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1. Quigley DI, Wolff DJ: Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci. Cancer Genet Cytogenet; 2006 Jul 1;168(1):77-9
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  • [Title] Pediatric T-cell acute lymphoblastic leukemia with aberrations of both MLL loci.
  • Translocations involving the MLL gene at 11q23 have been implicated in acute lymphoblastic leukemia (ALL), as well as acute myeloid leukemia (AML).
  • Except in cases of T-cell ALL, MLL rearrangement is typically associated with a poor prognosis.
  • We report a case of T-cell ALL with a t(11;19)(q23;p13.3) and deletion of the other chromosome 11 homolog at band q23.
  • Fluorescence in situ hybridization (FISH) analyses confirmed involvement of the MLL loci in both the translocation and deletion.
  • This case is unique in that deletions of 11q23 reported in ALL generally do not involve MLL.
  • We are unaware of a previous report showing rearrangement of the MLL loci on both chromosome 11 homologues.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 16772125.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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2. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • DESIGN AND METHODS: Breakpoints of balanced 6q rearrangements were mapped in sequential fluorescent in situ hybridization (FISH) experiments with BAC and PAC clones in 11 patients.
  • RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.
  • In two cases of childhood T-ALL, both carrying a t(6;7)(q23;q32 through 36), split FISH signals were produced by adjacent PAC, mapping the breakpoints to within an approximately 150 Kb region containing the genes c-MYB and AHI1.
  • Other 6q22-q23 translocations mapped in detail interrupted regions containing no recognized genes.
  • 6q breakpoints outside the q22-q23 region were widely dispersed and in two were mapped to positions overlapping the cloned fragile sites FRA6E and FRA6F.
  • The involvement of MLL was demonstrated in one case with t(6;11)(q15;q23).
  • INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
  • Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
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3. Liu XP, Li CW, Qin S, Dai Y, Xiao JG, Huang Q, Xu FY, Gong JY, Liu SH: [Conventional cytogenetics and fluorescence in situ hybridization as methods for detecting MLL gene rearrangements in leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Oct;13(5):798-803
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  • [Title] [Conventional cytogenetics and fluorescence in situ hybridization as methods for detecting MLL gene rearrangements in leukemia].
  • This study was aimed to compare the values of conventional cytogenetics (CC), interphase FISH and sequential R-banding and FISH analysis as methods for detecting MLL gene rearrangements.
  • 37 acute leukemia patients were studied by CC and interphase FISH.
  • The results showed that among them, 10 cases were 11q23(+)/MLL(+), 2 cases were 11q23(-)/MLL(+) (5.4%), 3 cases were 111q23(+)/MLL(-) (8.1%) and 22 cases were 11q23(-)/MLL(-).
  • For some patients, different results were obtained by using CC and interphase FISH for detecting 11q23/MLL gene rearrangements.
  • After sequential R-banding and FISH analysis for 6 patients, the chromosome related to MLL gene translocation was seen clearly in karyotypes and FISH image.
  • It is concluded that for accurate diagnosis both CC and FISH are needed for detecting 11q23/MLL gene rearrangements, and evaluation is needed in combination of these two results.

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  • (PMID = 16277845.001).
  • [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] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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4. Gessner A, Thomas M, Castro PG, Büchler L, Scholz A, Brümmendorf TH, Soria NM, Vormoor J, Greil J, Heidenreich O: Leukemic fusion genes MLL/AF4 and AML1/MTG8 support leukemic self-renewal by controlling expression of the telomerase subunit TERT. Leukemia; 2010 Oct;24(10):1751-9
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  • [Title] Leukemic fusion genes MLL/AF4 and AML1/MTG8 support leukemic self-renewal by controlling expression of the telomerase subunit TERT.
  • MLL/AF4 and AML/MTG8 represent two leukemic fusion genes, which are most frequently found in infant acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML), respectively.
  • We examined the influence of MLL/AF4 and AML1/MTG8 fusion genes on the expression of TERT coding for the telomerase protein subunit, and subsequently telomerase activity in t(4;11)-positive ALL and t(8;21)-positive cell lines, respectively.
  • MLL/AF4 suppression diminished telomerase activity and expression of TERT.
  • Blocking pro-apoptotic caspase activation in conjunction with MLL/AF4 knockdown enhanced the inhibition of TERT gene expression, which suggests that MLL/AF4 depletion does not reduce TERT expression levels by inducing apoptosis.
  • Knockdown of HOXA7, a direct transcriptional target of MLL/AF4 fusion gene, caused a reduction of telomerase and TERT to an extent similar to that observed with MLL/AF4 suppression.
  • We thus present findings that show a mechanistic link between leukemic fusion proteins, essential for development and maintenance of leukemia, and telomerase, a key element of both normal and malignant self-renewal.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Telomerase / genetics
  • [MeSH-minor] Apoptosis. Blotting, Western. Cell Aging. Chromatin Immunoprecipitation. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 8 / genetics. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. In Situ Hybridization, Fluorescence. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Telomere / genetics. Translocation, Genetic. Tumor Cells, Cultured

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  • (PMID = 20686504.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HOXA7 protein, human; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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5. Jung R, Jacobs U, Krumbholz M, Langer T, Keller T, De Lorenzo P, Valsecchi MG, van der Velden VH, Moericke A, Stanulla M, Teigler-Schlegel A, Panzer-Gruemayer ER, van Dongen JJ, Schrappe M, den Boer ML, Pieters R, Rascher W, Metzler M: Bimodal distribution of genomic MLL breakpoints in infant acute lymphoblastic leukemia treatment. Leukemia; 2010 Apr;24(4):903-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bimodal distribution of genomic MLL breakpoints in infant acute lymphoblastic leukemia treatment.
  • [MeSH-major] Chromosome Breakpoints. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20164851.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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6. Schlenk RF, Döhner K, Krauter J, Fröhling S, Corbacioglu A, Bullinger L, Habdank M, Späth D, Morgan M, Benner A, Schlegelberger B, Heil G, Ganser A, Döhner H, German-Austrian Acute Myeloid Leukemia Study Group: Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia. N Engl J Med; 2008 May 1;358(18):1909-18
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  • [Title] Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia.
  • BACKGROUND: Mutations occur in several genes in cytogenetically normal acute myeloid leukemia (AML) cells: the nucleophosmin gene (NPM1), the fms-related tyrosine kinase 3 gene (FLT3), the CCAAT/enhancer binding protein alpha gene (CEPBA), the myeloid-lymphoid or mixed-lineage leukemia gene (MLL), and the neuroblastoma RAS viral oncogene homolog (NRAS).
  • METHODS: We compared the mutational status of the NPM1, FLT3, CEBPA, MLL, and NRAS genes in leukemia cells with the clinical outcome in 872 adults younger than 60 years of age with cytogenetically normal AML.
  • RESULTS: A total of 53% of patients had NPM1 mutations, 31% had FLT3 internal tandem duplications (ITDs), 11% had FLT3 tyrosine kinase-domain mutations, 13% had CEBPA mutations, 7% had MLL partial tandem duplications (PTDs), and 13% had NRAS mutations.
  • Significant associations were found between the risk of relapse or the risk of death during complete remission and the leukemia genotype of mutant NPM1 without FLT3-ITD (hazard ratio, 0.44; 95% confidence interval [CI], 0.32 to 0.61), the mutant CEBPA genotype (hazard ratio, 0.48; 95% CI, 0.30 to 0.75), and the MLL-PTD genotype (hazard ratio, 1.56; 95% CI, 1.00 to 2.43), as well as receipt of a transplant from an HLA-matched related donor (hazard ratio, 0.60; 95% CI, 0.44 to 0.82).
  • CONCLUSIONS: Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. CCAAT-Enhancer-Binding Protein-alpha / genetics. Female. Genetic Markers. Genotype. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Viral / genetics. Remission Induction. Treatment Outcome. fms-Like Tyrosine Kinase 3 / genetics


7. Wei J, Wunderlich M, Fox C, Alvarez S, Cigudosa JC, Wilhelm JS, Zheng Y, Cancelas JA, Gu Y, Jansen M, Dimartino JF, Mulloy JC: Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia. Cancer Cell; 2008 Jun;13(6):483-95
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  • [Title] Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia.
  • Faithful modeling of mixed-lineage leukemia in murine cells has been difficult to achieve.
  • We show that expression of MLL-AF9 in human CD34+ cells induces acute myeloid, lymphoid, or mixed-lineage leukemia in immunodeficient mice.
  • Some leukemia stem cells (LSC) were multipotent and could be lineage directed by altering either the growth factors or the recipient strain of mouse, highlighting the importance of microenvironmental cues.
  • Other LSC were strictly lineage committed, demonstrating the heterogeneity of the stem cell compartment in MLL disease.
  • Targeting the Rac signaling pathway by pharmacologic or genetic means resulted in rapid and specific apoptosis of MLL-AF9 cells, suggesting that the Rac signaling pathway may be a valid therapeutic target in MLL-rearranged AML.


8. Miesner M, Haferlach C, Bacher U, Weiss T, Macijewski K, Kohlmann A, Klein HU, Dugas M, Kern W, Schnittger S, Haferlach T: Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC). Blood; 2010 Oct 14;116(15):2742-51
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  • [Title] Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC).
  • The World Health Organization classification of acute myeloid leukemia (AML) is hierarchically structured and integrates genetics, data on patients' history, and multilineage dysplasia (MLD).
  • The category "AML with myelodysplastic syndrome (MDS)-related changes" (AML-MRC) is separated from "AML not otherwise specified" (AML-NOS) by presence of MLD, MDS-related cytogenetics, or history of MDS or MDS/myeloproliferative neoplasm (MPN).
  • We analyzed 408 adult patients categorized as AML-MRC or AML-NOS.
  • Patients with MLD as sole AML-MRC criterion (AML-MLD-sole; n = 90) had less frequently FLT3 internal tandem duplication (P = .032) and lower median age than AML-NOS (n = 232).
  • Contrarily, patients with AML-NOS combined with AML-MLD-sole (n = 323) had better 3-year EFS (16.9 vs 10.7 months; P = .005) and 3-year OS (55.8% vs 32.5%; P = .001) than patients with history of MDS or MDS/MPN or MDS-related cytogenetics (n = 85).
  • Gene expression analysis showed distinct clusters for AML-MLD-sole combined with AML-NOS versus AML with MDS-related cytogenetics or MDS history.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


9. Rice KL, Licht JD: HOX deregulation in acute myeloid leukemia. J Clin Invest; 2007 Apr;117(4):865-8
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  • [Title] HOX deregulation in acute myeloid leukemia.
  • The deregulation of homeobox (HOX) genes in acute myeloid leukemia (AML) and the potential for these master regulators to perturb normal hematopoiesis is well established.
  • To date, overexpression of HOX genes in AML has been attributed to specific chromosomal aberrations and abnormalities involving mixed-lineage leukemia (MLL), an upstream regulator of HOX genes.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics

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  • [Cites] Leukemia. 2004 Jun;18(6):1059-63 [15085154.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1241-9 [14977821.001]
  • [Cites] J Biol Chem. 1991 Feb 15;266(5):3246-51 [1671571.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):154-8 [8563753.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2332-44 [9694798.001]
  • [Cites] Blood. 1999 Feb 1;93(3):1025-31 [9920852.001]
  • [Cites] Heredity (Edinb). 2005 Feb;94(2):145-52 [15578045.001]
  • [Cites] Leuk Lymphoma. 2005 Jul;46(7):1061-6 [16019559.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1536-42 [16015387.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:137-42 [16304371.001]
  • [Cites] Cancer Res. 2006 Jul 15;66(14):6947-54 [16849538.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16924-9 [17068127.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:178-84 [17124058.001]
  • [Cites] J Clin Invest. 2007 Apr;117(4):1037-48 [17347684.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Apr;27(4):380-6 [10719368.001]
  • [Cites] Mol Genet Metab. 2000 Feb;69(2):85-100 [10720435.001]
  • [Cites] Exp Hematol. 2002 Jan;30(1):49-57 [11823037.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1293-301 [12094253.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2395-402 [12805060.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):817-22 [14718672.001]
  • [CommentOn] J Clin Invest. 2007 Apr;117(4):1037-48 [17347684.001]
  • (PMID = 17404613.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1838955
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10. Nigro LL, Sainati L, Leszl A, Mirabile E, Spinelli M, Consarino C, Di Cataldo A, Magro S, Felix CA, Basso G: Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation. Leukemia; 2007 Feb;21(2):360-2
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  • [Title] Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation.
  • [MeSH-major] Dendritic Cells / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / immunology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antigens, CD / genetics. Antigens, CD / immunology. Cell Differentiation. Child. Histone-Lysine N-Methyltransferase. Humans

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  • (PMID = 17205059.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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11. Taki T, Akiyama M, Saito S, Ono R, Taniwaki M, Kato Y, Yuza Y, Eto Y, Hayashi Y: The MYO1F, unconventional myosin type 1F, gene is fused to MLL in infant acute monocytic leukemia with a complex translocation involving chromosomes 7, 11, 19 and 22. Oncogene; 2005 Aug 4;24(33):5191-7
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  • [Title] The MYO1F, unconventional myosin type 1F, gene is fused to MLL in infant acute monocytic leukemia with a complex translocation involving chromosomes 7, 11, 19 and 22.
  • We analysed a complex translocation involving chromosomes 7, 11, 19 and 22 in infant acute monocytic leukemia, and identified that the MLL gene on 11q23 was fused to the unconventional myosin type 1F, MYO1F, gene on 19p13.2-13.3.
  • MYO1F consists of at least 28 exons and was predicted to encode a 1098-amino-acid with an N-terminal head domain containing both ATP-binding and actin-binding sequences, a neck domain with a single IQ motif, and a tail with TH1, TH2 and SH3 domains.
  • The MLL-MYO1F fusion protein contains almost the entire MYO1F, however, C-terminal MYO1F has neither the transactivation domain nor the dimerization domain found in various MLL fusion partners.
  • Further analysis of this novel type of MLL fusion protein would provide new insights into leukemogenesis.
  • MYO1F is the fourth partner gene of MLL on 19p13.
  • At the cytogenetic level, it may be difficult to distinguish MLL-ENL, MLL-ELL, MLL-EEN and MLL-MYO1F fusions created by t(11;19)(q23;p13), and it is likely that cases of t(11;19) lacking a known fusion gene may result in this gene fusion.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Monocytic, Acute / genetics. Myosin Type I / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 7. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15897884.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.1.- / Myosin Type I
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12. Milne TA, Dou Y, Martin ME, Brock HW, Roeder RG, Hess JL: MLL associates specifically with a subset of transcriptionally active target genes. Proc Natl Acad Sci U S A; 2005 Oct 11;102(41):14765-70
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  • [Title] MLL associates specifically with a subset of transcriptionally active target genes.
  • MLL (mixed-lineage leukemia) is a histone H3 Lys-4 specific methyltransferase that is a positive regulator of Hox expression.
  • MLL rearrangements and amplification are common in acute lymphoid and myeloid leukemias and myelodysplastic disorders and are associated with abnormal up-regulation of Hox gene expression.
  • Although MLL is expressed throughout hematopoiesis, Hox gene expression is sharply down-regulated during differentiation, suggesting that either the activity of MLL or its association with target promoters must be regulated.
  • Here we show that MLL associates with actively transcribed genes but does not remain bound after transcriptional down-regulation.
  • Surprisingly, MLL is associated not only with promoter regions but also is distributed across the entire coding regions of genes.
  • MLL interacts with RNA polymerase II (pol II) and colocalizes with RNA pol II at a subset of actively transcribed target in vivo.
  • Loss of function Mll results in defects in RNA pol II distribution.
  • Together the results suggest that an intimate association between MLL and RNA pol II occurs at MLL target genes in vivo that is required for normal initiation and/or transcriptional elongation.
  • [MeSH-major] Gene Expression Regulation. Genes, Homeobox / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. RNA Polymerase II / metabolism. Transcription, Genetic / genetics

