marrow failure leading to death or the requirement for hematopoietic stem cell transplantation, acute myeloid leukemia, and solid tumors.
  • Prior epidemiological studies have quantified the risks of bone marrow failure, acute myeloid leukemia and solid tumors, but these estimates have not been replicated.
  • We calculated the ratio of observed to expected cancers, and the risks of bone marrow failure, acute myeloid leukemia, and solid tumors by age.
  • RESULTS: The first adverse event was bone marrow failure in 66 patients, acute meyloid leukemia in 14 patients and solid tumors in 10 patients.
  • The ratio of observed to expected cancers was 44 for all cancers, 26 for all solid tumors, and 868 for acute myeloid leukemia; these increased risks were statistically significant.
  • CONCLUSIONS: Findings from the German Fanconi Anemia Registry cohort validate prior risk estimates, and strongly support the concept that Fanconi anemia is a highly penetrant cancer susceptibility syndrome with early onset of acute myeloid leukemia and slightly later onset of specific solid tumors.
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Diseases / epidemiology. Bone Marrow Diseases / genetics. Child. Child, Preschool. Cohort Studies. Disease Progression. Fanconi Anemia Complementation Group Proteins / genetics. Fanconi Anemia Complementation Group Proteins / physiology. Female. Germany / epidemiology. Hematopoietic Stem Cell Transplantation / statistics & numerical data. Humans. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Neoplasms / epidemiology. Neoplasms / genetics. Penetrance. Postoperative Complications / mortality. Radius / abnormalities. Registries / statistics & numerical data. Risk

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  • [CommentIn] Haematologica. 2008 Apr;93(4):486-8 [18379006.001]
  • (PMID = 18322251.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Fanconi Anemia Complementation Group Proteins
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69. Lu C, Hassan HT: Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells. Leuk Res; 2006 Mar;30(3):296-302
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  • [Title] Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells.
  • Acute myeloid leukaemia (AML) is a heterogenous malignant disease with diverse biological features in which disease progression at the level of CD34+ cells has a major impact on the resistance to chemotherapy and relapse.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD34. Antineoplastic Agents / pharmacology. Biomarkers, Tumor. Cytarabine / pharmacology. Daunorubicin / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Stem Cell Factor / antagonists & inhibitors

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  • (PMID = 16112192.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; 0 / Receptors, Cytokine; 0 / Stem Cell Factor; 0 / bcl-2-Associated X Protein; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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70. Ryningen A, Wergeland L, Glenjen N, Gjertsen BT, Bruserud O: In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8. Leuk Res; 2005 Feb;29(2):185-96
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  • [Title] In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8.
  • Interactions between native human acute myelogenous leukemia (AML) blasts and nonleukemic cells in the bone marrow microenvironment seem important both for disease development chemosensitivity.
  • [MeSH-major] Cell Communication. Cytokines / physiology. Fibroblasts / physiology. Interleukin-8 / biosynthesis. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / physiology. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Disease Progression. Female. Humans. Male. Middle Aged. Signal Transduction. Stromal Cells / physiology

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  • (PMID = 15607368.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-8
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71. Wang J, Rao Q, Wang M, Wei H, Xing H, Liu H, Wang Y, Tang K, Peng L, Tian Z, Wang J: Overexpression of Rac1 in leukemia patients and its role in leukemia cell migration and growth. Biochem Biophys Res Commun; 2009 Sep 4;386(4):769-74
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  • [Title] Overexpression of Rac1 in leukemia patients and its role in leukemia cell migration and growth.
  • In this study, we analyze the expression of Rac1 protein in leukemia patients and determine its role in the abnormal behaviours of leukemic cells.
  • Rac1 protein is overexpressed in primary acute myeloid leukemia cells as compared to normal bone marrow mononuclear cells. siRNA-mediated silencing of Rac1 in leukemia cell lines induced inhibition of cell migration, proliferation, and colony formation.
  • We conclude that overexpression of Rac1 contributes to the accelerated migration and high proliferation potential of leukemia cells, which could be implicated in leukemia development and progression.
  • [MeSH-major] Cell Movement. Leukemia / pathology. rac1 GTP-Binding Protein / physiology

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  • (PMID = 19563775.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / NSC 23766; 0 / Pyrimidines; 0 / RNA, Small Interfering; EC 3.6.5.2 / rac1 GTP-Binding Protein
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72. Nicolini FE, Mauro MJ, Martinelli G, Kim DW, Soverini S, Müller MC, Hochhaus A, Cortes J, Chuah C, Dufva IH, Apperley JF, Yagasaki F, Pearson JD, Peter S, Sanz Rodriguez C, Preudhomme C, Giles F, Goldman JM, Zhou W: Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation. Blood; 2009 Dec 17;114(26):5271-8
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  • [Title] Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation.
  • The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome-positive (Ph)(+) acute lymphoblastic leukemia (ALL) patients with T315I mutation.
  • Median overall survival from T315I mutation detection was 22.4, 28.4, 4.0, and 4.9 months, and median progression-free survival was 11.5, 22.2, 1.8, and 2.5 months, respectively, for CP, AP, BP, and Ph(+) ALL patients.
  • [MeSH-major] Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality


