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1. Libura M, Asnafi V, Tu A, Delabesse E, Tigaud I, Cymbalista F, Bennaceur-Griscelli A, Villarese P, Solbu G, Hagemeijer A, Beldjord K, Hermine O, Macintyre E: FLT3 and MLL intragenic abnormalities in AML reflect a common category of genotoxic stress. Blood; 2003 Sep 15;102(6):2198-204
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  • MLL rearrangements in acute myeloid leukemia (AML) include translocations and intragenic abnormalities such as internal duplication and breakage induced by topoisomerase II inhibitors.
  • In adult AML, FLT3 internal tandem duplications (ITDs) are more common in cases with MLL intragenic abnormalities (33%) than those with MLL translocation (8%).
  • Mutation/deletion involving FLT3 D835 are found in more than 20% of cases with MLL intragenic abnormalities compared with 10% of AML with MLL translocation and 5% of adult AML with normal MLL status.
  • FLT3 abnormalities in CBF leukemias with AML1-ETO or CBFbeta-MYH11 were virtually restricted to cases with variant CBFbeta-MYH11 fusion transcripts and/or atypical morphology.
  • These data suggest that the FLT3 and MLL loci demonstrate similar susceptibility to agents that modify chromatin configuration, including topoisomerase II inhibitors and abnormalities involving PML and DEK, with consequent errors in DNA repair.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Deletion. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogenes. Receptor Protein-Tyrosine Kinases / genetics. Transcription Factors. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. DNA Topoisomerases, Type II / metabolism. DNA, Neoplasm / analysis. Exons. Gene Duplication. Gene Expression Regulation, Leukemic. Histone-Lysine N-Methyltransferase. Humans. Leukemia, Monocytic, Acute / genetics. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein. RNA, Neoplasm / analysis. Trisomy. fms-Like Tyrosine Kinase 3

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  • (PMID = 12791658.001).
  • [ISSN] 0006-4971
  • [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 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Neoplasm; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 5.99.1.3 / DNA Topoisomerases, Type II
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2. Schnittger S, Kohl TM, Haferlach T, Kern W, Hiddemann W, Spiekermann K, Schoch C: KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival. Blood; 2006 Mar 1;107(5):1791-9
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  • [Title] KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival.
  • Mutations in codon D816 of the KIT gene represent a recurrent genetic alteration in acute myeloid leukemia (AML).
  • To clarify the biologic implication of activation loop mutations of the KIT gene, 1940 randomly selected AML patients were analyzed.
  • Of these 33 patients, 8 (24.2%) had a t(8;21), which was significantly higher compared with the subgroup without D816 mutations.
  • Analyses of genetic subgroups showed that KIT-D816 mutations were associated with t(8;21)/AML1-ETO and other rare AML1 translocations.
  • In contrast, other activating mutations like FLT3 and NRAS mutations were very rarely detected in AML1-rearranged leukemia.
  • KIT mutations had an independent negative impact on overall (median 304 vs 1836 days; P = .006) and event-free survival (median 244 vs 744 days; P = .003) in patients with t(8;21) but not in patients with a normal karyotype.
  • The KIT-D816 mutations confer a poor prognosis to AML1-ETO-positive AML and should therefore be included in the diagnostic workup.
  • Patients with KIT-D816-positive/AML1-ETO-positive AML might benefit from early intensification of treatment or combination of conventional chemotherapy with KIT PTK inhibitors.
  • [MeSH-major] Amino Acid Substitution. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Point Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adult. Aged. Cell Line. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Codon / genetics. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression / genetics. Humans. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Retrospective Studies. Translocation, Genetic / genetics