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  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1519-24 [11171983.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Mol Cell Biol. 2001 Apr;21(7):2249-58 [11259575.001]
  • [Cites] Oncogene. 2001 Feb 15;20(7):874-8 [11314021.001]
  • [Cites] Genes Dev. 2001 Sep 1;15(17):2197-202 [11544176.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Exp Hematol. 2002 Jan;30(1):49-57 [11823037.001]
  • [Cites] Nucleic Acids Res. 2002 Feb 15;30(4):958-65 [11842107.001]
  • [Cites] Curr Opin Cell Biol. 2002 Jun;14(3):286-98 [12067650.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Curr Biol. 2002 Jun 25;12(12):1052-8 [12123582.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Cell. 2003 Nov 14;115(4):425-35 [14622597.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]
  • [Cites] Nat Cell Biol. 2004 Feb;6(2):162-7 [14730313.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]
  • [Cites] Dev Cell. 2004 Mar;6(3):437-43 [15030765.001]
  • [Cites] Gene Expr Patterns. 2004 Mar;4(2):215-22 [15161102.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]
  • [Cites] Trends Mol Med. 2004 Oct;10(10):500-7 [15464450.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10610-4 [7938000.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5434-43 [7565694.001]
  • [Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Blood. 1997 Sep 1;90(5):1799-806 [9292512.001]
  • [Cites] Gene. 1998 Mar 16;209(1-2):77-85 [9524228.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4152-7 [9539705.001]
  • [Cites] DNA Cell Biol. 1998 May;17(5):407-14 [9628584.001]
  • [Cites] Blood. 1998 Jul 1;92(1):108-17 [9639506.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Cell. 2004 Dec 29;119(7):941-53 [15620353.001]
  • [Cites] Cell. 2005 Jan 28;120(2):169-81 [15680324.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8 [15941828.001]
  • [Cites] Cell. 2005 Jun 17;121(6):859-72 [15960974.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):186-94 [12482972.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):721-9 [12667454.001]
  • [Cites] Science. 2003 Apr 18;300(5618):492-5 [12702877.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8342-7 [12829790.001]
  • [Cites] J Biol Chem. 2003 Jul 18;278(29):26303-6 [12764140.001]
  • [CommentIn] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14481-2 [16203969.001]
  • (PMID = 16199523.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.7.- / RNA Polymerase II
  • [Other-IDs] NLM/ PMC1253553
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13. Meleshko AN, Belevtsev MV, Savitskaja TV, Potapnev MP: The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression. Leuk Res; 2006 Jul;30(7):795-800
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  • [Title] The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression.
  • TCR genes rearrangements were reported to occur at high frequency in B-lineage acute lymphoblastic leukemia (ALL).
  • Therefore, we have analyzed 83 children with acute B-lineage ALL (67 de novo patients and 19 relapses) by PCR analysis for clonal IgH, incomplete TCRD (Vdelta2-Ddelta3 and Ddelta2-Ddelta3) and TCRG rearrangements.
  • [MeSH-major] Burkitt Lymphoma / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 16386788.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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14. Marcucci G, Mrózek K, Bloomfield CD: Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics. Curr Opin Hematol; 2005 Jan;12(1):68-75
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  • [Title] Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics.
  • PURPOSE OF REVIEW: Patients with acute myeloid leukemia (AML) and normal karyotype constitute the single largest cytogenetic group of AML, estimated to account for 45% of adults with de novo AML.
  • RECENT FINDINGS: Four prognostic biomarkers-the internal tandem duplication and point mutations in the FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEBPA gene, and overexpression of the BAALC gene-have been found to predict outcome in patients with AML and normal cytogenetics.
  • In addition, one study using gene expression profiling identified two subgroups of AML patients with a normal karyotype whose survival differs significantly.
  • Because mutations in FLT3 result in an autophosphorylated, leukemogenesis-driving protein, molecular targeting therapy with a new class of tyrosine kinase inhibitors is being explored in early clinical trials.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 15604894.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30CA16058
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 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
  • [Number-of-references] 65
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15. Valencia A, Cervera J, Such E, Ibañez M, Barragán E, Fuster O, Bolufer P, Moscardó F, Sanz MA: A new reliable fluorescence in situ hybridization method for identifying multiple specific cytogenetic abnormalities in acute myeloid leukemia. Leuk Lymphoma; 2010 Apr;51(4):680-5
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  • [Title] A new reliable fluorescence in situ hybridization method for identifying multiple specific cytogenetic abnormalities in acute myeloid leukemia.
  • The usefulness of the new Chromoprobe Multiprobe AML Panel was evaluated in 80 patients with acute myeloid leukemia (AML) in parallel with conventional cytogenetics.
  • Moreover, in six of nine patients (67%) without metaphases or with non-evaluable chromosomes, the panel identified three MLL rearrangements, two monosomy 7, one of them also with del(5q), and one inv(16)(p13q22).
  • Our results indicate that the multiprobe panel can be used as a complementary technique for detection of the most important chromosomal abnormalities in AML using small quantities of sample in only one hybridization experiment.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Chromosome Inversion. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 7. DNA Mutational Analysis / methods. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Models, Biological. Monosomy. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. Reproducibility of Results. Substrate Specificity / genetics

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  • (PMID = 20233056.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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16. Lee J, Hwang J, Kim HS, Kim S, Kim YH, Park SY, Kim KS, Ryoo ZY, Chang KT, Lee S: A comparison of gene expression profiles between primary human AML cells and AML cell line. Genes Genet Syst; 2008 Aug;83(4):339-45
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  • In acute myeloid leukemia (AML), hematologic malignancies are characterized by recurring chromosomal abnormalities.
  • Chromosome translocation t(9;11)(p22;q23) is one of the most common genetic aberrations and results in the formation of the MLL-AF9 fusion gene that functions as a facilitator of cell growth directly.
  • In order to study this type of AML, the cell lines with cytogenetically diagnosed t(9;11)(p22;q23), such as Mono Mac 6 (MM6), have been widely used.
  • To examine whether there is any difference in gene expression between the primary human t(9;11) AML cells and MM6 cell line, genome-wide transcriptome analysis was performed on MM6 cell line using SAGE and the results were compared to the profile of primary human t(9;11) AML cells.
  • 884 transcripts which were alternatively expressed between MM6 cells and primary human t(9;11) cells were identified through statistical analysis (P < 0.05) and 4-fold expression change.
  • Therefore, since MM6 cell line has a similar expression profile to primary human t(9;11) AML in general and expresses uniquely a strong Erk1/Erk2 MAPK pathway including HRAS, it can be used as a model for HRAS-positive t(9;11) AML.
  • [MeSH-major] Cell Line, Tumor. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Expressed Sequence Tags. Gene Library. Humans. Oligonucleotide Array Sequence Analysis. Translocation, Genetic


17. Argiropoulos B, Yung E, Xiang P, Lo CY, Kuchenbauer F, Palmqvist L, Reindl C, Heuser M, Sekulovic S, Rosten P, Muranyi A, Goh SL, Featherstone M, Humphries RK: Linkage of the potent leukemogenic activity of Meis1 to cell-cycle entry and transcriptional regulation of cyclin D3. Blood; 2010 May 20;115(20):4071-82
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  • Expression of Meis1 is rate-limiting in MLL-associated leukemias and potently interacts with Hox and NUP98-HOX genes in leukemic transformation to promote self-renewal and proliferation of hematopoietic progenitors.
  • We identified cyclin D3 as a direct downstream target of MEIS1 and M33-MEIS1 and showed that the G(1)-phase accumulation and growth suppression induced by M33-Meis1 was partially relieved by overexpression of cyclin D3.
  • [MeSH-major] Cell Cycle. Cyclin D3 / genetics. Gene Expression Regulation, Leukemic. Homeodomain Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 20237320.001).
  • [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 / Biomarkers, Tumor; 0 / Cyclin D3; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Retinoblastoma Protein; 0 / myeloid ecotropic viral integration site 1 protein; EC 1.13.12.- / Luciferases
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18. Ono R, Nosaka T, Hayashi Y: Roles of a trithorax group gene, MLL, in hematopoiesis. Int J Hematol; 2005 May;81(4):288-93
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  • [Title] Roles of a trithorax group gene, MLL, in hematopoiesis.
  • The mixed-lineage leukemia (MLL) gene is a trithorax group (trxG) gene that was originally identified at chromosomal translocations in patients developing acute leukemia.
  • Although Polycomb group (PcG) genes, which counteract trxG genes, were found to play essential roles in hematopoiesis, little has been understood about the roles of trxG genes in hematopoiesis except for MLL.
  • MLL has been found fused with 1 of more than 30 different partner genes to yield a diverse collection of MLL fusion oncoproteins that lead to the aberrant expression of HOX genes.
  • Recent studies have revealed that MLL assembles, as do some trxG proteins, into a chromatin-modifying transcriptional regulatory supercomplex to regulate epigenetic pathways, including the methylation of histone H3 lysine 4, which is conferred by the Su (var)3-9, enhancer of zeste, and tritho-rax (SET) domain.
  • Other studies also indicated that MLL plays a nonredundant and essential role in definitive hematopoiesis and induces the proliferation and differentiation of hematopoietic progenitors by maintaining appropriate up-regulation of HOX genes.
  • [MeSH-minor] Cell Differentiation. Cell Proliferation. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein

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  • [Cites] Blood. 2002 Nov 15;100(10):3710-8 [12393701.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Leukemia. 2004 May;18(5):998-1005 [14999297.001]
  • [Cites] Oncogene. 2001 May 28;20(24):3055-66 [11420721.001]
  • [Cites] Annu Rev Genet. 2004;38:413-43 [15568982.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]
  • [Cites] Trends Mol Med. 2004 Oct;10(10):500-7 [15464450.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14 ):4075-80 [12124344.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • [Cites] Cell. 1992 Nov 13;71(4):691-700 [1423624.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):919-29 [15761502.001]
  • [Cites] Dev Cell. 2004 Mar;6(3):437-43 [15030765.001]
  • [Cites] Oncogene. 1998 Jun 25;16(25):3233-41 [9681821.001]
  • [Cites] Genes Dev. 2004 May 1;18(9):965-74 [15132992.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1179-83 [8640793.001]
  • [Cites] J Exp Med. 2002 Mar 18;195(6):759-70 [11901201.001]
  • [Cites] Genes Dev. 2002 Nov 15;16(22):2893-905 [12435631.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):333-7 [11809673.001]
  • [Cites] Int J Hematol. 2003 Dec;78(5):390-401 [14704031.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):12902-7 [11687631.001]
  • [Cites] Cell. 2002 Oct 18;111(2):185-96 [12408863.001]
  • [Cites] Cell. 2003 Oct 31;115(3):293-303 [14636557.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Mol Cell. 2003 Nov;12(5):1325-32 [14636589.001]
  • [Cites] Blood. 1998 Jul 1;92(1):108-17 [9639506.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):90-4 [11752412.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3945-50 [9166831.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):368-80 [11071359.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4152-7 [9539705.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14535-40 [10588740.001]
  • [Cites] Nucleic Acids Res. 2002 Feb 15;30(4):958-65 [11842107.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4261-5 [10485469.001]
  • [Cites] Leukemia. 1996 Aug;10(8):1303-7 [8709635.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11535-40 [13679578.001]
  • [Cites] Mol Cell Biol. 2001 Apr;21(7):2249-58 [11259575.001]
  • [Cites] Cancer Cell. 2003 May;3(5):449-58 [12781363.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Curr Biol. 2004 Nov 23;14(22):2063-9 [15556871.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Sep;38(1):8-12 [12874781.001]
  • [Cites] Cell. 2002 Oct 18;111(2):197-208 [12408864.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10610-4 [7938000.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):186-94 [12482972.001]
  • [Cites] Science. 2002 Nov 1;298(5595):1039-43 [12351676.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14372-7 [10588712.001]
  • [Cites] Nature. 2003 May 15;423(6937):302-5 [12714971.001]
  • [Cites] Genesis. 2001 Aug;30(4):201-12 [11536426.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Sep;32(1):82-8 [11477664.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14 ):8342-7 [12829790.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):122-9 [9418860.001]
  • [Cites] Cell. 1996 Jun 14;85(6):853-61 [8681380.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3589-97 [11313484.001]
  • [Cites] Blood. 2004 May 15;103(10):3876-82 [14751928.001]
  • [Cites] Blood. 1997 Sep 1;90(5):1799-806 [9292512.001]
  • [Cites] Oncogene. 2003 May 8;22(18):2851-5 [12743608.001]
  • [Cites] J Biol Chem. 2002 Apr 5;277(14):11621-4 [11850414.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10632-6 [9724755.001]
  • [Cites] Genes Dev. 2003 Apr 1;17(7):896-911 [12670868.001]
  • [Cites] Blood. 1997 Dec 15;90(12 ):4699-704 [9389684.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6428-33 [10339604.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8732-7 [9238046.001]
  • [Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):7137-48 [11742990.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Nov;38(3):253-9 [14506700.001]
  • [Cites] Int J Hematol. 2003 Dec;78(5):414-20 [14704033.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Oncogene. 2002 Jul 11;21(30):4706-14 [12096348.001]
  • [Cites] Nat Rev Immunol. 2002 Aug;2(8):593-604 [12154378.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(23):10470-8 [15542854.001]
  • [Cites] Curr Opin Hematol. 2002 Jul;9(4):282-7 [12042701.001]
  • (PMID = 15914356.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 77
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19. Haferlach T, Kern W, Schnittger S, Schoch C: Modern diagnostics in acute leukemias. Crit Rev Oncol Hematol; 2005 Nov;56(2):223-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modern diagnostics in acute leukemias.
  • Acute leukemias are a heterogeneous group of diseases.
  • Only by using a comprehensive diagnostic panel including cytomorphology, cytochemistry, multiparameter flow cytometry (MFC), cytogenetics, fluorescence in situ hybridization (FISH) and molecular genetic methods the correct diagnosis in acute leukemias can be established today.
  • The results serve as a mandatory prerequisite for individual treatment strategies and for the evaluation of treatment response using especially newly defined and highly specific MRD markers.
  • [MeSH-major] Biomarkers, Tumor. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16213152.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 70
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20. Bielorai B, Meyer C, Trakhtenbrot L, Golan H, Rozner E, Amariglio N, Izraeli S, Marschalek R, Toren A: Therapy-related acute myeloid leukemia with t(2;11)(q37;q23) after treatment for osteosarcoma. Cancer Genet Cytogenet; 2010 Dec;203(2):288-91
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  • [Title] Therapy-related acute myeloid leukemia with t(2;11)(q37;q23) after treatment for osteosarcoma.
  • Secondary acute myeloid leukemia (AML) has been rarely reported after treatment for OS.
  • Cytogenetic analysis of the leukemic cells demonstrated deletion 11q23, whereas fluorescence in situ hybridization revealed rearrangement of the MLL gene.
  • Only the addition of the long-distance inverse polymerase chain reaction technique identified the SEPT2 as the MLL fusion partner resulting in t(2;11)(q37;q23) that was reported in a very few secondary AML cases.
  • Because of the cryptic nature of MLL translocations that cannot be detected by conventional cytogenetics or may misinterpreted as deletion, additional molecular techniques are required to identify the precise translocation partner.
  • Because long-distance inverse polymerase chain reaction is not available in most molecular laboratories, the true incidence of t(2;11)(q37;q23) and the involvement of SEPT2 as the MLL translocation partner could be more prevalent in secondary AML.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Osteosarcoma / drug therapy. Osteosarcoma / genetics. Translocation, Genetic


21. Mullighan CG, Kennedy A, Zhou X, Radtke I, Phillips LA, Shurtleff SA, Downing JR: Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias. Leukemia; 2007 Sep;21(9):2000-9
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  • [Title] Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias.
  • Somatic mutations in nucleophosmin (NPM1) occur in approximately 35% of adult acute myeloid leukemia (AML).
  • Six cases harbored NPM1 mutations, with each case lacking common cytogenetic abnormalities.
  • As dysregulated homeobox gene expression is also a feature of MLL-rearranged leukemia, the gene expression signatures of NPM1-mutated and MLL-rearranged leukemias were compared.
  • Significant differences were identified between these leukemia subtypes including the expression of different HOX genes, with NPM1-mutated AML showing higher levels of expression of HOXB2, B3, B6 and D4.
  • These results confirm recent reports of perturbed HOX expression in NPM1-mutated adult AML, and provide the first evidence that the NPM1-mutated signature is distinct from MLL-rearranged AML.
  • These findings suggest that mutated NPM1 leads to dysregulated HOX expression via a different mechanism than MLL rearrangement.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Cohort Studies. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Male. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Transcription Factors / genetics

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  • [CommentIn] Leukemia. 2007 Sep;21(9):1849-50 [17712359.001]
  • (PMID = 17597811.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P01 CA71907-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXB2 protein, human; 0 / HOXB6 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 140441-81-2 / HOXA10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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22. Gu WY, Chen ZX, Hu SY, Zhu J, Wang ZL, Yan F, Wang W, Cen JN, Shen HL, Qian J: [Significance of dynamic detection of WT1 expression on monitoring minimal residual disease in leukemia patients following allogeneic bone marrow transplantation]. Zhonghua Yi Xue Za Zhi; 2005 Feb 23;85(7):444-7
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  • [Title] [Significance of dynamic detection of WT1 expression on monitoring minimal residual disease in leukemia patients following allogeneic bone marrow transplantation].
  • OBJECTIVE: To investigate the significance of monitoring Wilms' tumor gene (WT1) expression level in bone marrow of leukemia patients following allogeneic bone marrow transplantation (allo-BMT).
  • METHODS: Real-time quantitative reverse transcription polymerase chain reaction method was established for measuring WT1 and GAPDH expression levels in bone marrow cells of 15 patients with leukemia, including a total of 111 specimens during the follow-up, and in 23 non-leukemia patients by using LightCycler.
  • Normalized WT1 expression level (WT1(N)) was determined as a ratio of WT1 to GAPDH times 10(4).
  • RESULTS: The median expression levels of WT1(N) in 17 samples of newly diagnosed patients, 6 samples of relapsed patients, 88 samples from leukemia patient in complete remission and 23 samples of non-leukemic controls were 40.18 (5.48 to 510.27), 125.89 (34.50 to 273.95), 4.80 (0 to 56.96) and 1.47 (0 to 8.56) respectively.
  • Spearman Rho correlation analysis revealed that the correlation coefficient between the WT1(N) expression levels and BCR/ABL, AML/ETO, PML/RARalpha and MLL/AF17 fusion genes expression were 0.678 (P = 0.00), 0.677 (P = 0.00), 0.806 (P = 0.00) and 0.553 (P = 0.049) respectively.
  • CONCLUSION: The WT1 expression level of leukemia patients following allo-BMT measured by real time RT-PCR can be a useful tool for monitoring MRD and warning the clinical relapse during follow-up.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / metabolism. WT1 Proteins / biosynthesis