73. Nishio S, Sugiyama T, Shouji T, Yoshizaki A, Kitagawa R, Ushijima K, Kamura T: Pilot study evaluating the efficacy and toxicity of irinotecan plus oral etoposide for platinum- and taxane-resistant epithelial ovarian cancer. Gynecol Oncol; 2007 Aug;106(2):342-7
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  • Treatment cycles were repeated until disease progression or unacceptable toxicity.
  • Acute myeloid leukemia (M5) developed as a secondary malignancy in 1 patient.

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  • (PMID = 17499346.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bridged Compounds; 0 / Organoplatinum Compounds; 0 / Taxoids; 1605-68-1 / taxane; 6PLQ3CP4P3 / Etoposide; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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74. Link BK, Martin P, Kaminski MS, Goldsmith SJ, Coleman M, Leonard JP: Cyclophosphamide, vincristine, and prednisone followed by tositumomab and iodine-131-tositumomab in patients with untreated low-grade follicular lymphoma: eight-year follow-up of a multicenter phase II study. J Clin Oncol; 2010 Jun 20;28(18):3035-41
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  • Five-year progression-free and overall survival rates were 56% and 83%, respectively.
  • Two patients developed myelodysplastic syndrome/acute myeloid leukemia.

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  • (PMID = 20458031.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / iodine-131 anti-B1 antibody; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
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75. Nowicki M, Ostalska-Nowicka D, Miśkowiak B: Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia. Folia Histochem Cytobiol; 2006;44(1):49-52
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  • [Title] Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia.
  • The aim of this study was to demonstrate the value of immunocytochemical staining of Ki67 antigen expression in blast cells of children with acute myeloid leukemia (AML) and to evaluate its correlation with treatment failure.

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  • (PMID = 16584092.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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76. Wang Y, Lin FR, Ren JH, Zhang JN, Chen J: [The expression and clinical significance of survivin gene in leukemia]. Zhonghua Nei Ke Za Zhi; 2006 Aug;45(8):628-30
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  • [Title] [The expression and clinical significance of survivin gene in leukemia].
  • OBJECTIVE: To investigate the expression of survivin in leukemia and the prognostic significance in acute leukemia (AL).
  • METHODS: The expression of survivin mRNA was measured in 105 AL and 21 chronic myelogenous leukemia (CML) patients with semi-quantity reverse transcription (RT)-PCR.
  • RESULTS: The expression of survivin in de novo AL (0.525 +/- 0.460) was higher than that in NC (0.101 +/- 0.187), while it decreased in complete remission (CR) patients (0.280 +/- 0.095).
  • There was no difference of the expression between chronic phase of CML (0.279 +/- 0.112) and NC, but in acute phase of CML (0.653 +/- 0.236), the expression was higher than that in NC.
  • Abnormal expression of survivin genes was related to pathogenesis and progression of AL and it can serve as a marker of relapse and poor prognosis in AL.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / metabolism. Microtubule-Associated Proteins / biosynthesis. Neoplasm Proteins / biosynthesis


77. Passamonti F, Cervantes F, Vannucchi AM, Morra E, Rumi E, Cazzola M, Tefferi A: Dynamic International Prognostic Scoring System (DIPSS) predicts progression to acute myeloid leukemia in primary myelofibrosis. Blood; 2010 Oct 14;116(15):2857-8
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  • [Title] Dynamic International Prognostic Scoring System (DIPSS) predicts progression to acute myeloid leukemia in primary myelofibrosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Primary Myelofibrosis / complications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Proportional Hazards Models. Time Factors


78. Al-Tawfiq JA, Al-Khatti AA: Spontaneous remission of acute monocytic leukemia after infection with Clostridium septicum. Int J Lab Hematol; 2007 Oct;29(5):386-9
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  • [Title] Spontaneous remission of acute monocytic leukemia after infection with Clostridium septicum.
  • Spontaneous remissions of acute myeloid leukemia (AML) have been reported in association with infection.
  • He was diagnosed with acute monocytic leukemia (AML, FAB M5b) and a perforated bowel.
  • Similarly, previous reports of spontaneous remission of AML were short lived and were followed by relapse and progression.
  • [MeSH-major] Clostridium Infections / complications. Clostridium septicum / pathogenicity. Intestinal Perforation / complications. Leukemia, Monocytic, Acute / complications