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  • (PMID = 16254134.001).
  • [ISSN] 0006-4971
  • [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 / AML1-ETO fusion protein, human; 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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3. Chen SJ, Chen LJ, Zhou GB: [Basic and clinical studies of the gene product-targeting therapy based on leukemogenesis--editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Feb;13(1):1-8
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  • [Title] [Basic and clinical studies of the gene product-targeting therapy based on leukemogenesis--editorial].
  • In the last twenty years, using all-trans retinoic acid (ATRA) as a differentiation inducer, Shanghai Institute of Hematology has achieved an important breakthrough in the treatment of acute promyelocytic leukemia (APL), which realized the theory of reversing phenotype of cells and provided a successful model of differentiation therapy in cancers.
  • Our group first discovered in the world the variant chromosome translocation t(11;17)(q23;q21) of APL, and cloned the PML-RAR alpha, PLZF-RAR alpha and NPM-RAR alpha fusion genes corresponding to the characterized chromosome translocations t(15;17); t(11;17) and t(5;17) in APL.
  • The ability of ATRA to modify the recruitment of nuclear receptor co-repressor with PML-RAR alpha but not PLZF-RAR alpha caused by the variant chromosome translocation elucidated the therapeutic mechanism of ATRA from the molecular level and provides new insight into transcription-modulating therapy.
  • This is the best clinical effect achieved in treating adult acute leukemia to this day, possibly making APL the first adult curable leukemia.
  • Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.
  • In acute myeloid leukemia M(2b), using new target therapy degradating AML1-ETO fusion protein and reducing the abnormal tyrosine kinase activity of c-kit will also lead to new therapeutic management in acute leukemias.

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  • (PMID = 15748426.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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4. Wang YY, Zhou GB, Yin T, Chen B, Shi JY, Liang WX, Jin XL, You JH, Yang G, Shen ZX, Chen J, Xiong SM, Chen GQ, Xu F, Liu YW, Chen Z, Chen SJ: AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec. Proc Natl Acad Sci U S A; 2005 Jan 25;102(4):1104-9
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  • [Title] AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.
  • To explore the genetic abnormalities that cooperate with AML1-ETO (AE) fusion gene to cause acute myeloid leukemia (AML) with t(8;21), we screened a number of candidate genes and identified 11 types of mutations in C-KIT gene (mC-KIT), including 6 previously undescribed ones among 26 of 54 (48.1%) cases with t(8;21).
  • Therefore, mC-KIT should be a subsequent event on the basis of t(8;21).
  • This may lead to an alternative way of C-KIT activation and may explain the significantly higher C-KIT expression in 81.3% of patients with t(8;21) than in patients with other leukemias.
  • These data strongly suggest that t(8;21) AML follows a stepwise model in leukemogenesis, i.e., AE represents the first, fundamental genetic hit to initiate the disease, whereas activation of the C-KIT pathway may be a second but also crucial hit for the development of a full-blown leukemia.
  • Gleevec also exerted a synergic effect in apoptosis induction with cytarabine, thus providing a potential therapeutic for t(8;21) leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Apoptosis / drug effects. Benzamides. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Female. Humans. Imatinib Mesylate. Male. Middle Aged

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  • (PMID = 15650049.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC545849
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5. Serrano E, Carnicer MJ, Lasa A, Orantes V, Pena J, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias. Leuk Res; 2008 Jun;32(6):944-53
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  • [Title] Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by an abnormal proliferation of the myeloid precursors and a maturation block.
  • The most common chromosomal lesions in AML are the t(8;21) and inv(16).
  • To better understand the leukemogenic mechanism of these fusion proteins, we performed gene expression studies in samples from (8;21), AML1 mutated and inv(16) patients, as well as from the Kasumi-1 cell line and a U937 cell line expressing the AML1-ETO fusion gene.
  • To assess the influence of associated epigenetic lesions, we performed gene expression studies in Kasumi-1 cells and cells extracted from an Inv(16) patient, both treated with demethylating and HDAC inhibitor agents.
  • We found a tight link between Inv(16) and mutant AML1 samples.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. DNA Methylation. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Biomarkers, Tumor / genetics. Chromatin Assembly and Disassembly. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Histone Deacetylase Inhibitors. Humans. Hydroxamic Acids / pharmacology. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / genetics. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Tumor Cells, Cultured. U937 Cells