23. Greif PA, Tizazu B, Krause A, Kremmer E, Bohlander SK: The leukemogenic CALM/AF10 fusion protein alters the subcellular localization of the lymphoid regulator Ikaros. Oncogene; 2008 May 1;27(20):2886-96
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  • The t(10;11)(p13;q14) translocation leads to the fusion of the CALM and AF10 genes.
  • This translocation can be found as the sole cytogenetic abnormality in acute lymphoblastic leukemia, acute myeloid leukemia and in malignant lymphomas.
  • The expression of CALM/AF10 in primary murine bone marrow cells results in the development of an aggressive leukemia in a murine bone marrow transplantation model.
  • Interestingly, Ikaros is required for normal development of lymphocytes, and aberrant expression of Ikaros has been found in leukemia.
  • The Ikaros interaction domain of AF10 was mapped to the leucine zipper domain of AF10, which is required for malignant transformation both by the CALM/AF10 and the MLL/AF10 fusion proteins.
  • [MeSH-major] Ikaros Transcription Factor / metabolism. Leukemia / metabolism. Lymphocytes / metabolism. Oncogene Proteins, Fusion / physiology

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  • (PMID = 18037964.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / IKZF1 protein, human; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; 148971-36-2 / Ikaros Transcription Factor
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24. Mrózek K, Marcucci G, Paschka P, Whitman SP, Bloomfield CD: Clinical relevance of mutations and gene-expression changes in adult acute myeloid leukemia with normal cytogenetics: are we ready for a prognostically prioritized molecular classification? Blood; 2007 Jan 15;109(2):431-48
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  • [Title] Clinical relevance of mutations and gene-expression changes in adult acute myeloid leukemia with normal cytogenetics: are we ready for a prognostically prioritized molecular classification?
  • Recent molecular analyses of leukemic blasts from pretreatment marrow or blood of patients with acute myeloid leukemia (AML) and a normal karyotype, the largest cytogenetic subset (ie, 40%-49%) of AML, have revealed a striking heterogeneity with regard to the presence of acquired gene mutations and changes in gene expression.
  • Multiple submicroscopic genetic alterations with prognostic significance have been discovered, including internal tandem duplication of the FLT3 gene, mutations in the NPM1 gene, partial tandem duplication of the MLL gene, high expression of the BAALC gene, and mutations in the CEBPA gene.

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  • [Cites] Leukemia. 2003 Jan;17(1):76-82 [12529663.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):1077-84 [10353741.001]
  • [Cites] Hum Mol Genet. 2004 Nov 15;13(22):2753-65 [15385438.001]
  • [Cites] N Engl J Med. 2004 Dec 2;351(23):2403-7 [15575056.001]
  • [Cites] Blood. 2005 Jan 1;105(1):54-60 [15345597.001]
  • [Cites] Blood. 2005 Jan 1;105(1):22-30 [15358622.001]
  • [Cites] Blood. 2005 Feb 1;105(3):986-93 [15459012.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):482-93 [15534356.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]
  • [Cites] Haematologica. 2005 May;90(5):695-6 [15921390.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4792-9 [15718420.001]
  • [Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3658-65 [16076872.001]
  • [Cites] Haematologica. 2005 Nov;90(11):1502-10 [16266897.001]
  • [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] Leukemia. 2005 Dec;19(12):2355-8 [16239911.001]
  • [Cites] Haematologica. 2005 Dec;90(12):1617-25 [16330434.001]
  • [Cites] Oncogene. 2005 Dec 15;24(56):8259-67 [16091734.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Blood. 2006 Jan 1;107(1):293-300 [16150941.001]
  • [Cites] Bone Marrow Transplant. 2005 Dec;36(11):977-83 [16184177.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Feb;165(1):1-8 [16490591.001]
  • [Cites] Blood. 2006 May 1;107(9):3724-6 [16368883.001]
  • [Cites] Blood. 2006 May 1;107(9):3700-7 [16410449.001]
  • [Cites] Blood. 2006 May 15;107(10):3847-53 [16434492.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Br J Haematol. 2000 Dec;111(4):1051-6 [11167739.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] J Clin Oncol. 2001 Apr 1;19(7):2033-40 [11283136.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2482-92 [11331327.001]
  • [Cites] Best Pract Res Clin Haematol. 2001 Mar;14(1):19-47 [11355922.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13901-6 [11707601.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2480-5 [12011125.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jun;34(2):137-53 [11979548.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1745-51 [12200689.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Hematol J. 2002;3(6):283-9 [12522450.001]
  • [Cites] Blood. 2003 Feb 1;101(3):837-45 [12393383.001]
  • [Cites] Stem Cells. 2006 May;24(5):1174-84 [16410383.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):327-37 [12538485.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Mar;36(3):261-72 [12557226.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jul;37(3):237-51 [12759922.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1813-9 [12970781.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5465-76 [14654525.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1901-8 [14604973.001]
  • [Cites] Br J Haematol. 2004 Feb;124(4):481-4 [14984498.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]
  • [Cites] Leuk Res. 2004 Jun;28(6):547-50 [15120929.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Aug;153(1):16-25 [15325089.001]
  • [Cites] Haematologica. 2004 Aug;89(8):926-33 [15339675.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14479-84 [15448205.001]
  • [Cites] Cancer Res. 1994 Jan 15;54(2):370-3 [8275471.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4277-80 [8044771.001]
  • [Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1911-8 [8946930.001]
  • [Cites] Leukemia. 1997 May;11(5):639-43 [9180285.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4876-85 [9389704.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):55-9 [9426057.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4514-23 [16455950.001]
  • [Cites] Haematologica. 2006 Jun;91(6):825-8 [16704962.001]
  • [Cites] Blood. 2006 Jul 15;108(2):685-96 [16597596.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Leukemia. 2000 Apr;14(4):675-83 [10764154.001]
  • [Cites] Leukemia. 2000 May;14(5):796-804 [10803509.001]
  • [Cites] Leukemia. 2000 Jun;14(6):1031-8 [10865969.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1297-308 [10942371.001]
  • (PMID = 16960150.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA31946
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 105
  • [Other-IDs] NLM/ PMC1785102
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25. Haferlach T, Bacher U, Kern W, Schnittger S, Haferlach C: Diagnostic pathways in acute leukemias: a proposal for a multimodal approach. Ann Hematol; 2007 May;86(5):311-27
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  • [Title] Diagnostic pathways in acute leukemias: a proposal for a multimodal approach.
  • Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) each represent a heterogeneous complex of disorders, which result from diverse mechanisms of leukemogenesis.
  • For some leukemia subtypes such as AML M3/M3v with t(15;17)/PML-RARA or Philadelphia-positive ALL targeted therapy options are available.
  • Thus, optimal therapeutic conditions are based on exact classification of the acute leukemia subtype at diagnosis and are guided by exact and sensitive quantification of minimal residual disease during complete hematologic remission.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Algorithms. Chromosome Aberrations / classification. Flow Cytometry. Humans. Immunohistochemistry. Molecular Diagnostic Techniques

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  • (PMID = 17375301.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 157
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26. Cho J, Hur M, Moon HW, Yun YM, Lee CH, Lee HG: A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer. Korean J Lab Med; 2010 Jun;30(3):255-9
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  • [Title] A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer.
  • ALL with MLL gene rearrangement secondary to chemotherapy has been rarely reported.
  • We report a case of therapy-related ALL (t-ALL) with MLL gene rearrangement in a patient who had undergone treatment for breast cancer.
  • However, the patient's complete blood cell count indicated acute leukemia: white blood cell count, 174.1 x 10(9)/L with 88% blasts; Hb level, 12.5 g/dL; and platelet count, 103.0 x 10(9)/L.
  • Cytogenetic and FISH analyses revealed t(4;11)(q21;q23) and MLL gene rearrangement, respectively.
  • To our knowledge, this is the first reported case of t-ALL with MLL gene rearrangement following treatment of breast cancer in Korea.
  • [MeSH-major] Breast Neoplasms / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Translocation, Genetic

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  • (PMID = 20603585.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; U3P01618RT / Fluorouracil
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27. Kreuziger LM, Porcher JC, Ketterling RP, Steensma DP: An MLL-SEPT9 fusion and t(11;17)(q23;q25) associated with de novo myelodysplastic syndrome. Leuk Res; 2007 Aug;31(8):1145-8
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  • [Title] An MLL-SEPT9 fusion and t(11;17)(q23;q25) associated with de novo myelodysplastic syndrome.
  • Rearrangements of the MLL gene at chromosome 11q23 are uncommon in de novo myelodysplastic syndrome (MDS).
  • Here, we describe molecular findings in a patient with multilineage dysplasia and t(11;17)(q23;q25) who responded to decitabine therapy.
  • Fluorescent in situ hybridization (FISH) demonstrated rearrangement of MLL, while RT-PCR analysis and sequencing identified the transcript fusion partner as SEPT9, a member of the septin family of GTPases.
  • MLL-SEPT9 fusion appears to be rare, having been described to date in only seven cases of AML and not, to our knowledge, in MDS.
  • Analysis of MLL-septin family member fusion products such as the one seen here may provide further insights into the etiology of myeloid neoplasia, and MLL-SEPT9 fusion may be worth seeking in other cases of MLL rearrangements with a translocation partner on chromosome 17q.

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  • [Cites] Leukemia. 2006 May;20(5):777-84 [16511515.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6428-33 [10339604.001]
  • [Cites] Oncogene. 2001 Sep 13;20(41):5930-9 [11593400.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):346-56 [10691865.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4261-5 [10485469.001]
  • [Cites] Br J Haematol. 1996 Jun;93(4):966-72 [8703835.001]
  • [Cites] Ann Hematol. 2004 Mar;83(3):170-5 [15064866.001]
  • [Cites] Leukemia. 2003 Apr;17(4):700-6 [12682627.001]
  • [Cites] Mol Biol Cell. 2002 Dec;13(12):4111-3 [12475938.001]
  • [Cites] Int J Hematol. 2002 Jun;75(5):503-7 [12095151.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Nov;45(11):1041-9 [16897742.001]
  • (PMID = 17250889.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090628; United States / NCI NIH HHS / CA / K12 CA090628-05; United States / NCI NIH HHS / CA / K12 CA90628
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-MSF fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS26467; NLM/ PMC2768487
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28. Haferlach T, Kohlmann A, Klein HU, Ruckert C, Dugas M, Williams PM, Kern W, Schnittger S, Bacher U, Löffler H, Haferlach C: AML with translocation t(8;16)(p11;p13) demonstrates unique cytomorphological, cytogenetic, molecular and prognostic features. Leukemia; 2009 May;23(5):934-43
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  • Balanced chromosomal rearrangements define distinct entities in acute myeloid leukemia (AML).
  • Here, we present 13 AML cases with t(8;16)(p11;p13) with observed low incidence (13/6124 patients), but more frequent presentation in therapy-related AML than in de novo AML (7/438 versus 6/5686, P=0.00001).
  • Cytomorphology was characterized by parallel positive myeloperoxidase and non-specific esterase staining, therefore, French-American-British (FAB)-classification was impossible and origin of the AML with t(8;16) from an early stem cell with myeloid and monoblastic potential is hypothesized.
  • Using gene expression profiling on 407 cases, patients with t(8;16) were compared to AML FAB subtypes with normal karyotype.
  • Principal component analyses demonstrated that AML with t(8;16) were distinct from FAB subtypes M1, M4, M5a/b.
  • When further compared to AML showing balanced rearrangements, that is, current WHO categories t(15;17), t(8;21), inv(16) and t(11q23)/MLL, AML with t(8;16) cases were clustered close to t(11q23)/MLL sharing commonly expressed genes.
  • Subsequently, a pairwise comparison discriminated AML with t(8;16) from AML with t(11q23)/MLL, thus defining a highly unique signature for AML with t(8;16).
  • In conclusion, AML with t(8;16) demonstrates unique cytomorphological, cytogenetic, molecular and prognostic features and is a specific subtype of AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Mapping. Cytogenetic Analysis. Female. Gene Expression Profiling. Gene Regulatory Networks. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 19194466.001).
  • [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 / MLL protein, human; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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29. Rege-Cambrin G, Giugliano E, Michaux L, Stul M, Scaravaglio P, Serra A, Saglio G, Hagemeijer A: Trisomy 11 in myeloid malignancies is associated with internal tandem duplication of both MLL and FLT3 genes. Haematologica; 2005 Feb;90(2):262-4
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  • [Title] Trisomy 11 in myeloid malignancies is associated with internal tandem duplication of both MLL and FLT3 genes.
  • In 20 patients with myeloid malignancies and isolated trisomy 11 an internal tandem duplication of the MLL and FLT3 genes was observed in 41% and 31% of the cases, respectively; 80% of the FLT3+ cases showed MLL self-fusion.
  • Concomitant presence of MLL and FLT3 anomalies could be relevant in determining the poor outcome of patients with acute myeloid leukemia with trisomy 11.
  • [MeSH-major] Chromosomes, Human, Pair 11. Gene Duplication. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Trisomy. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 15710585.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MLL protein, human; 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 / fms-Like Tyrosine Kinase 3
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30. De Braekeleer E, Meyer C, Douet-Guilbert N, Morel F, Le Bris MJ, Marschalek R, Férec C, De Braekeleer M: A complex 1;19;11 translocation involving the MLL gene in a patient with congenital acute monoblastic leukemia identified by molecular and cytogenetic techniques. Ann Hematol; 2009 Aug;88(8):795-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A complex 1;19;11 translocation involving the MLL gene in a patient with congenital acute monoblastic leukemia identified by molecular and cytogenetic techniques.
  • [MeSH-major] Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Cyanosis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. Infant, Newborn. Skin Neoplasms / diagnosis

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  • (PMID = 19107484.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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31. Balgobind BV, Zwaan CM, Reinhardt D, Arentsen-Peters TJ, Hollink IH, de Haas V, Kaspers GJ, de Bont ES, Baruchel A, Stary J, Meyer C, Marschalek R, Creutzig U, den Boer ML, Pieters R, van den Heuvel-Eibrink MM: High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome. Leukemia; 2010 Dec;24(12):2048-55
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  • [Title] High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome.
  • Translocations involving the mixed lineage leukemia (MLL) gene, localized at 11q23, frequently occur in pediatric acute myeloid leukemia (AML).
  • To unravel the latter, we used microarrays to generate gene expression profiles of 245 pediatric AML cases, including 53 MLL-rearranged cases.
  • Thereby, we identified a specific gene expression signature for t(9;11)(p22;q23), and identified BRE (brain and reproductive organ expressed) to be discriminative for t(9;11)(p22;q23) (P<0.001) when compared with other MLL subtypes.
  • Patients with high BRE expression showed a significantly better 3-year relapse-free survival (pRFS) (80±13 vs 30±10%, P=0.02) within MLL-rearranged AML cases.
  • In conclusion, overexpression of the BRE gene is predominantly found in MLL-rearranged AML with t(9;11)(p22;q23).
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Translocation, Genetic

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  • (PMID = 20861917.001).
  • [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 / BRE protein, human; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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32. Haferlach C, Rieder H, Lillington DM, Dastugue N, Hagemeijer A, Harbott J, Stilgenbauer S, Knuutila S, Johansson B, Fonatsch C: Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes. Genes Chromosomes Cancer; 2007 May;46(5):494-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Diagnosis, Differential. Humans. Karyotyping


33. Santillan DA, Theisler CM, Ryan AS, Popovic R, Stuart T, Zhou MM, Alkan S, Zeleznik-Le NJ: Bromodomain and histone acetyltransferase domain specificities control mixed lineage leukemia phenotype. Cancer Res; 2006 Oct 15;66(20):10032-9
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  • [Title] Bromodomain and histone acetyltransferase domain specificities control mixed lineage leukemia phenotype.
  • A critical unanswered question about mixed lineage leukemia (MLL) is how specific MLL fusion partners control leukemia phenotype.
  • The MLL-cyclic AMP-responsive element binding protein-binding protein (CBP) fusion requires both the CBP bromodomain and histone acetyltransferase (HAT) domain for transformation and causes acute myelogenous leukemia (AML), often preceded by a myelodysplastic phase.
  • We did domain-swapping experiments to define whether unique specificities of these CBP domains drive this specific MLL phenotype.
  • Within MLL-CBP, we replaced the CBP bromodomain or HAT domain with P300/CBP-associated factor (P/CAF) or TAF(II)250 bromodomains or the P/CAF or GCN5 HAT domains.
  • HAT, but not bromodomain, substitutions conferred enhanced proliferative capacity in vitro but lacked expression of myeloid cell surface markers normally seen with MLL-CBP.
  • Mice reconstituted with domain-swapped hematopoietic progenitors developed different disease from those with MLL-CBP.
  • We conclude that both the CBP bromodomain and HAT domain play different but critical roles in determining the phenotype of MLL-CBP leukemia.
  • Our results support an important role for MLL partner genes in determining the leukemia phenotype besides their necessity in leukemogenesis.
  • Here, we find that subtleties in MLL fusion protein domain specificity direct cells toward a specific disease phenotype.
  • [MeSH-major] Histone Acetyltransferases / physiology. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / physiology. p300-CBP Transcription Factors / physiology