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  • (PMID = 17824921.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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79. García-Reina S, Gómez-Caro A, Sánchez-Lorente D: [Air leak syndrome due to graft versus host disease]. Arch Bronconeumol; 2009 Jul;45(7):358-9
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  • [Transliterated title] Síndrome de fuga aérea por enfermedad del injerto contra huésped.
  • [MeSH-minor] Adult. Anemia, Refractory, with Excess of Blasts / surgery. Disease Progression. Female. Hemoglobinuria, Paroxysmal / surgery. Humans. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / surgery. Prognosis. Pulmonary Alveoli / pathology. Reoperation. Rupture, Spontaneous

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  • (PMID = 19376631.001).
  • [ISSN] 1579-2129
  • [Journal-full-title] Archivos de bronconeumología
  • [ISO-abbreviation] Arch. Bronconeumol.
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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80. Makis W, Hickeson M, Derbekyan V: Myeloid sarcoma presenting as an anterior mediastinal mass invading the pericardium: Serial Imaging With F-18 FDG PET/CT. Clin Nucl Med; 2010 Sep;35(9):706-9
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  • [Title] Myeloid sarcoma presenting as an anterior mediastinal mass invading the pericardium: Serial Imaging With F-18 FDG PET/CT.
  • Myeloid sarcoma is a tumor formed by extramedullary accumulation of myeloblasts or immature myeloid cells.
  • These tumors can develop in lymphoid organs, bone, skin, soft tissue, and other organs, and may precede or occur concurrently with acute myeloid leukemia.
  • Biopsy of the mediastinal mass and pericardium revealed myeloid sarcoma.
  • A follow-up positron emission tomography-CT was done 2 months after the last cycle, showing poor response to therapy and significant progression of disease with invasion through the anterior chest wall.
  • Myeloid sarcoma can be added to the differential diagnosis of F-18 FDG avid anterior mediastinal masses, as well as F-18 FDG uptake in the pericardium.
  • [MeSH-major] Fluorodeoxyglucose F18. Mediastinal Neoplasms / radionuclide imaging. Pericardium / pathology. Positron-Emission Tomography. Sarcoma, Myeloid / radiography. Sarcoma, Myeloid / radionuclide imaging. Tomography, X-Ray Computed

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  • (PMID = 20706048.001).
  • [ISSN] 1536-0229
  • [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] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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81. Göhring G, Giagounidis A, Büsche G, Kreipe HH, Zimmermann M, Hellström-Lindberg E, Aul C, Schlegelberger B: Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression. Ann Hematol; 2010 Apr;89(4):365-74
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  • [Title] Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression.
  • Thirty-six percent of patients progressed into acute myeloid leukaemia.
  • However, erythroid and cytogenetic responders had a significantly decreased risk of progression to acute myeloid leukaemia (p = 0.001 and p = 0.009, respectively) compared to non-responders.
  • Three and 5 years after study entry, the cumulative incidence of acute myeloid leukaemia for patients with a cytogenetic response was 10% and 21%, respectively, and for patients without cytogenetic response, it was 46% and 60%.
  • Patients with del(5q) myelodysplastic syndromes without erythroid or cytogenetic remission after treatment with lenalidomide have a high risk for clonal evolution and acute myeloid leukaemia progression.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Erythroid Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Remission Induction. Risk Factors. Treatment Failure


82. Liu X, Guo Y, Li Y, Jiang Y, Chubb S, Azuma A, Huang P, Matsuda A, Hittelman W, Plunkett W: Molecular basis for G2 arrest induced by 2'-C-cyano-2'-deoxy-1-beta-D-arabino-pentofuranosylcytosine and consequences of checkpoint abrogation. Cancer Res; 2005 Aug 1;65(15):6874-81
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  • Inhibition of Chk1 kinase with 7-hydroxystaurosporine (UCN-01) abrogated the checkpoint pathway as indicated by dephosphorylation of checkpoint proteins and progression of cells through mitosis and into G1.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. CDC2 Protein Kinase / metabolism. Cell Line, Tumor. Chromosome Aberrations. DNA Damage. Drug Interactions. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mitosis / drug effects. Protein Kinases / metabolism. Signal Transduction / drug effects. Staurosporine / analogs & derivatives. Staurosporine / pharmacology