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  • (PMID = 18206229.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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6. Brioschi M, Fischer J, Cairoli R, Rossetti S, Pezzetti L, Nichelatti M, Turrini M, Corlazzoli F, Scarpati B, Morra E, Sacchi N, Beghini A: Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits. Neoplasia; 2010 Nov;12(11):866-76
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  • [Title] Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.
  • Core-binding factor leukemia (CBFL) is a subgroup of acute myeloid leukemia (AML) characterized by genetic mutations involving the subunits of the core-binding factor (CBF).
  • The leukemogenesis model for CBFL posits that one, or more, gene mutations inducing increased cell proliferation and/or inhibition of apoptosis cooperate with CBF mutations for leukemia development.
  • Previous studies indicate that microRNA (MIR) 222/221 targets the 3' untranslated region of the KIT messenger RNA and our observation that AML1 can bind the MIR-222/221 promoter, we hypothesized that MIR-222/221 represents the link between CBF and KIT.
  • Here, we show that MIR-222/221 expression is upregulated after myeloid differentiation of normal bone marrow AC133(+) stem progenitor cells.
  • CBFL blasts with either t(8;21) or inv(16) CBF rearrangements with high expression levels of KIT (CD117) display a significantly lower level of MIR-222/221 expression than non-CBFL blasts.
  • Consistently, we found that the t(8;21) AML1-MTG8 fusion protein binds the MIR-222/221 promoter and induces transcriptional repression of a MIR-222/221-LUC reporter.
  • Because of the highly conserved sequence homology, we demonstrated concomitant MIR-222/221 down-regulation and KIT up-regulation in the 32D/WT1 mouse cell model carrying the AML1-MTG16 fusion protein.
  • This study provides the first hint that CBFL-associated fusion proteins may lead to up-regulation of the KIT receptor by down-regulating MIR-222/221, thus explaining the concomitant occurrence of CBF genetic rearrangements and overexpression of wild type or mutant KIT in AML.
  • [MeSH-major] Core Binding Factor alpha Subunits / genetics. Leukemia, Myeloid / genetics. MicroRNAs / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Line, Tumor. Cells, Cultured. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Down-Regulation. Erythropoietin / pharmacology. Female. Flow Cytometry. Glycoproteins / genetics. Glycoproteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Humans. Male. Middle Aged. Mutation. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Peptides / genetics. Peptides / metabolism. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells

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  • (PMID = 21076613.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor alpha Subunits; 0 / Glycoproteins; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 11096-26-7 / Erythropoietin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC2978910
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7. Zhang Y, Rowley JD: Chromatin structural elements and chromosomal translocations in leukemia. DNA Repair (Amst); 2006 Sep 8;5(9-10):1282-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromatin structural elements and chromosomal translocations in leukemia.
  • Recurring chromosome abnormalities are strongly associated with certain subtypes of leukemia, lymphoma and sarcomas.
  • Chromosome translocations are frequently observed in both de novo and therapy-related acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS).
  • The mechanisms that result in such chromosome translocations in leukemia and other cancers are largely unknown.
  • Genomic breakpoints in all the common chromosome translocations in leukemia, including t(4;11), t(9;11), t(8;21), inv(16), t(15;17), t(12;21), t(1;19) and t(9;22), have been cloned.
  • Genomic breakpoints tend to cluster in certain intronic regions of the relevant genes including MLL, AF4, AF9, AML1, ETO, CBFB, MYHI1, PML, RARA, TEL, E2A, PBX1, BCR and ABL.
  • However, whereas the genomic breakpoints in MLL tend to cluster in the 5' portion of the 8.3 kb breakpoint cluster region (BCR) in de novo and adult patients and in the 3' portion in infant leukemia patients and t-AML patients, those in both the AML1 and ETO genes occur in the same clustered regions in both de novo and t-AML patients.
  • Strong in vivo topo II cleavage sites and DNase I hypersensitive sites often co-localize with each other and also with many of the BCRs in most of these genes, whereas SARs are associated with BCRs in MLL, AF4, AF9, AML1, ETO and ABL, but not in the BCR gene.
  • In addition, the BCRs in MLL, AML1 and ETO have the lowest free energy level for unwinding double strand DNA.
  • Virtually all chromosome translocations in leukemia that have been analyzed to date show no consistent homologous sequences at the breakpoints, whereas a strong non-homologous end joining (NHEJ) repair signature exists at all of these chromosome translocation breakpoint junctions; this includes small deletions and duplications in each breakpoint, and micro-homologies and non-template insertions at genomic junctions of each chromosome translocation.
  • Surprisingly, the size of these deletions and duplications in the same translocation is much larger in de novo leukemia than in therapy-related leukemia.
  • We propose a non-homologous chromosome recombination model as one of the mechanisms that results in chromosome translocations in leukemia.
  • The topo II cleavage sites at open chromatin regions (DNase I hypersensitive sites), SARs or the regions with low energy level are vulnerable to certain genotoxic or other agents and become the initial breakage sites, which are followed by an excision end joining repair process.
  • [MeSH-major] Chromatin / genetics. DNA Topoisomerases, Type II / genetics. Leukemia / genetics. Lymphoma / genetics. Translocation, Genetic