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  • (PMID = 17047066.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA95040; United States / NIAID NIH HHS / AI / T32 AI07508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors
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34. Burmeister T, Meyer C, Schwartz S, Hofmann J, Molkentin M, Kowarz E, Schneider B, Raff T, Reinhardt R, Gökbuget N, Hoelzer D, Thiel E, Marschalek R: The MLL recombinome of adult CD10-negative B-cell precursor acute lymphoblastic leukemia: results from the GMALL study group. Blood; 2009 Apr 23;113(17):4011-5
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  • [Title] The MLL recombinome of adult CD10-negative B-cell precursor acute lymphoblastic leukemia: results from the GMALL study group.
  • MLL translocations in adult B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) are largely restricted to the immature CD10(-) immunophenotypes.
  • MLL-AF4 is known to be the most frequent fusion transcript, but the exact frequencies of MLL aberrations in CD10(-) adult BCP-ALL are unknown.
  • Patient samples were investigated by RT-PCR for MLL-AF4, MLL-ENL, and MLL-AF9 and by long-distance inverse polymerase chain reaction, thus also allowing the identification of unknown MLL fusion partners at the genomic level.
  • MLL-AF4 was detected in 101 (54.9%) and MLL-ENL in 11 (6.0%) cases.
  • In addition, rare MLL fusion genes were found: 2 MLL-TET1 cases, not previously reported in ALL, 1 MLL-AF9, 1 MLL-PTD, a novel MLL-ACTN4, and an MLL-11q23 fusion.
  • Chromosomal breakpoints were determined in all 118 positive cases, revealing 2 major breakpoint cluster regions in the MLL gene.
  • Characteristic features of MLL(+) patients were significantly lower CD10 expression, expression of the NG2 antigen, a higher white blood count at diagnosis, and female sex.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recombinant Fusion Proteins / metabolism

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  • (PMID = 19144982.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00198991/ NCT00199056
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Recombinant Fusion Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.4.24.11 / Neprilysin
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35. Pui CH, Campana D: Age-related differences in leukemia biology and prognosis: the paradigm of MLL-AF4-positive acute lymphoblastic leukemia. Leukemia; 2007 Apr;21(4):593-4
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  • [Title] Age-related differences in leukemia biology and prognosis: the paradigm of MLL-AF4-positive acute lymphoblastic leukemia.
  • [MeSH-major] Aging / physiology. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17301807.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA115422; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA78224
  • [Publication-type] Editorial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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36. 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.
  • The properties of these cells provide a biological basis for several clinical hallmarks of MLL leukemias.
  • [MeSH-major] Disease Models, Animal. Leukemia, Lymphoid. Leukemia, Myeloid. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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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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37. Stam RW, Den Boer ML, Schneider P, de Boer J, Hagelstein J, Valsecchi MG, de Lorenzo P, Sallan SE, Brady HJ, Armstrong SA, Pieters R: Association of high-level MCL-1 expression with in vitro and in vivo prednisone resistance in MLL-rearranged infant acute lymphoblastic leukemia. Blood; 2010 Feb 4;115(5):1018-25
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  • [Title] Association of high-level MCL-1 expression with in vitro and in vivo prednisone resistance in MLL-rearranged infant acute lymphoblastic leukemia.
  • MLL-rearranged acute lymphoblastic leukemia (ALL) represents an unfavorable type of leukemia that often is highly resistant to glucocorticoids such as prednisone and dexamethasone.
  • Here, we show how gene expression profiling identifies high-level MCL-1 expression to be associated with prednisolone resistance in MLL-rearranged infant ALL, as well as in more favorable types of childhood ALL.
  • To validate this observation, we determined MCL-1 expression with quantitative reverse transcription-polymerase chain reaction in a cohort of MLL-rearranged infant ALL and pediatric noninfant ALL samples and confirmed that high-level MCL-1 expression is associated with prednisolone resistance in vitro.
  • In addition, MCL-1 expression appeared to be significantly higher in MLL-rearranged infant patients who showed a poor response to prednisone in vivo compared with prednisone good responders.
  • Finally, down-regulation of MCL-1 in prednisolone-resistant MLL-rearranged leukemia cells by RNA interference, to some extent, led to prednisolone sensitization.
  • Collectively, our findings suggest a potential role for MCL-1 in glucocorticoid resistance in MLL-rearranged infant ALL, but at the same time strongly imply that high-level MCL-1 expression is not the sole mechanism providing resistance to these drugs.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prednisone / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Cell Survival / drug effects. Child. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Gene Rearrangement. Glucocorticoids / pharmacology. Glucocorticoids / therapeutic use. Histone-Lysine N-Methyltransferase. Humans. Immunoblotting. Infant. Myeloid Cell Leukemia Sequence 1 Protein. Oligonucleotide Array Sequence Analysis. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction


38. Chang MJ, Wu H, Achille NJ, Reisenauer MR, Chou CW, Zeleznik-Le NJ, Hemenway CS, Zhang W: Histone H3 lysine 79 methyltransferase Dot1 is required for immortalization by MLL oncogenes. Cancer Res; 2010 Dec 15;70(24):10234-42
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  • [Title] Histone H3 lysine 79 methyltransferase Dot1 is required for immortalization by MLL oncogenes.
  • Chimeric oncoproteins resulting from fusion of MLL to a wide variety of partnering proteins cause biologically distinctive and clinically aggressive acute leukemias.
  • However, the mechanism of MLL-mediated leukemic transformation is not fully understood.
  • Dot1, the only known histone H3 lysine 79 (H3K79) methyltransferase, has been shown to interact with multiple MLL fusion partners including AF9, ENL, AF10, and AF17.
  • In this study, we utilize a conditional Dot1l deletion model to investigate the role of Dot1 in hematopoietic progenitor cell immortalization by MLL fusion proteins.
  • We find that loss of Dot1 activity attenuates cell viability and colony formation potential of cells immortalized by MLL oncoproteins but not by the leukemic oncoprotein E2a-Pbx1.
  • Although this effect is most pronounced for MLL-AF9, we find that Dot1 contributes to the viability of cells immortalized by other MLL oncoproteins that are not known to directly recruit Dot1.
  • Cells immortalized by MLL fusions also show increased apoptosis, suggesting the involvement of Dot1 in survival pathways.
  • In summary, our data point to a pivotal requirement for Dot1 in MLL fusion protein-mediated leukemogenesis and implicate Dot1 as a potential therapeutic target.

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  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8732-7 [9238046.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):81-8 [8972188.001]
  • [Cites] Nat Struct Mol Biol. 2010 Jan;17(1):62-8 [20010842.001]
  • [Cites] Cancer Cell. 2010 Feb 17;17(2):198-212 [20153263.001]
  • [Cites] Am J Physiol Renal Physiol. 2010 Mar;298(3):F617-24 [20053791.001]
  • [Cites] Genes Dev. 2010 Mar 15;24(6):574-89 [20203130.001]
  • [Cites] J Biol Chem. 2010 Apr 16;285(16):11966-73 [20159978.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):7042-7 [20348416.001]
  • [Cites] FEBS J. 2010 Apr;277(8):1822-31 [20236311.001]
  • [Cites] Blood. 2010 Jul 8;116(1):63-70 [20395419.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4699-704 [9389684.001]
  • [Cites] Genetics. 1998 Oct;150(2):613-32 [9755194.001]
  • [Cites] Nucleic Acids Res. 2005;33(4):e36 [15731329.001]
  • [Cites] Cell. 2005 Apr 22;121(2):167-78 [15851025.001]
  • [Cites] Genome Biol. 2005;6(6):113 [15960810.001]
  • [Cites] J Biol Chem. 2006 Jun 30;281(26):18059-68 [16636056.001]
  • [Cites] Hum Mol Genet. 2007 Jan 1;16(1):92-106 [17135274.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4445-54 [17855633.001]
  • [Cites] Mol Cell Biol. 2008 Apr;28(8):2825-39 [18285465.001]
  • [Cites] PLoS Genet. 2008;4(9):e1000190 [18787701.001]
  • [Cites] Cancer Cell. 2008 Nov 4;14(5):355-68 [18977325.001]
  • [Cites] Blood. 2009 Apr 2;113(14):3314-22 [19188669.001]
  • [Cites] Blood. 2009 Sep 17;114(12):2489-96 [19528532.001]
  • [Cites] PLoS Biol. 2009 Nov;7(11):e1000249 [19956800.001]
  • [Cites] Genes Dev. 2002 Jun 15;16(12):1518-27 [12080090.001]
  • [Cites] Cell. 2002 Jun 14;109(6):745-56 [12086673.001]
  • [Cites] Curr Biol. 2002 Jun 25;12(12):1052-8 [12123582.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):30421-4 [12097318.001]
  • [Cites] Mol Cell Biol. 2002 Sep;22(18):6542-52 [12192052.001]
  • [Cites] Blood. 2003 Jan 15;101(2):633-9 [12393557.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1820-5 [12574507.001]
  • [Cites] Genome Res. 2003 Mar;13(3):476-84 [12618378.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):161-71 [12620410.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4882-7 [12941810.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Biochem J. 2004 Feb 1;377(Pt 3):641-51 [14572310.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43296-306 [15292170.001]
  • [Cites] Oncogene. 1994 Nov;9(11):3159-66 [7936638.001]
  • [Cites] Mol Cell Biol. 1994 Dec;14(12):8304-14 [7969166.001]
  • [Cites] J Biol Chem. 2009 Dec 18;284(51):35659-69 [19864429.001]
  • (PMID = 21159644.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK080236; United States / NCI NIH HHS / CA / CA098459-06; United States / NIDDK NIH HHS / DK / DK080236-02; United States / NIDDK NIH HHS / DK / R01 DK080236-02; United States / NCI NIH HHS / CA / CA105049-05; United States / NIDDK NIH HHS / DK / DK080236-03; United States / NCI NIH HHS / CA / CA 105049; United States / NCI NIH HHS / CA / CA 098459; United States / NCI NIH HHS / CA / CA105049-04; United States / NCI NIH HHS / CA / R01 CA098459; United States / NIDDK NIH HHS / DK / R01 DK080236-03; United States / NCI NIH HHS / CA / P01 CA105049; United States / NCI NIH HHS / CA / P01 CA105049-04; United States / NCI NIH HHS / CA / P01 CA105049-05; United States / NCI NIH HHS / CA / R01 CA098459-06; United States / NIDDK NIH HHS / DK / DK 080236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / Dot1l protein, mouse; EC 2.1.1.- / Methyltransferases; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ NIHMS263101; NLM/ PMC3040779
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39. Patel A, Dharmarajan V, Vought VE, Cosgrove MS: On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex. J Biol Chem; 2009 Sep 4;284(36):24242-56
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  • [Title] On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.
  • The mixed lineage leukemia protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in acute leukemias.

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  • [Cites] Biophys J. 2000 Mar;78(3):1606-19 [10692345.001]
  • [Cites] J Biol Chem. 2008 Dec 12;283(50):35258-64 [18840606.001]
  • [Cites] Nature. 2000 Aug 10;406(6796):593-9 [10949293.001]
  • [Cites] Science. 2001 Sep 28;293(5539):2453-5 [11498546.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3286-95 [11751634.001]
  • [Cites] Curr Opin Genet Dev. 2002 Apr;12(2):198-209 [11893494.001]
  • [Cites] Nature. 2002 Sep 26;419(6905):407-11 [12353038.001]
  • [Cites] Cell. 2002 Oct 4;111(1):91-103 [12372303.001]
  • [Cites] Cell. 2002 Oct 4;111(1):105-15 [12372304.001]
  • [Cites] Cell. 2002 Oct 4;111(1):117-27 [12372305.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):140-9 [12482968.001]
  • [Cites] Nature. 2003 Feb 6;421(6923):652-6 [12540855.001]
  • [Cites] Nat Struct Biol. 2003 Mar;10(3):187-96 [12567185.001]
  • [Cites] Cell. 2003 Mar 7;112(5):711-23 [12628190.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):709-19 [12667453.001]
  • [Cites] Genes Dev. 2003 Apr 1;17(7):896-911 [12670868.001]
  • [Cites] Nat Struct Biol. 2003 Jul;10(7):545-52 [12819771.001]
  • [Cites] Mol Cell. 2003 Jul;12(1):177-85 [12887903.001]
  • [Cites] Mol Cell. 2003 Nov;12(5):1325-32 [14636589.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1591-8 [14690610.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]
  • [Cites] PLoS Biol. 2004 Jul;2(7):E171 [15252442.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6357-66 [8413234.001]
  • [Cites] EMBO J. 1994 Aug 15;13(16):3822-31 [7915232.001]
  • [Cites] Mech Dev. 1995 Aug;52(2-3):209-23 [8541210.001]
  • [Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]
  • [Cites] Anal Biochem. 1996 Jun 1;237(2):260-73 [8660575.001]
  • [Cites] Mol Biol Cell. 1997 Dec;8(12):2421-36 [9398665.001]
  • [Cites] Protein Expr Purif. 1999 Feb;15(1):34-9 [10024467.001]
  • [Cites] Nature. 2005 Jan 27;433(7024):434-8 [15647753.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):5563-70 [15590646.001]
  • [Cites] Cell. 2005 Jun 17;121(6):873-85 [15960975.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1444-54 [15933069.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1455-65 [15933070.001]
  • [Cites] Biophys J. 2005 Jul;89(1):619-34 [15863475.001]
  • [Cites] Genome Biol. 2005;6(8):227 [16086857.001]
  • [Cites] Mol Cell. 2009 Jan 30;33(2):181-91 [19187761.001]
  • [Cites] Biochemistry. 2000 Nov 14;39(45):13633-40 [11076501.001]
  • [Cites] Cell. 2005 Aug 26;122(4):517-27 [16122420.001]
  • [Cites] Plant Cell. 2005 Sep;17(9):2439-53 [16100335.001]
  • [Cites] Mol Cell. 2005 Sep 16;19(6):849-56 [16168379.001]
  • [Cites] PLoS Biol. 2005 Oct;3(10):e328 [16122352.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14765-70 [16199523.001]
  • [Cites] J Biol Chem. 2005 Dec 16;280(50):41725-31 [16253997.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6629-34 [16618927.001]
  • [Cites] J Mol Biol. 2006 May 26;359(1):86-96 [16603186.001]
  • [Cites] Nature. 2006 Jul 6;442(7098):96-9 [16728974.001]
  • [Cites] Nature. 2006 Jul 6;442(7098):86-90 [16728976.001]
  • [Cites] Nat Struct Mol Biol. 2006 Aug;13(8):713-9 [16878130.001]
  • [Cites] Nat Struct Mol Biol. 2006 Sep;13(9):852-4 [16892064.001]
  • [Cites] Nat Genet. 2007 Mar;39(3):311-8 [17277777.001]
  • [Cites] Biochemistry. 2007 Mar 27;46(12):3905-15 [17338551.001]
  • [Cites] Mutat Res. 2007 May 1;618(1-2):102-15 [17374386.001]
  • [Cites] J Biol Chem. 2007 May 4;282(18):13419-28 [17355966.001]
  • [Cites] J Biol Chem. 2007 Jul 13;282(28):20395-406 [17500065.001]
  • [Cites] Curr Opin Genet Dev. 2008 Apr;18(2):159-68 [18281209.001]
  • [Cites] J Biol Chem. 2008 Nov 21;283(47):32162-75 [18829457.001]
  • [Cites] J Biol Chem. 2008 Nov 21;283(47):32158-61 [18829459.001]
  • [Cites] Anal Chem. 2000 Jul 15;72(14):3311-9 [10939405.001]
  • (PMID = 19556245.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA140522
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2782018
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40. Stubbs MC, Kim YM, Krivtsov AV, Wright RD, Feng Z, Agarwal J, Kung AL, Armstrong SA: MLL-AF9 and FLT3 cooperation in acute myelogenous leukemia: development of a model for rapid therapeutic assessment. Leukemia; 2008 Jan;22(1):66-77
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  • [Title] MLL-AF9 and FLT3 cooperation in acute myelogenous leukemia: development of a model for rapid therapeutic assessment.
  • Human leukemias harboring chromosomal translocations involving the mixed lineage leukemia (MLL, HRX, ALL-1) gene possess high-level expression, and frequent activating mutations of the receptor tyrosine kinase FLT3.
  • We used a murine bone marrow transplant model to assess cooperation between MLL translocation and FLT3 activation.
  • We demonstrate that MLL-AF9 expression induces acute myelogenous leukemia (AML) in approximately 70 days, whereas the combination of MLL-AF9 and FLT3-ITD does so in less than 30 days.
  • Secondary transplantation of splenic cells from diseased mice established that leukemia stem cells are present at a very high frequency of approximately 1:100 in both diseases.
  • Importantly, prospectively isolated granulocyte macrophage progenitors (GMPs) coinfected with MLL-AF9 and FLT3-ITD give rise to a similar AML, with shorter latency than from GMP transduced with MLL-AF9 alone.
  • Cooperation between MLL-AF9 and FLT3-ITD was further verified by real-time assessment of leukemogenesis using noninvasive bioluminescence imaging.
  • We used this model to demonstrate that MLL-AF9/FLT3-ITD-induced leukemias are sensitive to FLT3 inhibition in a 2-3 week in vivo assay.
  • These data show that activated FLT3 cooperates with MLL-AF9 to accelerate onset of an AML from whole bone marrow as well as a committed hematopoietic progenitor, and provide a new genetically defined model system that should prove useful for rapid assessment of potential therapeutics in vivo.