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  • (PMID = 16061671.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA28596; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P30 CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 134665-72-8 / 2'-cyano-2'-deoxyarabinofuranosylcytosine; 7BU5H4V94A / 7-hydroxystaurosporine; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Checkpoint kinase 1; EC 2.7.11.22 / CDC2 Protein Kinase; H88EPA0A3N / Staurosporine
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83. Kakihana K, Kubo F, Wakabayashi S, Kurosu T, Miki T, Murakami N, Miura O: A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jul 15;184(2):109-12
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  • [Title] A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia.
  • MLL located at 11q23 is fused with a variety of partner genes by recurrent chromosomal translocations in acute leukemias.
  • Here we report a case of chronic myelomonocytic leukemia (CMML) with a 46,XY,t(11;19)(q23;p13.1) karyotype that transformed to acute myeloid leukemia (AML) without showing any karyotypic evolution.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Base Sequence. Disease Progression. Humans. Male


84. Oki Y, Issa JP: Epigenetic mechanisms in AML - a target for therapy. Cancer Treat Res; 2010;145:19-40
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  • In acute myelogenous leukemia (AML), aberrant DNA methylation can be observed in multiple functionally relevant genes such as p15, p 73, E-cadherin, ID 4, RARbeta2.
  • It is now clear that these epigenetic changes play a significant role in development and progression of AML, and thus constitute important targets of therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Epigenesis, Genetic. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20306243.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Neoplasm Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase
  • [Number-of-references] 174
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85. Song JH, Choi CH, Yeom HJ, Hwang SY, Kim TS: Monitoring the gene expression profiles of doxorubicin-resistant acute myelocytic leukemia cells by DNA microarray analysis. Life Sci; 2006 Jun 6;79(2):193-202
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  • [Title] Monitoring the gene expression profiles of doxorubicin-resistant acute myelocytic leukemia cells by DNA microarray analysis.
  • In order to investigate the genes involved in drug resistance, a human leukemia cell line that is resistant to doxorubicin, an anthracycline anticancer agent (AML-2/DX100), was selected and its gene expression profile was analyzed using a cDNA microarray.
  • Pro-apoptotic genes such as TNFSF7 and p21 (Cip1/Waf1) were significantly down-regulated, whereas the IKBKB, PCNA, stathmin 1, MCM5, MMP-2 and MRP1 genes, which are involved in anti-apoptotic or cell cycle progression, were over-expressed.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. DNA, Neoplasm / biosynthesis. Doxorubicin / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


86. Swords RT, Kelly KR, Smith PG, Garnsey JJ, Mahalingam D, Medina E, Oberheu K, Padmanabhan S, O'Dwyer M, Nawrocki ST, Giles FJ, Carew JS: Inhibition of NEDD8-activating enzyme: a novel approach for the treatment of acute myeloid leukemia. Blood; 2010 May 6;115(18):3796-800
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  • [Title] Inhibition of NEDD8-activating enzyme: a novel approach for the treatment of acute myeloid leukemia.
  • NEDD8 activating enzyme (NAE) has been identified as an essential regulator of the NEDD8 conjugation pathway, which controls the degradation of many proteins with important roles in cell-cycle progression, DNA damage, and stress responses.
  • Here we report that MLN4924, a novel inhibitor of NAE, has potent activity in acute myeloid leukemia (AML) models.
  • [MeSH-major] Cyclopentanes / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Proteasome Inhibitors. Pyrimidines / pharmacology. Ubiquitins / metabolism

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  • (PMID = 20203261.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ((1S,2S,4R)-4-(4-((1S)-2,3-dihydro-1H-inden-1-ylamino)-7H-pyrrolo(2,3-d)pyrimidin-7-yl)-2-hydroxycyclopentyl)methyl sulphamate; 0 / Cullin Proteins; 0 / Cyclopentanes; 0 / NEDD8 protein, human; 0 / NF-kappa B; 0 / Proteasome Inhibitors; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Ubiquitins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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87. Rieger KE, Ridky TW, Sundram UN: Skin nodules in a patient with acute myeloid leukemia and neurological deterioration--quiz case. Disseminated fusariosis. Arch Dermatol; 2010 Sep;146(9):1037-42
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  • [Title] Skin nodules in a patient with acute myeloid leukemia and neurological deterioration--quiz case. Disseminated fusariosis.
  • [MeSH-major] Dermatomycoses / diagnosis. Dermatomycoses / etiology. Fungemia / complications. Fusarium / isolation & purification. Leukemia, Myeloid, Acute / complications. Opportunistic Infections / complications
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy, Needle. Disease Progression. Edema / complications. Edema / diagnosis. Fatal Outcome. Humans. Immunocompromised Host. Immunohistochemistry. Male. Middle Aged. Orbital Diseases / complications. Orbital Diseases / diagnosis. Paresis / complications. Paresis / diagnosis. Remission Induction. Skin / microbiology. Skin / pathology