8. Bug G, Schwarz K, Schoch C, Kampfmann M, Henschler R, Hoelzer D, Ottmann OG, Ruthardt M: Effect of histone deacetylase inhibitor valproic acid on progenitor cells of acute myeloid leukemia. Haematologica; 2007 Apr;92(4):542-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of histone deacetylase inhibitor valproic acid on progenitor cells of acute myeloid leukemia.
  • Here, VPA maintains a significantly higher proportion of CD34+ LPC and colony forming units compared to control cultures in six AML samples, but selectively reduces leukemic cell numbers in another AML sample with expression of AML1/ETO.
  • [MeSH-major] Hematopoietic Stem Cells / drug effects. Histone Deacetylase Inhibitors. Leukemia, Myeloid / pathology. Neoplasm Proteins / antagonists & inhibitors. Neoplastic Stem Cells / drug effects. Valproic Acid / adverse effects
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / analysis. Cell Culture Techniques / methods. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Chromosomes, Human, Pair 21 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Core Binding Factor Alpha 2 Subunit / analysis. Core Binding Factor Alpha 2 Subunit / physiology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / physiology. Translocation, Genetic. Tumor Stem Cell Assay

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  • (PMID = 17488665.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Histone Deacetylase Inhibitors; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 614OI1Z5WI / Valproic Acid
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9. Lasa A, Carnicer MJ, Aventín A, Estivill C, Brunet S, Sierra J, Nomdedéu JF: MEIS 1 expression is downregulated through promoter hypermethylation in AML1-ETO acute myeloid leukemias. Leukemia; 2004 Jul;18(7):1231-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MEIS 1 expression is downregulated through promoter hypermethylation in AML1-ETO acute myeloid leukemias.
  • Retroviral insertional mutagenesis in BXH2 mice commonly induces myeloid leukemias.
  • We found a constant downregulation of the Meis 1 gene mRNA in AML1-ETO acute myeloid leukemias and in those cases harboring in frame mutations in the bZIP domain of CEBPalpha.
  • In a cell line model (U937 Tet AML1-ETO), AML1-ETO expression was not associated with Meis 1 suppression at 72 h.
  • Nevertheless, Meis 1 repression is dependent on the AML1-ETO transcript levels in treated leukemic patients.
  • Chimeric products that arise from chromosomal translocations may be associated with locus-specific epigenetic inactivation.
  • It remains to be investigated when this methylation process is acquired and which are the basic mechanisms underlying these molecular events in AML1-ETO and CEBPalpha-mutated AML.
  • [MeSH-major] Azacitidine / analogs & derivatives. DNA Methylation. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion. Promoter Regions, Genetic / genetics. Transcription Factors
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow. Case-Control Studies. Cell Line, Tumor. Core Binding Factor Alpha 2 Subunit. Down-Regulation / drug effects. Humans. Hydroxamic Acids / pharmacology. RNA, Messenger / analysis

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  • (PMID = 15103390.001).
  • [ISSN] 0887-6924
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / Hydroxamic Acids; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / myeloid ecotropic viral integration site 1 protein; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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