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  • [Cites] Ann Hematol. 2004;83 Suppl 1:S75-6 [15124682.001]
  • [Cites] Semin Hematol. 2003 Oct;40(4):268-73 [14582077.001]
  • [Cites] Genes Dev. 2004 May 1;18(9):965-74 [15132992.001]
  • [Cites] Blood. 1993 May 1;81(9):2386-93 [8481519.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Nature. 1994 Nov 10;372(6502):143-9 [7969446.001]
  • [Cites] Nucleic Acids Res. 1996 May 1;24(9):1787-8 [8650001.001]
  • [Cites] Blood. 1996 May 15;87(10):4025-39 [8639758.001]
  • [Cites] Cell. 1996 Jun 14;85(6):853-61 [8681380.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4226-37 [9250666.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • [Cites] EMBO J. 1999 Jul 1;18(13):3564-74 [10393173.001]
  • [Cites] Br J Haematol. 1999 Sep;106(3):614-26 [10468849.001]
  • [Cites] Curr Biol. 2004 Nov 23;14(22):2063-9 [15556871.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] EMBO J. 2005 Jan 26;24(2):368-81 [15635450.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):919-29 [15761502.001]
  • [Cites] Blood. 2005 Jul 15;106(2):673-80 [15797998.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1085-8 [14504097.001]
  • [Cites] Blood. 2004 May 1;103(9):3544-6 [14670924.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Best Pract Res Clin Haematol. 2001 Mar;14(1):49-64 [11355923.001]
  • [Cites] Leukemia. 2001 Jun;15(6):987-9 [11417488.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Cancer Cell. 2002 Jun;1(5):433-43 [12124173.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:179-98 [12194988.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4882-7 [12941810.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2198-204 [12791658.001]
  • (PMID = 17851551.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA92551; United States / NCI NIH HHS / CA / CA092551-04; United States / NCI NIH HHS / CA / K08 CA092551; United States / NCI NIH HHS / CA / CA092551-05; United States / NCI NIH HHS / CA / K08 CA092551-05; United States / NCI NIH HHS / CA / K08 CA092551-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS230264; NLM/ PMC2936245
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41. Whitman SP, Ruppert AS, Marcucci G, Mrózek K, Paschka P, Langer C, Baldus CD, Wen J, Vukosavljevic T, Powell BL, Carroll AJ, Kolitz JE, Larson RA, Caligiuri MA, Bloomfield CD: Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study. Blood; 2007 Jun 15;109(12):5164-7
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  • [Title] Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study.
  • The clinical impact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults aged 18 to 59 years with cytogenetically normal (CN) de novo acute myeloid leukemia (AML) who were treated intensively on similar Cancer and Leukemia Group B protocols 9621 and 19808.
  • Twenty-four (10.1%) patients harbored an MLL-PTD.
  • Of those, 92% achieved complete remission (CR) compared with 83% of patients without MLL-PTD (P=.39).
  • Thirteen MLL-PTD(+) patients relapsed within 1.4 years of achieving CR.
  • MLL-PTD(+) patients who relapsed more often had other adverse CN-AML-associated molecular markers.
  • In contrast with previously reported studies, 9 (41%) MLL-PTD(+) patients continue in long-term first remission (CR1; range, 2.5-7.7 years).
  • Intensive consolidation therapy that included autologous peripheral stem-cell transplantation during CR1 may have contributed to the better outcome of this historically poor-prognosis group of CN-AML patients with MLL-PTD.

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  • [Cites] Leukemia. 2000 May;14(5):796-804 [10803509.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]
  • [Cites] Leukemia. 2003 Jan;17(1):76-82 [12529663.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4290-301 [15514371.001]
  • [Cites] Cancer Res. 1994 Jan 15;54(2):370-3 [8275471.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2707-16 [16981007.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):55-9 [9426057.001]
  • [Cites] Leukemia. 2002 Feb;16(2):196-202 [11840285.001]
  • (PMID = 17341662.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA098933; United States / NCI NIH HHS / CA / CA089341; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / U10 CA041287; United States / NCI NIH HHS / CA / R01 CA098933; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA096887
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1890839
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42. Starkova J, Zamostna B, Mejstrikova E, Krejci R, Drabkin HA, Trka J: HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL. Pediatr Blood Cancer; 2010 Dec 1;55(6):1072-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, HOX expression patterns in leukemia cells compared to normal lymphoid progenitors have not been systematically studied in acute lymphoblastic leukemia (ALL) subtypes.
  • HOXA3-4, HOXA7, and HOXB3-4 genes were differentially expressed between BCP-ALL and T-ALL subgroups, and among genotypically defined MLL/AF4, TEL/AML1, BCR/ABL, hyperdiploid and normal karyotype subgroups.
  • HOXA7 gene was low expressed at the RNA level in patients with hyperdiploid leukemia, whereas HOXB7 and CDX2 genes were low expressed in TEL/AML1-positive and BCR/ABL-positive cases, respectively.
  • In contrast to previous findings in acute myeloid leukemia, high HOXA RNA expression was associated with an excellent prognosis in Cox's regression model (P = 0.03).
  • In MLL/AF4-positive ALL, lower HOXA RNA expression correlated with the methylation status of their promoters.
  • CONCLUSIONS: HOX gene RNA expression cannot discriminate leukemia subgroups or relative maturity of leukemic cells.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 20672366.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / HOXB2 protein, human; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
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43. Chinen Y, Taki T, Nishida K, Shimizu D, Okuda T, Yoshida N, Kobayashi C, Koike K, Tsuchida M, Hayashi Y, Taniwaki M: Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA. Oncogene; 2008 Apr 3;27(15):2249-56
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  • [Title] Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
  • The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia.
  • We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA.
  • The LAF4 gene is a member of the AF4/FMR2 family and was previously identified as a fusion partner of MLL in B-precursor ALL with t(2;11)(q11;q23), although AML1-LAF4 was in T-ALL.
  • LAF4 is the first gene fused with both AML1 and MLL in acute leukemia.
  • Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22).
  • These findings provide new insight into the common mechanism of AML1 and MLL fusion proteins in the pathogenesis of ALL.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction / methods. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Child. DNA Mutational Analysis / methods. DNA, Complementary / analysis. Humans. Male. Models, Biological. Molecular Sequence Data

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  • (PMID = 17968322.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AFF3 protein, human; 0 / AML1-LAF4 fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
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44. Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML: Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus. J Clin Pathol; 2007 May;60(5):562-4
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  • [Title] Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
  • Myeloid sarcomas are tumour masses of myeloid leukaemic cells at extramedullary sites.
  • These tumours can, on occasion, occur without concurrent or antecedent leukaemia.
  • Myeloid sarcomas have been described at unusual locations including the female genital tract.
  • An unusual case of therapy-related acute myeloid leukaemia (t-AML) presenting as isolated monoblastic myeloid sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
  • Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a mixed-lineage leukaemia (MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
  • This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these myeloid sarcomas can be useful for risk assessment and guiding definitive therapy.

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  • [Cites] Am J Clin Pathol. 2000 Nov;114(5):807-11 [11068557.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):255-76 [11378539.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):1967-72 [12057901.001]
  • [Cites] Leuk Lymphoma. 2002 Nov;43(11):2151-3 [12533040.001]
  • [Cites] Int J Surg Pathol. 2003 Oct;11(4):271-82 [14615822.001]
  • [Cites] Leukemia. 2005 Feb;19(2):183-90 [15618964.001]
  • [Cites] Urology. 1986 Mar;27(3):268-70 [3082059.001]
  • [Cites] Gynecol Oncol. 1992 Jul;46(1):128-37 [1634133.001]
  • [Cites] Blood. 1993 Dec 15;82(12):3705-11 [8260707.001]
  • [Cites] Am J Clin Pathol. 1995 Oct;104(4):431-43 [7572794.001]
  • [Cites] Am J Surg Pathol. 1997 Oct;21(10):1156-65 [9331287.001]
  • [Cites] Leuk Res. 2004 Nov;28(11):1165-9 [15380340.001]
  • (PMID = 17513515.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994540
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45. Tracey L, Streck CJ, Du Z, Williams RF, Pfeffer LM, Nathwani AC, Davidoff AM: NF-kappaB activation mediates resistance to IFN beta in MLL-rearranged acute lymphoblastic leukemia. Leukemia; 2010 Apr;24(4):806-12
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  • [Title] NF-kappaB activation mediates resistance to IFN beta in MLL-rearranged acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) harboring the t(4;11) translocation is associated with a very poor prognosis; innovative treatment strategies are required to improve the current 5-year survival rate of 30-40%.
  • To overcome these limitations, we investigated the effect of continuous, gene transfer-mediated delivery of IFN beta using adeno-associated virus (AAV)-mediated expression, on ALL cells with the t(4;11) translocation.
  • We found that this method of IFN beta delivery resulted in complete remission of leukemia in a murine model.
  • Activation of NF-kappaB was identified as a mechanism for IFN beta resistance, and inhibition of NF-kappaB activity in resistant cells sensitized cells to IFN beta.
  • IFN beta combined with agents that inhibit NF-kappaB could have therapeutic potential in the treatment of children with mixed lineage leukemia subtype ALL.

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  • (PMID = 20130599.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] None / None / / R01 CA133322-02; United States / NCI NIH HHS / CA / R01 CA133322-02; United States / NCI NIH HHS / CA / R01 CA133322-01A1; United States / NCI NIH HHS / CA / R01 CA133322; United States / NCI NIH HHS / CA / CA21766; United States / NCI NIH HHS / CA / R01CA1333222-01A1; None / None / / R01 CA133322-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 77238-31-4 / Interferon-beta; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS262254; NLM/ PMC4657731
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46. Chen W, Wang E, Lu Y, Gaal KK, Huang Q: Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review. Am J Clin Pathol; 2010 Jan;133(1):75-82
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  • [Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.
  • Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.
  • However, t-ALL cases without 11q23 abnormality have been rarely described.
  • We describe 6 adults with secondary t-ALL without 11q23 abnormalities following various treatment regimens for primary malignancies.
  • In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).
  • Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.
  • [MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20023261.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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47. Matsuda K, Hidaka E, Ishida F, Yamauchi K, Makishima H, Ito T, Suzuki T, Imagawa E, Sano K, Katsuyama T, Ota H: A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion. Cancer Genet Cytogenet; 2006 Nov;171(1):24-30
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  • [Title] A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion.
  • Structural abnormalities involving the mixed-lineage leukemia (MLL) gene on 11q23 have been associated with hematological malignancies.
  • The rearrangement of MLL occurs during translocations and insertions involving a variety of genes on the partner chromosome.
  • We report a rare case of acute myelogenous leukemia (AML-M2) with 11q23 abnormalities.
  • Fluorescence in situ hybridization (FISH) using a commercial dual-color MLL probe detected an atypical signal pattern: one fusion signal, two green signals smaller than those usually detected, and no orange signals.
  • Spectral karyotyping (SKY) analysis indicated that one green signal was detected on the short arm of derivative chromosome 10, and the other green signal on the long arm of a derivative chromosome 11, on which no orange signal was detected.
  • A long-distance inverse polymerase chain reaction (LDI-PCR) identified the fusion partner gene, in which intron 6 of MLL was fused with intron 8 of AF10 on 10p12 in the 5' to 3' direction.
  • Our observations indicated that the MLL-AF10 fusion gene resulted from the insertion of part of the region that included the 5' MLL insertion into 10p12; this was concurrent with the deletion of 3' MLL.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Gene Deletion. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Amino Acid Sequence. Base Sequence. Chromosome Aberrations. Chromosome Banding. Chromosome Breakage. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Male. Mutagenesis, Insertional / genetics. Sequence Analysis, DNA. Spectral Karyotyping / methods. Transcription Factors / genetics

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  • (PMID = 17074587.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF10 fusion protein, human; 0 / MLLT10 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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48. Jo A, Tsukimoto I, Ishii E, Asou N, Mitani S, Shimada A, Igarashi T, Hayashi Y, Ichikawa H: Age-associated difference in gene expression of paediatric acute myelomonocytic lineage leukaemia (FAB M4 and M5 subtypes) and its correlation with prognosis. Br J Haematol; 2009 Mar;144(6):917-29
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  • [Title] Age-associated difference in gene expression of paediatric acute myelomonocytic lineage leukaemia (FAB M4 and M5 subtypes) and its correlation with prognosis.
  • Acute myeloid leukaemia, French-American-British M4 and M5 subtypes (AML-M4/M5) is frequently associated with MLL gene rearrangement and its incidence is relatively high among infants.
  • All subgroups included patients with MLL gene rearrangement as well as normal and other karyotypes.
  • Surprisingly, gene expression signatures of MLL gene rearrangement differed substantially among these subgroups.
  • In addition, subgroup C presented extremely poor outcome (3-year event-free survival 28%) whilst eight patients with MLL gene rearrangement in subgroup C had all relapsed within 18 months.
  • [MeSH-major] Gene Expression Profiling. Gene Rearrangement. Leukemia, Myelomonocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19120366.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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49. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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  • [Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
  • We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
  • The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.
  • The BM blasts showed a complex "karyotype," including dic(17;20) (p11;q11), -5 and add (11q23).
  • Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).
  • For the MLL gene, southern blot analysis showed that the MLL gene locus was amplified but not rearranged at its breakpoint cluster region, which is usually rearranged in balanced translocations with many partner genes.
  • These findings suggest that MLL gene amplification may in this case be based on the genetic instability caused by the preceding biallelic loss of the wild type p53 gene.
  • [MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Marrow. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Genes, p53. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 20505276.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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50. Ono R, Nakajima H, Ozaki K, Kumagai H, Kawashima T, Taki T, Kitamura T, Hayashi Y, Nosaka T: Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis. J Clin Invest; 2005 Apr;115(4):919-29
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  • [Title] Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.
  • The mechanisms by which mixed-lineage leukemia (MLL) fusion products resulting from in utero translocations in 11q23 contribute to leukemogenesis and infant acute leukemia remain elusive.
  • It is still controversial whether the MLL fusion protein is sufficient to induce acute leukemia without additional genetic alterations, although carcinogenesis in general is known to result from more than 1 genetic disorder accumulating during a lifetime.
  • Here we demonstrate that the fusion partner-mediated homo-oligomerization of MLL-SEPT6 is essential to immortalize hematopoietic progenitors in vitro.
  • MLL-SEPT6 induced myeloproliferative disease with long latency in mice, but not acute leukemia, implying that secondary genotoxic events are required to develop leukemia.
  • We developed in vitro and in vivo model systems of leukemogenesis by MLL fusion proteins, where activated FMS-like receptor tyrosine kinase 3 (FLT3) together with MLL-SEPT6 not only transformed hematopoietic progenitors in vitro but also induced acute biphenotypic or myeloid leukemia with short latency in vivo.
  • In these systems, MLL-ENL, another type of the fusion product that seems to act as a monomer, also induced the transformation in vitro and leukemogenesis in vivo in concert with activated FLT3.
  • These findings show direct evidence for a multistep leukemogenesis mediated by MLL fusion proteins and may be applicable to development of direct MLL fusion-targeted therapy.
  • [MeSH-major] Cell Transformation, Neoplastic. DNA-Binding Proteins. GTP-Binding Proteins. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion. Proto-Oncogene Proteins / metabolism. Proto-Oncogenes. Receptor Protein-Tyrosine Kinases / metabolism. Recombinant Fusion Proteins. Transcription Factors
  • [MeSH-minor] Animals. Cell Transplantation. Cells, Cultured. Cytoskeletal Proteins. DNA Damage. Dimerization. Enzyme Activation. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Histone-Lysine N-Methyltransferase. Humans. Infant. Liver / pathology. Liver / physiology. Mice. Mice, Inbred C57BL. Myeloid-Lymphoid Leukemia Protein. Protein Structure, Tertiary. Septins. Spleen / pathology. Spleen / physiology. fms-Like Tyrosine Kinase 3