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  • (PMID = 20855710.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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88. Kroeger H, Jelinek J, Estécio MR, He R, Kondo K, Chung W, Zhang L, Shen L, Kantarjian HM, Bueso-Ramos CE, Issa JP: Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse. Blood; 2008 Aug 15;112(4):1366-73
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  • [Title] Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.
  • DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology.
  • Its impact in leukemia progression is not fully understood.
  • We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.
  • Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

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  • [Cites] Blood. 2001 May 1;97(9):2823-9 [11313277.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1997-2005 [17332327.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2957-64 [12351408.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1472-9 [12697869.001]
  • [Cites] Blood. 2003 May 15;101(10):4131-6 [12586619.001]
  • [Cites] Biotechniques. 2003 Jul;35(1):146-50 [12866414.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2879-81 [12912930.001]
  • [Cites] Nucleic Acids Res. 2004;32(3):e38 [14973332.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2411-7 [15059893.001]
  • [Cites] FEBS Lett. 2004 Jun 4;567(2-3):327-32 [15178346.001]
  • [Cites] Nucleic Acids Res. 1994 Aug 11;22(15):2990-7 [8065911.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):722-7 [8631003.001]
  • [Cites] Cancer Res. 1996 Mar 1;56(5):973-77 [8640788.001]
  • [Cites] J Mol Biol. 1996 Nov 29;264(2):268-78 [8951376.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2307-12 [10344734.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3352-6 [10416592.001]
  • [Cites] Nat Rev Cancer. 2004 Dec;4(12):988-93 [15573120.001]
  • [Cites] Nat Genet. 2005 Mar;37(3):265-74 [15723065.001]
  • [Cites] Br J Cancer. 2005 Mar 28;92(6):1165-72 [15756280.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3948-56 [15883410.001]
  • [Cites] Mol Cancer Res. 2005 Jun;3(6):325-34 [15972851.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6285-95 [16155011.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7043-9 [16192589.001]
  • [Cites] Semin Oncol. 2005 Oct;32(5):521-30 [16210093.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]
  • [Cites] Ann Hematol. 2005 Dec;84 Suppl 1:39-46 [16231140.001]
  • [Cites] Br J Haematol. 2006 May;133(3):276-83 [16643429.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5077-84 [16707430.001]
  • [Cites] Clin Cancer Res. 2006 Aug 15;12(16):4845-50 [16914570.001]
  • [Cites] Br J Cancer. 2006 Oct 23;95(8):1108-13 [17047656.001]
  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):876-80 [17283117.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Blood. 2007 May 1;109(9):3895-905 [17234736.001]
  • [Cites] Genome Res. 2007 Oct;17(10):1529-36 [17785535.001]
  • [Cites] PLoS Genet. 2007 Oct;3(10):2023-36 [17967063.001]
  • [Cites] Oncogene. 2002 Apr 18;21(17):2741-9 [11965547.001]
  • (PMID = 18523155.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2515110
  •  go-up   go-down


89. Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NS, Mufti GJ, Padua RA: Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia? Cancer Res; 2007 Sep 15;67(18):8762-71
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  • [Title] Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of disorders characterized by ineffective hematopoiesis, with an increased propensity to develop acute myelogenous leukemia (AML).
  • The molecular basis for MDS progression is unknown, but a key element in MDS disease progression is loss of chromosomal material (genomic instability).
  • Using our two-step mouse model for myeloid leukemic disease progression involving overexpression of human mutant NRAS and BCL2 genes, we show that there is a stepwise increase in the frequency of DNA damage leading to an increased frequency of error-prone repair of double-strand breaks (DSB) by nonhomologous end-joining.
  • There is a concomitant increase in reactive oxygen species (ROS) in these transgenic mice with disease progression.
  • Our data link gene abnormalities to constitutive DNA damage and increased DSB repair errors in vivo and provide a mechanism for an increase in the error rate of DNA repair with MDS disease progression.
  • [MeSH-major] DNA Damage. DNA Repair. Genomic Instability. Leukemia, Myeloid / genetics. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Genes, bcl-2. Genes, ras. Mice. Mice, Transgenic


90. Treon SP, Branagan AR, Ioakimidis L, Soumerai JD, Patterson CJ, Turnbull B, Wasi P, Emmanouilides C, Frankel SR, Lister A, Morel P, Matous J, Gregory SA, Kimby E: Long-term outcomes to fludarabine and rituximab in Waldenström macroglobulinemia. Blood; 2009 Apr 16;113(16):3673-8
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  • Median time to progression for all patients was 51.2 months and was longer for untreated patients (P = .017) and those achieving at least a very good partial response (P = .049).
  • With a median follow-up of 40.3 months, we observed 3 cases of transformation to aggressive lymphoma and 3 cases of myelodysplastic syndrome/acute myeloid leukemia.
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Murine-Derived. Disease-Free Survival. Female. Follow-Up Studies. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / mortality. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / mortality. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / mortality. Neutropenia / chemically induced. Neutropenia / mortality. Pneumonia / chemically induced. Pneumonia / mortality. Prospective Studies. Rituximab. Survival Rate. Thrombocytopenia / chemically induced. Thrombocytopenia / mortality. Time Factors

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  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1553-8 [8336194.001]
  • [Cites] Ann Oncol. 1999 Dec;10(12):1525-7 [10643548.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):709-23 [11297268.001]
  • [Cites] Blood. 2001 Jul 1;98(1):41-8 [11418461.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):800-9 [11564066.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1038-43 [11807010.001]
  • [Cites] J Immunother. 2002 Jan-Feb;25(1):72-81 [11924912.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2327-33 [11981004.001]
  • [Cites] Chest. 2002 Sep;122(3):785-90 [12226014.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3115-20 [12384407.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Leuk Lymphoma. 2003 Mar;44(3):477-81 [12688318.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):110-5 [12720118.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2694-8 [7989946.001]
  • [Cites] Br J Haematol. 1997 Nov;99(2):358-63 [9375754.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2060-4 [9626204.001]
  • [Cites] Br J Haematol. 1998 Dec;103(3):690-5 [9858218.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):546-53 [10080598.001]
  • [Cites] Eur J Haematol. 1999 Jul;63(1):35-41 [10414453.001]
  • [Cites] Cancer. 2004 Dec 1;101(11):2593-8 [15493038.001]
  • [Cites] Ann Oncol. 2005 Jan;16(1):132-8 [15598950.001]
  • [Cites] Blood. 2005 Jan 1;105(1):49-53 [15138165.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):694-704 [15681517.001]
  • [Cites] Blood. 2006 May 1;107(9):3442-6 [16410453.001]
  • [Cites] Clin Lymphoma Myeloma. 2006 Mar;6(5):380-3 [16640813.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1467-73 [16855634.001]
  • [Cites] J Clin Oncol. 2009 Jan 1;27(1):120-6 [19047284.001]
  • [Cites] J Clin Oncol. 2009 Jan 10;27(2):250-5 [19064987.001]
  • [Cites] N Engl J Med. 2003 Dec 25;349(26):2495-502 [14695409.001]
  • [Cites] Ann Oncol. 2004 Oct;15(10):1481-3 [15367407.001]
  • [Cites] Leuk Lymphoma. 2004 Oct;45(10):2047-55 [15370249.001]
  • [Cites] Invest New Drugs. 1990 May;8(2):199-200 [1696569.001]
  • [Cites] Am J Med. 1993 Jul;95(1):49-52 [8328496.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):317-24 [10637245.001]
  • (PMID = 19015393.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00020800
  • [Grant] United States / NCI NIH HHS / CA / K23 CA087977; United States / NCI NIH HHS / CA / K23CA087977-03
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2670786
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91. Ko RM, Kim HG, Wolff L, Klug CA: Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1101-11
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  • [Title] Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia.
  • Inactivation of p15(Ink4b) expression by promoter hypermethylation occurs in up to 80% of acute myeloid leukemia (AML) cases and is particularly common in the FAB-M2 subtype of AML, which is characterized by the presence of the RUNX1-ETO translocation in 40% of cases.
  • To establish whether the loss of p15(Ink4b) contributes to AML progression in association with RUNX1-ETO, we have expressed the RUNX1-ETO fusion protein from a retroviral vector in hematopoietic progenitor cells isolated from wild-type, p15(Ink4b) or p16(Ink4a) knockout bone marrow.
  • Analysis of lethally irradiated recipient mice reconstituted with RUNX1-ETO-expressing cells showed that neither p15(Ink4b) or p16(Ink4a) loss significantly accelerated disease progression over the time period of one year post-transplantation.
  • Loss of p15(Ink4b) alone resulted in increased myeloid progenitor cell frequencies in bone marrow by 10-month post-transplant and a 19-fold increase in the frequency of Lin(-)c-Kit(+)Sca-1(+) (LKS) cells that was not associated with expansion of long-term reconstituting HSC.