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  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6428-33 [10339604.001]
  • [Cites] EMBO J. 1999 Sep 1;18(17):4754-65 [10469654.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Dev Cell. 2002 Dec;3(6):791-802 [12479805.001]
  • [Cites] J Biol Chem. 2003 Jan 31;278(5):3483-8 [12446710.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(8):2969-80 [12665593.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3229-35 [12515728.001]
  • [Cites] Dev Cell. 2003 Apr;4(4):549-60 [12689593.001]
  • [Cites] Cancer Cell. 2003 May;3(5):449-58 [12781363.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Sep;38(1):8-12 [12874781.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):32892-8 [12815052.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2298-307 [12952893.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Nov;38(3):253-9 [14506700.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Exp Hematol. 2003 Nov;31(11):1007-14 [14585362.001]
  • [Cites] Cell. 2003 Oct 31;115(3):293-303 [14636557.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1085-8 [14504097.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4261-5 [10485469.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):368-80 [11071359.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Sep;32(1):82-8 [11477664.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):333-7 [11809673.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Oncogene. 2002 Jul 11;21(30):4706-14 [12096348.001]
  • [Cites] EMBO J. 2002 Aug 15;21(16):4297-306 [12169632.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2393-8 [12239147.001]
  • [Cites] Curr Biol. 2002 Oct 29;12(21):1858-63 [12419187.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1286-95 [14576045.001]
  • [Cites] Leukemia. 2004 May;18(5):998-1005 [14999297.001]
  • [Cites] Genes Dev. 2004 May 1;18(9):965-74 [15132992.001]
  • [Cites] Nature. 1981 Apr 2;290(5805):372-8 [6783959.001]
  • [Cites] Blood. 1986 Jan;67(1):1-11 [3079640.001]
  • [Cites] Cell. 1992 Nov 13;71(4):691-700 [1423624.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • [Cites] Cell. 1996 Jun 14;85(6):853-61 [8681380.001]
  • [Cites] Blood. 1997 May 1;89(9):3361-70 [9129043.001]
  • [Cites] Genes Dev. 1997 Jun 15;11(12):1535-47 [9203580.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4226-37 [9250666.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • (PMID = 15761502.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.1.- / SEPT6 protein, human; EC 3.6.1.- / Septins
  • [Other-IDs] NLM/ PMC1062890
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51. Santamaría CM, Chillón MC, García-Sanz R, Pérez C, Caballero MD, Ramos F, de Coca AG, Alonso JM, Giraldo P, Bernal T, Queizán JA, Rodriguez JN, Fernández-Abellán P, Bárez A, Peñarrubia MJ, Balanzategui A, Vidriales MB, Sarasquete ME, Alcoceba M, Díaz-Mediavilla J, San Miguel JF, Gonzalez M: Molecular stratification model for prognosis in cytogenetically normal acute myeloid leukemia. Blood; 2009 Jul 2;114(1):148-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular stratification model for prognosis in cytogenetically normal acute myeloid leukemia.
  • We have evaluated 9 new molecular markers (ERG, EVI1, MLL-PTD, MN1, PRAME, RHAMM, and WT1 gene-expression levels plus FLT3 and NPM1 mutations) in 121 de novo cytogenetically normal acute myeloblastic leukemias.
  • In the multivariate analysis, high ERG or EVI1 and low PRAME expressions were associated with a shorter relapse-free survival (RFS) and overall survival (OS).
  • Here we propose a new molecular score for cytogenetically normal acute myeloblastic leukemias, which could improve patient risk-stratification.
  • [MeSH-major] Biomarkers, Tumor / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic

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  • (PMID = 19398719.001).
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Genetic Markers; 0 / MECOM protein, human; 0 / PRAME protein, human; 0 / Trans-Activators; 0 / Transcription Factors
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52. Manola KN, Georgakakos VN, Stavropoulou C, Spyridonidis A, Angelopoulou MK, Vlachadami I, Katsigiannis A, Roussou P, Pantelias GE, Sambani C: Jumping translocations in hematological malignancies: a cytogenetic study of five cases. Cancer Genet Cytogenet; 2008 Dec;187(2):85-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These cases involve JT of 1q in a case of acute myeloblastic leukemia (AML)-M1, a case of Burkitt lymphoma, and a case of BCR/ABL-positive acute lymphoblastic leukemia, as well as a JT of 13q in a case of AML-M5, and a JT of 11q segment in a case of undifferentiated leukemia.
  • To our knowledge, with regard to hematologic malignancies, this study presents the first case of JT associated with AML-M1, the first case of JT involving 13q as a donor chromosome, and the first report of JT involving a segment of 11q containing two copies of the MLL gene, jumping on to two recipient chromosomes in each cell line and resulting in six copies of the MLL gene.
  • Our investigation suggests that JT may not contribute to the pathogenesis but rather to the progression of the disease, and it demonstrates that chromosome band 1q10 as a breakpoint of the donor chromosome 1q is also implicated in AML, not only in multiple myeloma as it has been known until now.
  • [MeSH-minor] Adult. Aged. Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Cytogenetic Analysis. Female. Humans. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Young Adult

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  • (PMID = 19027489.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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53. Schnittger S, Bacher U, Haferlach C, Kern W, Haferlach T: Rare CBFB-MYH11 fusion transcripts in AML with inv(16)/t(16;16) are associated with therapy-related AML M4eo, atypical cytomorphology, atypical immunophenotype, atypical additional chromosomal rearrangements and low white blood cell count: a study on 162 patients. Leukemia; 2007 Apr;21(4):725-31
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  • The spectrum of CBFB-MYH11 fusion transcripts in acute myeloid leukemia (AML) M4eo with inv(16)/t(16;16) is heterogeneous.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. Core Binding Factor beta Subunit / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Leukocytes / pathology. Myosin Heavy Chains / genetics. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 17287858.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; EC 3.6.4.1 / Myosin Heavy Chains
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54. Whelan JT, Ludwig DL, Bertrand FE: HoxA9 induces insulin-like growth factor-1 receptor expression in B-lineage acute lymphoblastic leukemia. Leukemia; 2008 Jun;22(6):1161-9
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  • [Title] HoxA9 induces insulin-like growth factor-1 receptor expression in B-lineage acute lymphoblastic leukemia.
  • Deregulation of Hox gene expression is frequently associated with acute leukemia.
  • HoxA9 is the most commonly overexpressed Hox gene in acute leukemia.
  • IGF-1R expression correlated with endogenous HoxA9 expression in a small panel of mixed lineage leukemia (MLL)/AF4 cell lines. siRNA knockdown of endogenous HoxA9 expression in the MLL/AF4-positive cell line RS4;11 resulted in loss of IGF-1R expression.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / physiology. Homeodomain Proteins / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, IGF Type 1 / genetics
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Blotting, Southern. Blotting, Western. Cell Proliferation. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoprecipitation. Insulin-Like Growth Factor I / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism. Phosphorylation. Proto-Oncogene Proteins c-myc. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Retroviridae / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / metabolism. Tumor Cells, Cultured

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  • (PMID = 18337761.001).
  • [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 / Antibodies, Monoclonal; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / MYC protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1
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55. Mulloy JC, Wunderlich M, Zheng Y, Wei J: Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling. Cell Cycle; 2008 Nov 1;7(21):3314-9
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  • [Title] Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.
  • MLL-AF9 (MA9) is a leukemia fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11.
  • MA9 is commonly found in acute myeloid leukemia (AML) and occasionally in acute lymphoid leukemia and is associated with intermediate to poor outcome.
  • We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to acute myeloid or lymphoid leukemia when injected into immunodeficient mice.
  • The Mixed Lineage Leukemia (MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other leukemia-associated oncogenes tested thus far have induced only partial phenotypes.
  • Here we provide an update on the use of this system for modeling human leukemia and its potential application for therapeutic testing of novel compounds to treat the disease.

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  • [Cites] Leukemia. 2002 Sep;16(9):1818-26 [12200698.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2029-40 [18685615.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7618-23 [15128949.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] EMBO J. 1994 Feb 15;13(4):928-33 [8112307.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Nature. 1999 Jul 29;400(6743):464-8 [10440377.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1166-73 [16234360.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]
  • [Cites] Exp Hematol. 2007 May;35(5):782-92 [17577927.001]
  • [Cites] Exp Hematol. 2007 Oct;35(10):1538-49 [17889721.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):467-78 [17996650.001]
  • [Cites] Methods Enzymol. 2008;439:365-93 [18374178.001]
  • [Cites] Cancer Cell. 2008 May;13(5):432-40 [18455126.001]
  • [Cites] Leukemia. 2008 May;22(5):898-904 [18354486.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1803-6 [18668135.001]
  • [Cites] Leukemia. 2003 Apr;17(4):760-3 [12682634.001]
  • (PMID = 18948748.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA118319; United States / NCI NIH HHS / CA / K01 CA090370; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NCI NIH HHS / CA / CA118319-04; United States / NCI NIH HHS / CA / R01 CA118319-04; United States / NCI NIH HHS / CA / CA118319; United States / NCI NIH HHS / CA / CA90370
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / rac GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS169825; NLM/ PMC2812025
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56. Burmeister T, Meyer C, Thiel G, Reinhardt R, Thiel E, Marschalek R: A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32). Blood Cells Mol Dis; 2008 Sep-Oct;41(2):210-4
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  • [Title] A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32).
  • MLL aberrations are found in approximately 10% of acute leukemias.
  • More than 80 different MLL fusion genes have been cytogenetically described but a significant number of MLL fusion partners remain unidentified on the molecular level.
  • We describe here the case of a patient who developed secondary acute myeloid leukemia five years after the patient had received adjuvant radiochemotherapy because of breast cancer.
  • Cytogenetic bone marrow analysis revealed a translocation t(11;14)(q23;q32), with a MLL split signal in FISH analysis.
  • Both breakpoints, on chromosomes 11 and 14, were characterized.
  • The breakpoint in the KIAA0284 gene was located 5' of the putative start codon and an in-frame MLL-KIAA0284 transcript was detectable by RT-PCR.
  • The KIAA0284 gene has hitherto not been implicated in hematologic diseases and has never been reported as a translocation partner.
  • The expression of KIAA0284 in various tissues and hematologic diseases was investigated by real time quantitative PCR and turned out to be very low in all lymphatic and myeloid diseases investigated.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Breast Neoplasms / pathology. Breast Neoplasms / therapy. Chromosome Breakage. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Female. Histone-Lysine N-Methyltransferase. Humans. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 18640063.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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57. Strehl S, König M, Meyer C, Schneider B, Harbott J, Jäger U, von Bergh AR, Loncarevic IF, Jarosova M, Schmidt HH, Moore SD, Marschalek R, Haas OA: Molecular dissection of t(11;17) in acute myeloid leukemia reveals a variety of gene fusions with heterogeneous fusion transcripts and multiple splice variants. Genes Chromosomes Cancer; 2006 Nov;45(11):1041-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular dissection of t(11;17) in acute myeloid leukemia reveals a variety of gene fusions with heterogeneous fusion transcripts and multiple splice variants.
  • The majority of translocations that involve the long arms of chromosomes 11 and 17 in acute myeloid leukemia appear identical on the cytogenetic level.
  • At present, two genes are known in 11q23 and four in 17q12-25 that generate five distinct fusion genes: MLL-MLLT6/AF17, MLL-LASP1, MLL-ACACA or MLL-SEPT9/MSF, and ZBTB16/PLZF-RARA.
  • We analyzed 14 cases with a t(11;17) by fluorescence in situ hybridization and molecular genetic techniques and determined the molecular characteristics of their fusion genes.
  • We identified six different gene fusions that comprised seven cases with a MLL-MLLT6/AF17, three with a MLL-SEPT9/MSF, and one each with MLL-LASP1, MLL-ACACA, and ZBTB16/PLZF-RARA fusions.
  • In the remaining case, a MLL-SEPT6/Xq24 fusion suggested a complex rearrangement.
  • The MLL-MLLT6/AF17 transcripts were extremely heterogeneous and the detection of seven different in-frame transcript and splice variants enabled us to predict the protein domains relevant for leukemogenesis.
  • The putative MLL-MLLT6 consensus chimeric protein consists of the AT-hook DNA-binding, the methyltransferase, and the CXXC zinc-finger domains of MLL and the highly conserved octapeptide and the leucine-zipper dimerization motifs of MLLT6.
  • The MLL-SEPT9 transcripts showed a similar high degree of variability.
  • These analyses prove that the diverse types of t(11;17)-associated fusion genes can be reliably identified and delineated with a proper combination of cytogenetic and molecular genetic techniques.
  • The heterogeneity of transcripts encountered in cases with MLL-MLLT6/AF17 and MLL-SEPT9/MSF fusions clearly demonstrates that thorough attention has to be paid to the appropriate selection of primers to cover all these hitherto unrecognized fusion variants.
  • [MeSH-major] Alternative Splicing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Humans. In Situ Hybridization. Infant. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16897742.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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58. Marques-Salles Tde J, Mkrtchyan H, Leite EP, Soares-Ventura EM, Muniz MT, Silva EF, Liehr T, Silva ML, Santos N: Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis. Cancer Genet Cytogenet; 2010 Jul 15;200(2):167-9
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  • [Title] Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis.
  • Acute myeloid leukemia in childhood is a heterogeneous group of diseases, and different epidemiologic factors are involved in the etiopathogenesis.
  • Genetic syndromes are one of the predisposing factors of acute myeloid leukemia (AML), including Down syndrome, Bloom syndrome, and neurofibromatosis.
  • Acute megakaryoblastic leukemia (AMKL) is the main subtype in Down syndrome infants, and acquired chromosomal anomalies are closely related to the physiopathology of the illness.
  • The main chromosomal anomalies in AMKL are structural, such as t(1;22); however, complex karyotypes are also common.
  • Here we describe the case of an infant with neurofibromatosis developing AMKL with a complex karyotype including 5q and 17q deletions, TP53 deletion, and an unusual unbalanced chromosomal translocation t(11;19)(q13;p13), leading to three copies of the MLL gene.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Megakaryoblastic, Acute / genetics. Neurofibromatoses / genetics
  • [MeSH-minor] Female. Genes, p53. Histone-Lysine N-Methyltransferase. Humans. Infant. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20620601.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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59. Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG: A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial. Lancet; 2007 Jul 21;370(9583):240-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
  • BACKGROUND: Acute lymphoblastic leukaemia in infants younger than 1 year is rare, and infants with the disease have worse outcomes than do older children.
  • We initiated an international study to investigate the effects of a new hybrid treatment protocol with elements designed to treat both acute lymphoblastic leukaemia and acute myeloid leukaemia, and to identify any prognostic factors for outcome in infants.
  • Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given a hybrid regimen based on the standard protocol for acute lymphoblastic leukaemia, with some elements designed for treatment of acute myeloid leukaemia.
  • All types of rearrangements in the (mixed lineage leukaemia) MLL gene, very high white blood cell count, age of younger than 6 months, and a poor response to the prednisone prophase were independently associated with inferior outcomes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [CommentIn] Lancet. 2007 Jul 21;370(9583):198-200 [17658376.001]
  • (PMID = 17658395.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
  • [Grant] United Kingdom / Medical Research Council / / G0300130
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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60. Stasevich I, Utskevich R, Kustanovich A, Litvinko N, Savitskaya T, Chernyavskaya S, Saharova O, Aleinikova O: Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism. Cancer Genet Cytogenet; 2006 Sep;169(2):114-20
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  • [Title] Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism.
  • Using both conventional and molecular cytogenetic methods, we found five new cases of t(10;11)(p12;q23).
  • This translocation represented 28% of all cases of childhood AML treated at our center in 2004, and 63% of AML with rearrangements of 11q23.
  • One patient showed a cytogenetically cryptic insertion of 5' part of MLL into the 3' part of MLLT10 in 10p12.
  • The median event-free survival of patients was 8.1 months, and we conclude that the t(10;11)(p12;q23) is associated with unfavorable prognosis in childhood acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16938568.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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61. Alonso CN, Longo PL, Gallego MS, Medina A, Felice MS: A novel AF9 breakpoint in MLL-AF9-positive acute monoblastic leukemia. Pediatr Blood Cancer; 2008 Apr;50(4):869-71
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  • [Title] A novel AF9 breakpoint in MLL-AF9-positive acute monoblastic leukemia.
  • MLL-AF9 is the most frequent MLL rearrangement in childhood acute myeloid leukemia (AML) and it may be also found in acute lymphoblastic leukemia (ALL) of patients younger than 1-year-old (infants).
  • The occurrence of this new breakpoint should be considered when designing RT-PCR assays for the screening of MLL abnormalities.
  • The precise characterization of the MLL-AF9 transcript is important to carry out the minimal residual disease analysis during the follow-up of the patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18000862.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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62. Cleary ML: Regulating the leukaemia stem cell. Best Pract Res Clin Haematol; 2009 Dec;22(4):483-7
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  • [Title] Regulating the leukaemia stem cell.
  • Leukaemia stem cells (LSCs) are responsible for sustaining and propagating malignant disease, and, as such, are promising targets for therapy.
  • LSCs in acute myeloid leukaemia (AML) have recently been studied using mouse syngeneic models of leukaemia induced by MLL oncogenes.