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  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6 [10861016.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):296-308 [10460585.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):5869-79 [15988004.001]
  • [Cites] J Exp Med. 2005 Dec 5;202(11):1599-611 [16330818.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):249-60 [16616331.001]
  • [Cites] J Cell Physiol. 2006 Sep;208(3):594-601 [16741927.001]
  • [Cites] Exp Hematol. 2007 Mar;35(3):394-406 [17309820.001]
  • [Cites] Blood. 2007 May 15;109(10):4392-8 [17284535.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3438-45 [10652337.001]
  • [Cites] Blood. 2000 Mar 15;95(6):1942-9 [10706859.001]
  • [Cites] Oncogene. 2000 May 18;19(22):2695-703 [10851069.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] Mol Cell Biol. 2002 Dec;22(23):8278-91 [12417730.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4342-6 [12560221.001]
  • [Cites] Ann Hematol. 2003 Dec;82(12):738-42 [14513284.001]
  • [Cites] Oncogene. 2003 Dec 18;22(58):9265-74 [14681685.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15678-87 [14747476.001]
  • [Cites] Ann Genet. 1973 Jun;16(2):109-12 [4125056.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1825-31 [1391946.001]
  • [Cites] Blood. 1993 Jun 1;81(11):2860-5 [8499624.001]
  • [Cites] EMBO J. 1993 Jul;12(7):2715-21 [8334990.001]
  • [Cites] Blood. 1993 Aug 1;82(3):712-5 [8338940.001]
  • [Cites] Blood. 1995 Jul 1;86(1):1-14 [7795214.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1548-56 [7632963.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):722-7 [8631003.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):837-41 [9041182.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):322-33 [9418879.001]
  • [Cites] Leukemia. 1998 Jun;12(6):845-59 [9639410.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7176-84 [9819404.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7185-91 [9819405.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3496-506 [10880462.001]
  • (PMID = 18037485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096798; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01CA087549; United States / NCI NIH HHS / CA / CA096798-05; United States / NCI NIH HHS / CA / R01 CA096798-05; United States / NCI NIH HHS / CA / R01CA096798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ NIHMS49471; NLM/ PMC2430055
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92. Rau R, Brown P: Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity. Hematol Oncol; 2009 Dec;27(4):171-81
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  • [Title] Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity.
  • It plays key roles in ribosome biogenesis, centrosome duplication, genomic stability, cell cycle progression and apoptosis.
  • Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in adult acute myeloid leukaemia (AML), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK) AML.

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • [Cites] Leukemia. 2007 Jul;21(7):1564-6 [17410190.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1566-70 [17443224.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6230-7 [17616680.001]
  • [Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2000-9 [17597811.001]
  • [Cites] Int J Hematol. 2007 Aug;86(2):143-6 [17875528.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]
  • [Cites] Leukemia. 2008 Jan;22(1):195-8 [17637812.001]
  • [Cites] J Biol Chem. 2008 Feb 29;283(9):5728-37 [18165222.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1234-40 [18401421.001]
  • [Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]
  • [Cites] J Pathol. 1996 Jan;178(1):48-52 [8778315.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]
  • [Cites] Cell. 1997 Nov 28;91(5):649-59 [9393858.001]
  • [Cites] J Soc Gynecol Investig. 1997 Nov-Dec;4(6):298-304 [9408885.001]
  • [Cites] FEBS Lett. 1997 Dec 22;420(1):25-7 [9450543.001]
  • [Cites] Nat Cell Biol. 1999 May;1(1):20-6 [10559859.001]
  • [Cites] Cell. 2000 Sep 29;103(1):127-40 [11051553.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • [Cites] FEBS Lett. 2001 Oct 12;506(3):272-6 [11602260.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1053-68 [12040437.001]
  • [Cites] Nat Cell Biol. 2002 Jul;4(7):529-33 [12080348.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Biosci Biotechnol Biochem. 2002 Oct;66(10):2239-42 [12450141.001]
  • [Cites] Mol Cell. 2003 Feb;11(2):415-24 [12620229.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1738-52 [12970773.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):985-96 [14729947.001]
  • [Cites] Science. 2004 Apr 23;304(5670):594-6 [15105502.001]
  • [Cites] Cancer Cell. 2004 May;5(5):465-75 [15144954.001]
  • [Cites] Genes Dev. 2004 Aug 1;18(15):1862-74 [15289458.001]
  • [Cites] J Biol Chem. 2004 Aug 20;279(34):35726-34 [15190079.001]
  • [Cites] FEBS Lett. 2004 Sep 24;575(1-3):112-8 [15388344.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]
  • [Cites] Haematologica. 2008 Mar;93(3):439-42 [18268276.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] Leuk Lymphoma. 2007 Nov;48(11):2141-4 [17990177.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3859-62 [18212245.001]
  • [Cites] Oncogene. 2008 Apr 10;27(17):2382-9 [17968318.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Leukemia. 2008 May;22(5):1075-8 [17972951.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1285-9 [18059485.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9327-38 [15485902.001]
  • [Cites] Cell. 1989 Feb 10;56(3):379-90 [2914325.001]
  • [Cites] J Biol Chem. 1990 Oct 25;265(30):18227-33 [2211699.001]
  • [Cites] Cancer Res. 1992 Jun 15;52(12):3372-7 [1596895.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Biol Chem. 1994 Dec 9;269(49):30994-8 [7527039.001]
  • [Cites] Cancer Res. 1995 Apr 15;55(8):1625-8 [7712464.001]
  • [Cites] Nucleic Acids Res. 1995 Oct 11;23(19):3974-9 [7479045.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Oncogene. 2006 Jul 20;25(31):4376-80 [16501600.001]
  • [Cites] J Cell Biol. 2008 Jul 14;182(1):19-26 [18625840.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2041-7 [18668134.001]
  • [Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]
  • [Cites] Nucleic Acids Res. 1998 Oct 1;26(19):4508-15 [9742256.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3706-11 [10097101.001]
  • [Cites] Protein Sci. 1999 Apr;8(4):905-12 [10211837.001]
  • [Cites] Prostate. 1999 Jun 1;39(4):298-304 [10344220.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):10988-96 [15644315.001]
  • [Cites] Biochem J. 2005 May 15;388(Pt 1):7-15 [15737070.001]
  • [Cites] Blood. 2005 Aug 1;106(3):899-902 [15831697.001]
  • [Cites] Nat Cell Biol. 2005 Aug;7(8):823-30 [16041368.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(17):7534-45 [16107701.001]
  • [Cites] Nature. 2005 Sep 1;437(7055):147-53 [16007073.001]
  • [Cites] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • [Cites] Cell Cycle. 2005 Nov;4(11):1593-8 [16205118.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3044-50 [16540653.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]
  • [Cites] Mol Cell Biol. 2006 May;26(10):3798-809 [16648475.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Br J Haematol. 2006 Jun;133(6):638-41 [16704439.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4514-23 [16455950.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1147-8 [16870548.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Leuk Res. 2007 Jan;31(1):109-11 [16678898.001]
  • [Cites] Trends Mol Med. 2006 Dec;12(12):580-7 [17071139.001]
  • [Cites] Nature. 2006 Nov 30;444(7119):638-42 [17136094.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4146-55 [16926285.001]
  • [Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]
  • [Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]
  • [Cites] Leuk Res. 2007 Apr;31(4):427-34 [17161457.001]
  • [Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]
  • [Cites] Leukemia. 2007 May;21(5):998-1004 [17361227.001]
  • [Cites] APMIS. 2007 Apr;115(4):341-6 [17504301.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1307 [17315018.001]
  • (PMID = 19569254.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111728-05; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / K23 CA111728-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Number-of-references] 102
  • [Other-IDs] NLM/ NIHMS234930; NLM/ PMC3069851
  •  go-up   go-down


93. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


94. Garcia-Manero G, Shan J, Faderl S, Cortes J, Ravandi F, Borthakur G, Wierda WG, Pierce S, Estey E, Liu J, Huang X, Kantarjian H: A prognostic score for patients with lower risk myelodysplastic syndrome. Leukemia; 2008 Mar;22(3):538-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Of these patients, 87 (10%) transformed to acute myelogenous leukemia, and 429 (50%) had died.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Anemia / etiology. Bone Marrow / pathology. Chromosome Aberrations. Disease Progression. Female. Ferritins / blood. Follow-Up Studies. Humans. Leukemia, Myeloid / epidemiology. Leukemia, Myeloid / mortality. Male. Middle Aged. Platelet Count. Prognosis. Risk. Survival Analysis. beta 2-Microglobulin / blood


95. Mesa RA, Quintás-Cardama A, Verstovsek S: Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia. Curr Hematol Malig Rep; 2007 Feb;2(1):25-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia.
  • Myelofibrosis with myeloid metaplasia (MMM) is currently classified as a classic (ie, BCR-ABL-negative) myeloproliferative disorder characterized by anemia, multiorgan extramedullary hematopoiesis, constitutional symptoms, and premature death from either leukemic transformation or other disease complications.
  • [MeSH-minor] Aged. Alkylating Agents / therapeutic use. Anemia / drug therapy. Anemia / etiology. Antimetabolites, Antineoplastic / therapeutic use. Blood Coagulation Disorders / drug therapy. Blood Coagulation Disorders / etiology. Disease Progression. Drug Delivery Systems. Drugs, Investigational / therapeutic use. Erythropoietin / therapeutic use. Hematopoiesis, Extramedullary / drug effects. Humans. Immunologic Factors / therapeutic use. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / drug therapy. Middle Aged. Mutation, Missense. Palliative Care. Point Mutation. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Signal Transduction / drug effects. Thrombocytopenia / drug therapy. Thrombocytopenia / etiology