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  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Br J Haematol. 1999 Sep;106(3):614-26 [10468849.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Science. 2007 Jul 20;317(5836):337 [17641192.001]
  • [Cites] Cell Stem Cell. 2008 Apr 10;2(4):333-44 [18397753.001]
  • [Cites] Nat Genet. 2008 May;40(5):499-507 [18443585.001]
  • [Cites] Blood. 2008 Aug 1;112(3):568-75 [18523148.001]
  • [Cites] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802.001]
  • [Cites] Exp Hematol. 2000 Jun;28(6):660-71 [10880752.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10984-9 [10995463.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1849-56 [12738660.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Trends Mol Med. 2004 Oct;10(10):500-7 [15464450.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1166-73 [16234360.001]
  • (PMID = 19959097.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 16
  • [Other-IDs] NLM/ NIHMS157679; NLM/ PMC2802107
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63. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • However, the incidence and type of MLL rearrangements have not been determined in common ALL (cALL) and CD10+ or CD10- pre-B ALL.
  • EXPERIMENTAL DESIGN: To address this question, we analyzed 29 patients with pro-B ALL, 11 patients with CD10- pre-B ALL, 23 pre-B, and 26 cALL patients with CD10 on 20% to 80%, as well as 136 pre-B and 143 cALL patients with CD10 > or = 80% of blasts.
  • Conventional cytogenetics were done to detect 11q23 abnormalities and in parallel the potential involvement of the MLL gene was evaluated with a split apart fluorescence in situ hybridization probe set.
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • However, no 11q23/MLL translocation was identified among the CD10+ pre-B and cALL patients.
  • MLL-rearranged pro-B and CD10- pre-B ALL cases had similar clinical and immunophenotypic (coexpression of CDw65 and CD15) features at initial diagnosis.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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64. Sagawa M, Shimizu T, Shimizu T, Awaya N, Mitsuhashi T, Ikeda Y, Okamoto S, Kizaki M: Establishment of a new human acute monocytic leukemia cell line TZ-1 with t(1;11)(p32;q23) and fusion gene MLL-EPS15. Leukemia; 2006 Sep;20(9):1566-71
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  • [Title] Establishment of a new human acute monocytic leukemia cell line TZ-1 with t(1;11)(p32;q23) and fusion gene MLL-EPS15.
  • Human leukemia cell lines are of great value in investigating basic and applied aspects of cell biology and clinical medicine.
  • There have been 37 leukemia cell lines carrying 11q23 translocation and MLL rearrangements; however, cell lines harboring with t(1;11)(p32;q23) have not been established.
  • We report here for the first time a new acute monocytic leukemia (AMoL) cell line with t(1;11)(p32;q23), designated TZ-1, and herein describe its biological characteristics.
  • Mononuclear cells isolated from the ascites from a patient with AMoL (French-American-British classification; acute myeloid leukemia M5a) were isolated and passaged by liquid culture medium for a year.
  • TZ-1 cells revealed typical monocytic features in morphology and had a t(1;11)(p32;q23) translocation.
  • The immunoprofiling as determined by flow cytometry showed that TZ-1 cells are positive for myeloid and monocytic markers with lymphoid-associated markers.
  • Fluorescence in situ hybridization and reverse transcription-polymerase chain reaction analyses revealed MLL-EPS15 fusion transcript and protein.
  • Taken together, these results suggest that TZ-1 is a new monocytic leukemia cell line with t(1;11) translocation and fusion gene MLL-EPS15.
  • The established cell line, TZ-1, could provide a valuable model in the analysis of the pathogenesis of MLL-EPS15-positive leukemia and in the development of new agents for this type of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Monocytic, Acute / pathology. Translocation, Genetic

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  • (PMID = 16826222.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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65. Shimada A, Taki T, Tabuchi K, Taketani T, Hanada R, Tawa A, Tsuchida M, Horibe K, Tsukimoto I, Hayashi Y: Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group. Pediatr Blood Cancer; 2008 Feb;50(2):264-9
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  • [Title] Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.
  • BACKGROUND: Mixed-lineage leukemia (MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult acute myeloid leukemia (AML), but its relationship to pediatric AML is unknown.
  • PROCEDURE: One hundred fifty-eight newly diagnosed AML patients, including 13 FAB-M3 and 10 Down syndrome (DS) patients, who were treated on the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed for MLL-PTD, as well as internal tandem duplication (ITD) and the kinase domain mutation (D835Mt) in the FLT3 gene.
  • RESULTS: We found MLL-PTD in 21 (13.3%) of 158 AML patients, but not in FAB-M3 or DS patients.
  • The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018), disease-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.
  • AML patients with MLL-PTD were also correlated with poor prognosis in this study.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763464.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 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 / fms-Like Tyrosine Kinase 3
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66. Bueno C, Montes R, Martín L, Prat I, Hernandez MC, Orfao A, Menendez P: NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic cell precursors: is NG2 expression in leukemia dependent on the target cell where leukemogenesis is triggered? Leukemia; 2008 Aug;22(8):1475-8
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  • [Title] NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic cell precursors: is NG2 expression in leukemia dependent on the target cell where leukemogenesis is triggered?
  • [MeSH-major] Antigens / immunology. Antigens, CD34 / immunology. Dendritic Cells / immunology. Leukemia, Biphenotypic, Acute / immunology. Proteoglycans / immunology
  • [MeSH-minor] Cell Line, Tumor. Flow Cytometry. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 18698324.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Editorial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD34; 0 / MLL protein, human; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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67. Stam RW, den Boer ML, Passier MM, Janka-Schaub GE, Sallan SE, Armstrong SA, Pieters R: Silencing of the tumor suppressor gene FHIT is highly characteristic for MLL gene rearranged infant acute lymphoblastic leukemia. Leukemia; 2006 Feb;20(2):264-71
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  • [Title] Silencing of the tumor suppressor gene FHIT is highly characteristic for MLL gene rearranged infant acute lymphoblastic leukemia.
  • MLL rearranged acute lymphoblastic leukemia (MLL) is an aggressive type of acute lymphoblastic leukemia (ALL), diagnosed predominantly in infants (<1 years of age).
  • Since current chemotherapy fails in >50% of patients with MLL, new therapeutic strategies are desperately needed.
  • For this, understanding the biological features characterizing MLL is necessary.
  • Analysis of gene expression profiles revealed that the expression of the tumor suppressor gene FHIT is reduced in children with MLL rearranged ALL as compared to ALL patients carrying germ line MLL.
  • In 100% of the infant MLL cases tested, methylation of the FHIT 5'CpG region was observed, resulting in strongly reduced mRNA and protein expression.
  • In contrast, FHIT methylation in infant and non-infant ALL patients carrying germ line MLL was found in only approximately 60% (P< or =0.004).
  • Likewise and more specifically, leukemic cell death was induced by transfecting MLL rearranged leukemic cells with expression vectors encoding wild-type FHIT, confirming tumor suppressor activity of this gene.
  • These observations imply that suppression of FHIT may be required for the development of MLL, and provide new insights into leukemogenesis and therapeutic possibilities for MLL.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. Gene Silencing. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16357833.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / fragile histidine triad protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.- / Acid Anhydride Hydrolases
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68. Tobal K: Prognostic value of minimal residual disease monitoring in acute myeloid leukemia patients with t(9;11)(p22;q23). Haematologica; 2005 Dec;90(12):1586A
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  • [Title] Prognostic value of minimal residual disease monitoring in acute myeloid leukemia patients with t(9;11)(p22;q23).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / blood. Oncogene Proteins, Fusion / blood. Translocation, Genetic

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  • [CommentOn] Haematologica. 2005 Dec;90(12):1626-34 [16330435.001]
  • (PMID = 16330423.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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69. Brown P, Levis M, McIntyre E, Griesemer M, Small D: Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner. Leukemia; 2006 Aug;20(8):1368-76
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  • [Title] Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner.
  • Mixed lineage leukemia (MLL) rearrangements occur in 80% of infants and 5% of older children with acute lymphoblastic leukemia (ALL).
  • The FLT3 kinase is overexpressed and constitutively activated in MLL-rearranged ALL cells.
  • To identify potentially synergistic combination strategies, we studied CEP-701 and six standard chemotherapeutic agents in three sequences of exposure (S1: chemotherapy followed by CEP-701, S2: simultaneous exposure to both; and S3: CEP-701 followed by chemotherapy) using MLL-rearranged ALL cell lines and patient bone marrow samples.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carbazoles / administration & dosage. Indoles / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors

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  • (PMID = 16761017.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA70970
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; 0 / MLL protein, human; 0 / Protein Kinase Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; DO989GC5D1 / lestaurtinib; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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70. Thiede C: MLL-PTD as a marker for minimal residual disease studies: quantification counts. Haematologica; 2005 Jul;90(7):865B
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  • [Title] MLL-PTD as a marker for minimal residual disease studies: quantification counts.
  • [MeSH-major] Biomarkers, Tumor. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • [CommentOn] Haematologica. 2005 Jul;90(7):881-9 [15996925.001]
  • (PMID = 15996915.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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71. Vey N, Thomas X, Picard C, Kovascovicz T, Charin C, Cayuela JM, Dombret H, Dastugue N, Huguet F, Bastard C, Stamatoulas A, Giollant M, Tournilhac O, Macintyre E, Buzyn A, Bories D, Kuentz M, Dreyfus F, Delannoy A, Raynaud S, Gratecos N, Bordessoule D, de Botton S, Preudhomme C, Reman O, Troussard X, Pigneux A, Bilhou C, Vernant JP, Boucheix C, Gabert J, GET-LALA Group the Swiss Group for Clinical Cancer Research (SAKK): Allogeneic stem cell transplantation improves the outcome of adults with t(1;19)/E2A-PBX1 and t(4;11)/MLL-AF4 positive B-cell acute lymphoblastic leukemia: results of the prospective multicenter LALA-94 study. Leukemia; 2006 Dec;20(12):2155-61
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  • [Title] Allogeneic stem cell transplantation improves the outcome of adults with t(1;19)/E2A-PBX1 and t(4;11)/MLL-AF4 positive B-cell acute lymphoblastic leukemia: results of the prospective multicenter LALA-94 study.
  • Adult patients with acute lymphoblastic leukemia (ALL) and t(1;19)/E2A-PBX1 or t(4;11)/MLL-AF4 have a poor outcome.
  • We have evaluated the impact of an intensified post-remission therapy using a high-dose chemotherapy course followed by allogeneic or autologous SCT on the outcome of 58 patients with t(1;19)/E2A-PBX1 (E2A group, n=24) or t(4;11)/MLL-AF4 (MLL group, n=34) treated in the LALA-94 multicenter prospective study.
  • Patients in the MLL group had higher WBC counts and more frequent DIC.
  • CR rates achieved by MLL and E2A groups were similar to other B-cell ALL (87, 82 and 86% respectively).
  • While in CR, patients with a donor were assigned to alloSCT (n=22), the remaining patients with were randomized between autoSCT (n=15) or chemotherapy (n=8).
  • Five-year overall survival was 31 and 45% for E2A and MLL groups, respectively.
  • The results of this study show that chemotherapy intensification did not overcome the poor prognosis of adults with t(1;19)/E2A-PBX1.
  • Allogeneic SCT should thus be offered in first CR to patients with t(1;19)/E2A-PBX1 or t(4;11)/MLL-AF4.
  • [MeSH-minor] Adolescent. Adult. Basic Helix-Loop-Helix Transcription Factors / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Prospective Studies. Proto-Oncogene Proteins / genetics. Transplantation, Homologous

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  • (PMID = 17039234.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / TCF3 protein, human; 0 / pbx1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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72. Kern W, Estey EH: High-dose cytosine arabinoside in the treatment of acute myeloid leukemia: Review of three randomized trials. Cancer; 2006 Jul 1;107(1):116-24
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  • [Title] High-dose cytosine arabinoside in the treatment of acute myeloid leukemia: Review of three randomized trials.
  • BACKGROUND: The use of high-dose cytosine arabinoside (HDAraC) during induction may improve outcomes in patients with acute myeloid leukemia (AML) compared with standard-dose AraC (SDAraC).
  • [MeSH-major] Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16721819.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine
  • [Number-of-references] 9
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73. Hotfilder M, Röttgers S, Rosemann A, Schrauder A, Schrappe M, Pieters R, Jürgens H, Harbott J, Vormoor J: Leukemic stem cells in childhood high-risk ALL/t(9;22) and t(4;11) are present in primitive lymphoid-restricted CD34+CD19- cells. Cancer Res; 2005 Feb 15;65(4):1442-9
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  • [Title] Leukemic stem cells in childhood high-risk ALL/t(9;22) and t(4;11) are present in primitive lymphoid-restricted CD34+CD19- cells.
  • Open questions in the pathogenesis of childhood acute lymphoblastic leukemia (ALL) are which hematopoietic cell is target of the malignant transformation and whether primitive stem cells contribute to the leukemic clone.
  • Therefore, immature CD34(+)CD19(-) bone marrow cells from 8 children with ALL/t(9;22) and 12 with ALL/t(4;11) were purified and analyzed by fluorescence in situ hybridization, reverse transcription-PCR (RT-PCR), and colony assays.
  • Fifty-six percent (n = 8, SD 31%) and 68% (n = 12, SD 26%) of CD34(+)CD19(-) cells in ALL/t(9;22) and ALL/t(4;11), respectively, carried the translocation.
  • In addition, 5 of 168 (3%) and 22 of 228 (10%) myeloerythroid colonies expressed BCR/ABL and MLL/AF4.
  • Interestingly, in some patients with ALL/t(4;11), alternative splicing was seen in myeloid progenitors compared with the bulk leukemic population, suggesting that these myeloid colonies might be part of the leukemic cell clone.
  • Fluorescence in situ hybridization analysis, however, shows that none of these myeloid colonies (0 of 41 RT-PCR-positive colonies) originated from a progenitor cell that carries the leukemia-specific translocation.
  • In conclusion, we show that childhood high-risk ALL/t(9;22) and t(4;11) originate in a primitive CD34(+)CD19(-) progenitor/stem cell without a myeloerythroid developmental potential.
  • [MeSH-major] Antigens, CD19 / biosynthesis. Antigens, CD34 / biosynthesis. Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 9 / genetics. Flow Cytometry. Genes, abl / genetics. Humans. In Situ Hybridization, Fluorescence. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15735032.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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74. Faber J, Krivtsov AV, Stubbs MC, Wright R, Davis TN, van den Heuvel-Eibrink M, Zwaan CM, Kung AL, Armstrong SA: HOXA9 is required for survival in human MLL-rearranged acute leukemias. Blood; 2009 Mar 12;113(11):2375-85
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  • [Title] HOXA9 is required for survival in human MLL-rearranged acute leukemias.
  • Leukemias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologic characteristics and often have an unfavorable prognosis.
  • Gene expression analyses demonstrate a distinct profile for MLL-rearranged leukemias with consistent high-level expression of select Homeobox genes, including HOXA9.
  • Here, we investigated the effects of HOXA9 suppression in MLL-rearranged and MLL-germline leukemias using RNA interference.
  • Gene expression profiling after HOXA9 suppression demonstrated co-down-regulation of a program highly expressed in human MLL-AML and murine MLL-leukemia stem cells, including HOXA10, MEIS1, PBX3, and MEF2C.
  • We demonstrate that HOXA9 depletion in 17 human AML/ALL cell lines (7 MLL-rearranged, 10 MLL-germline) induces proliferation arrest and apoptosis specifically in MLL-rearranged cells (P = .007).
  • Similarly, assessment of primary AMLs demonstrated that HOXA9 suppression induces apoptosis to a greater extent in MLL-rearranged samples (P = .01).
  • Moreover, mice transplanted with HOXA9-depleted t(4;11) SEMK2 cells revealed a significantly lower leukemia burden, thus identifying a role for HOXA9 in leukemia survival in vivo.
  • Our data indicate an important role for HOXA9 in human MLL-rearranged leukemias and suggest that targeting HOXA9 or downstream programs may be a novel therapeutic option.

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  • [Cites] Leukemia. 2002 Jul;16(7):1293-301 [12094253.001]
  • [Cites] Blood. 2002 Aug 1;100(3):862-8 [12130496.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1685-90 [12200682.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):161-71 [12620410.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2298-307 [12952893.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1823-8 [14615372.001]
  • [Cites] Nat Genet. 2004 Mar;36(3):257-63 [14770183.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3192-9 [15070702.001]
  • [Cites] Leukemia. 1988 Oct;2(10):672-6 [3172843.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] Blood. 1993 May 1;81(9):2386-93 [8481519.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1080-5 [8353274.001]
  • [Cites] Blood. 1993 Dec 15;82(12):3705-11 [8260707.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2274-84 [8161794.001]
  • [Cites] Blood. 1994 Jul 15;84(2):570-3 [8025282.001]
  • [Cites] Blood. 1994 Dec 1;84(11):3835-42 [7949140.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12223-7 [7527557.001]
  • [Cites] Genes Dev. 1995 Jul 15;9(14):1753-65 [7622039.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):154-8 [8563753.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):159-67 [8563754.001]
  • [Cites] Am J Hematol. 1996 Dec;53(4):264-6 [8948668.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1922-30 [9058712.001]
  • [Cites] Blood. 1998 Jul 15;92(2):383-93 [9657735.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1222-30 [15479723.001]
  • [Cites] EMBO J. 2005 Jan 26;24(2):368-81 [15635450.001]
  • [Cites] Nat Biotechnol. 2005 Jun;23(6):709-17 [15908939.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8 [15941828.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2841-8 [15998836.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3988-94 [16091451.001]
  • [Cites] Exp Hematol. 2000 May;28(5):569-74 [10812247.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10984-9 [10995463.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):224-34 [11113197.001]
  • [Cites] EMBO J. 2001 Feb 1;20(3):350-61 [11157742.001]
  • [Cites] Oncogene. 2001 Feb 15;20(7):874-8 [11314021.001]
  • [Cites] Blood. 2001 Aug 1;98(3):885-7 [11468194.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Exp Hematol. 1995 Oct;23(11):1160-6 [7556525.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Blood. 2002 Jan 1;99(1):121-9 [11756161.001]
  • [Cites] Exp Hematol. 2002 Jan;30(1):49-57 [11823037.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Oncogene. 2002 Jun 20;21(27):4247-56 [12082612.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11367-74 [16357144.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Nat Methods. 2006 Sep;3(9):677-81 [16929311.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1929-35 [17008526.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Leukemia. 2007 Apr;21(4):593-4 [17301807.001]
  • [Cites] Nat Cell Biol. 2007 Oct;9(10):1208-15 [17891136.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]
  • [Cites] Cancer Cell. 2008 Nov 4;14(5):355-68 [18977325.001]
  • [CommentIn] Blood. 2009 Mar 12;113(11):2372-3 [19282462.001]
  • (PMID = 19056693.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA66996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2656267
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75. Martino V, Bianchera A, Reia L, Bussolati O, Fazzina R, Marino F, Montemurro L, Tonelli R, Pession A, Gazzola GC, Sala R: Down-regulation of HOXA4, HOXA7, HOXA10, HOXA11 and MEIS1 during monocyte-macrophage differentiation in THP-1 cells. Mol Med Rep; 2009 Mar-Apr;2(2):241-4
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  • The translocation t(9;11)(p22;q23) generates the MLL-AF9 oncogene and is commonly associated with monocytic acute myeloid leukemia (AML-M5; FAB-classification).
  • For the oncogenicity of MLL-AF9, the (over)expression of several other genes, including selected HOXA cluster genes as well as MEIS1 (a HOX cofactor), is required.
  • We previously showed that the down-regulation of MLL-AF9 expression is not obligatory for monocyte-macrophage maturation in AML-M5 cells carrying t(9;11)(p22;q23).
  • In this study, we analyzed the expression patterns of HOXA4, 5, 6, 7, 9, 10 and 11 (defined as 'HOXA-code' genes) and MEIS1 by semiquantitative RT-PCR during the monocyte-macrophage differentiation induced by phorbol 12-myristate 13-acetate (PMA) in THP-1 cells carrying t(9;11)(p22;q23) and expressing MLL-AF9.
  • The analyses were performed in THP-1 cells expressing MLL-AF9 even after PMA treatment.
  • After the induction of differentiation, we observed a down-regulation of HOXA4, 7, 10, 11 and MEIS1, an up-regulation of HOXA6, and no significant variation in the expression of HOXA5 and 9.
  • These data indicate that the expression of most HOXA-code genes, as well as MEIS1, could be implicated in the differentiation blockage observed in MLL-AF9-related leukemias.

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  • (PMID = 21475819.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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76. De Braekeleer E, Meyer C, Douet-Guilbert N, Morel F, Le Bris MJ, Berthou C, Arnaud B, Marschalek R, Férec C, De Braekeleer M: Complex and cryptic chromosomal rearrangements involving the MLL gene in acute leukemia: a study of 7 patients and review of the literature. Blood Cells Mol Dis; 2010 Apr 15;44(4):268-74
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  • [Title] Complex and cryptic chromosomal rearrangements involving the MLL gene in acute leukemia: a study of 7 patients and review of the literature.
  • Chromosomal rearrangements involving the MLL gene have been associated with many different types of hematological malignancies.
  • However, in some cases, complex, unusual or cryptic rearrangements make the MLL involvement difficult or impossible to be detected by conventional cytogenetics.
  • Fluorescent in situ hybridization with a panel of probes coupled with long distance inverse-PCR was used to identify chromosomal rearrangements involving the MLL gene.
  • Seven unusual chromosomal rearrangements were identified, including two complex translocations, three insertions of material of chromosome 11 in another chromosome and one insertion of chromosome material into the MLL gene.
  • Conventional cytogenetics showed three patients to have a deletion of 11q; one had an unexpected t(6;11)(q27;q23) whereas the other two patients had also an insertion of MLL material in another chromosome.
  • Concurrent 3' deletion in the MLL rearrangement was observed in two patients.
  • We recommend a systematic approach to be used in all cases of acute leukemia starting with FISH analyses using a commercially available MLL split signal probe.
  • Should an abnormality be discovered, the analysis has to be completed by further molecular cytogenetic and genomic PCR methods in order to unravel the recombination mechanism.
  • [MeSH-major] Chromosome Aberrations. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Adenocarcinoma. Adult. Aged. Blast Crisis / genetics. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Duodenal Neoplasms. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Leukemia, Monocytic, Acute / congenital. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Male. Mutagenesis, Insertional. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prostatic Neoplasms. Sequence Deletion. Translocation, Genetic

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  • (PMID = 20206559.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 70
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77. Fernandez HF, Sun Z, Yao X, Litzow MR, Luger SM, Paietta EM, Racevskis J, Dewald GW, Ketterling RP, Bennett JM, Rowe JM, Lazarus HM, Tallman MS: Anthracycline dose intensification in acute myeloid leukemia. N Engl J Med; 2009 Sep 24;361(13):1249-59
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  • [Title] Anthracycline dose intensification in acute myeloid leukemia.
  • BACKGROUND: In young adults with acute myeloid leukemia (AML), intensification of the anthracycline dose during induction therapy has improved the rate of complete remission but not of overall survival.
  • RESULTS: In the intention-to-treat analysis, high-dose daunorubicin, as compared with a standard dose of the drug, resulted in a higher rate of complete remission (70.6% vs. 57.3%, P<0.001) and improved overall survival (median, 23.7 vs. 15.7 months; P=0.003).
  • CONCLUSIONS: In young adults with AML, intensifying induction therapy with a high daily dose of daunorubicin improved the rate of complete remission and the duration of overall survival, as compared with the standard dose. (ClinicalTrials.gov number, NCT00049517. )

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  • [Copyright] 2009 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2009 Dec 24;361(26):2578; author reply 2578 [20032330.001]
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1301-3 [19776412.001]
  • (PMID = 19776406.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] ENG
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00049517
  • [Grant] United States / NCI NIH HHS / CA / CA14548; United States / NCI NIH HHS / CA / U10 CA013650; United States / NCI NIH HHS / CA / U10 CA014958; United States / NCI NIH HHS / CA / CA66636; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / CA13650; United States / NCI NIH HHS / CA / U10 CA017145; United States / NCI NIH HHS / CA / U10 CA066636; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / U10 CA073590; United States / NCI NIH HHS / CA / U10 CA014548; United States / NCI NIH HHS / CA / U10 CA023318; United States / NCI NIH HHS / CA / U10 CA011083; United States / NCI NIH HHS / CA / CA15488; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / U10 CA015488
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / MLL protein, human; 04079A1RDZ / Cytarabine; 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 / fms-Like Tyrosine Kinase 3; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS435676; NLM/ PMC4480917
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78. Okada Y, Jiang Q, Lemieux M, Jeannotte L, Su L, Zhang Y: Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L. Nat Cell Biol; 2006 Sep;8(9):1017-24
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  • Chromosomal translocation is a common cause of leukaemia and the most common chromosome translocations found in leukaemia patients involve the mixed lineage leukaemia (MLL) gene.
  • AF10 is one of more than 30 MLL fusion partners in leukaemia.
  • We have recently demonstrated that the H3K79 methyltransferase hDOT1L contributes to MLL-AF10-mediated leukaemogenesis through its interaction with AF10 (ref. 5).
  • In addition to MLL, AF10 has also been reported to fuse to CALM (clathrin-assembly protein-like lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML).
  • Thus, our study establishes CALM-AF10 fusion as a cause of leukaemia and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind leukaemia caused by CALM-AF10 fusion.

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  • [ErratumIn] Nat Cell Biol. 2006 Oct;8(10):1178
  • (PMID = 16921363.001).
  • [ISSN] 1465-7392
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI48407; United States / NIAID NIH HHS / AI / R56 AI048407; United States / NHLBI NIH HHS / HL / R21 HL072240; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIGMS NIH HHS / GM / R01 GM068804; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIGMS NIH HHS / GM / GM68804; United States / NHLBI NIH HHS / HL / HL72240; United States / NIAID NIH HHS / AI / R01 AI048407
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / MLLT10 protein, human; 0 / Mllt10 protein, mouse; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Phosphoproteins; 0 / Transcription Factors; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Methyltransferases
  • [Other-IDs] NLM/ NIHMS684864; NLM/ PMC4425349
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79. Germano G, Pigazzi M, del Giudice L, Campo Dell'Orto M, Spinelli M, Zangrando A, Paolucci P, Ladogana S, Basso G: Two consecutive immunophenotypic switches in a child with MLL-rearranged acute lymphoblastic leukemia. Haematologica; 2006 May;91(5 Suppl):ECR09
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  • [Title] Two consecutive immunophenotypic switches in a child with MLL-rearranged acute lymphoblastic leukemia.
  • An 18-month-old girl was diagnosed with pre-pre-B ALL/t(4;11) leukemia, which during the treatment and after matched bone marrow transplantation (BMT), underwent two consecutive switches from lymphoid to myeloid lineage and vice versa.
  • The high expression of HOXA9 and FLT3 genes remaining genotypically stable in a leukemia throughout phenotypic switches, suggests that this leukemia may have originated as a common B/myeloid progenitors.
  • [MeSH-major] Antigens, CD / analysis. Antigens, Neoplasm / analysis. B-Lymphocytes / pathology. Gene Rearrangement. Immunophenotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 4 / ultrastructure. Clone Cells / pathology. Combined Modality Therapy. Fatal Outcome. Female. Gene Expression Regulation, Leukemic. Gene Rearrangement, B-Lymphocyte. Genes, Immunoglobulin. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Humans. Infant. Models, Biological. Neoplasm Proteins / genetics. Recurrence. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16709517.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / MLL-AF4 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9; 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 / fms-Like Tyrosine Kinase 3
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80. Gulley ML, Shea TC, Fedoriw Y: Genetic tests to evaluate prognosis and predict therapeutic response in acute myeloid leukemia. J Mol Diagn; 2010 Jan;12(1):3-16
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  • [Title] Genetic tests to evaluate prognosis and predict therapeutic response in acute myeloid leukemia.
  • Management of patients with acute myeloid leukemia relies on genetic tests that inform diagnosis and prognosis, predict response to therapy, and measure minimal residual disease.
  • The value of genetics is reinforced in the revised 2008 World Health Organization acute myeloid leukemia classification scheme.
  • Karyotype and array technology represent genome-wide screens, whereas the other methods target specific prognostic features such as t(15;17) PML-RARA, t(8;21) RUNX1-RUNX1T1, inv(16) CBFB-MYH11, 11q23 MLL rearrangement, FLT3 internal tandem duplication, or NPM1 mutation.
  • Acute myeloid leukemia leads the way for modern molecular medicine.


81. Wong P, Iwasaki M, Somervaille TC, Ficara F, Carico C, Arnold C, Chen CZ, Cleary ML: The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression. Cancer Res; 2010 May 1;70(9):3833-42
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  • [Title] The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression.
  • Despite advances in defining the critical molecular determinants for leukemia stem cell (LSC) generation and maintenance, little is known about the roles of microRNAs in LSC biology.
  • Here, we identify microRNAs that are differentially expressed in LSC-enriched cell fractions (c-kit(+)) in a mouse model of MLL leukemia.
  • Expression of miR-17 family microRNAs was substantially reduced concomitant with leukemia cell differentiation and loss of self-renewal, whereas forced expression of a polycistron construct encoding miR-17-19b miRNAs significantly shortened the latency for MLL leukemia development.
  • Leukemias expressing increased levels of the miR-17-19b construct displayed a higher frequency of LSCs, more stringent block of differentiation, and enhanced proliferation associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated as a direct target of miR-17 microRNAs.
  • Knockdown of p21 in MLL-transformed cells phenocopied the overexpression of the miR-17 polycistron, including a significant decrease in leukemia latency, validating p21 as a biologically relevant and direct in vivo target of the miR-17 polycistron in MLL leukemia.
  • Thus, microRNAs quantitatively regulate LSC self-renewal in MLL-associated leukemia in part by modulating the expression of p21, a known regulator of normal stem cell function.

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  • [Copyright] (c)2010 AACR.
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Genes Dev. 2009 Dec 15;23(24):2839-49 [20008935.001]
  • [Cites] Cell. 1993 Dec 3;75(5):855-62 [8252622.001]
  • [Cites] Cell. 2005 Jan 14;120(1):21-4 [15652478.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):839-43 [15944709.001]
  • [Cites] J Biol Chem. 2005 Jul 1;280(26):24315-21 [15851483.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] J Biol Chem. 2007 Jan 26;282(4):2135-43 [17135249.001]
  • [Cites] Cell Death Differ. 2007 Apr;14(4):879-82 [17218954.001]
  • [Cites] Leukemia. 2007 May;21(5):912-6 [17330104.001]
  • [Cites] Blood. 2007 May 15;109(10):4399-405 [17284533.001]
  • [Cites] Nat Cell Biol. 2007 Jul;9(7):775-87 [17589498.001]
  • [Cites] Mol Cell. 2007 Jul 6;27(1):91-105 [17612493.001]
  • [Cites] Cell. 2007 Sep 21;130(6):1005-18 [17889646.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2762-74 [17942707.001]
  • [Cites] Dev Biol. 1999 Dec 15;216(2):671-80 [10642801.001]
  • [Cites] EMBO J. 2000 Sep 1;19(17):4655-64 [10970858.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6480-6 [11522644.001]
  • [Cites] Oncogene. 2003 Apr 17;22(15):2285-95 [12700664.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2298-307 [12952893.001]
  • [Cites] Mol Cancer. 2007;6:60 [17894887.001]
  • [Cites] Mol Cell Biol. 2008 Apr;28(7):2167-74 [18212054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]
  • [Cites] J Exp Med. 2008 Mar 17;205(3):585-94 [18299402.001]
  • [Cites] Mol Cell. 2008 May 23;30(4):460-71 [18498749.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15535-40 [18832181.001]
  • [Cites] J Cell Mol Med. 2008 Sep-Oct;12(5A):1445-55 [18554315.001]
  • [Cites] Nature. 2009 Jan 1;457(7225):51-6 [19122635.001]
  • [Cites] Blood. 2009 Jan 8;113(2):396-402 [18941111.001]
  • [Cites] Cancer Res. 2009 Feb 1;69(3):1109-16 [19155294.001]
  • [Cites] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802.001]
  • [Cites] Blood. 2009 Apr 2;113(14):3314-22 [19188669.001]
  • [Cites] Genes Dev. 2009 Dec 15;23(24):2806-11 [20008931.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • (PMID = 20406979.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / CA55029; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NHLBI NIH HHS / HL / R01 HL081612-05; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA116606; United States / NHLBI NIH HHS / HL / R01 HL081612-04; United States / NIH HHS / OD / DP1 OD006435; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MicroRNAs; 0 / Mirn17 microRNA, mouse; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS185039; NLM/ PMC2862107
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82. Li Z, Lu J, Sun M, Mi S, Zhang H, Luo RT, Chen P, Wang Y, Yan M, Qian Z, Neilly MB, Jin J, Zhang Y, Bohlander SK, Zhang DE, Larson RA, Le Beau MM, Thirman MJ, Golub TR, Rowley JD, Chen J: Distinct microRNA expression profiles in acute myeloid leukemia with common translocations. Proc Natl Acad Sci U S A; 2008 Oct 7;105(40):15535-40
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  • [Title] Distinct microRNA expression profiles in acute myeloid leukemia with common translocations.
  • Here, we report a genome-wide miRNA expression analysis in 52 acute myeloid leukemia (AML) samples with common translocations, including t(8;21)/AML1(RUNX1)-ETO(RUNX1T1), inv(16)/CBFB-MYH11, t(15;17)/PML-RARA, and MLL rearrangements.
  • Distinct miRNA expression patterns were observed for t(15;17), MLL rearrangements, and core-binding factor (CBF) AMLs including both t(8;21) and inv(16) samples.
  • Expression signatures of a minimum of two (i.e., miR-126/126*), three (i.e., miR-224, miR-368, and miR-382), and seven (miR-17-5p and miR-20a, plus the aforementioned five) miRNAs could accurately discriminate CBF, t(15;17), and MLL-rearrangement AMLs, respectively, from each other.
  • Our results demonstrate that specific alterations in miRNA expression distinguish AMLs with common translocations and imply that the deregulation of specific miRNAs may play a role in the development of leukemia with these associated genetic rearrangements.

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  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10984-9 [10995463.001]
  • [Cites] Leukemia. 2005 Jun;19(6):953-64 [15815718.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(16):5556-71 [12897130.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Nat Rev Cancer. 2001 Dec;1(3):245-50 [11902580.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1189-98 [15878973.001]
  • [Cites] Cell. 2005 Aug 26;122(4):553-63 [16122423.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6296-305 [16155012.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]
  • [Cites] Blood. 2006 Jan 1;107(1):250-6 [16160013.001]
  • [Cites] Leuk Res. 2006 May;30(5):643-7 [16226311.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):435-43 [16766263.001]
  • [Cites] Cell Cycle. 2006 Jun;5(12):1262-4 [16868416.001]
  • [Cites] Methods Enzymol. 2006;411:134-93 [16939790.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Oct 13;349(1):59-68 [16934749.001]
  • [Cites] Br J Haematol. 2006 Nov;135(3):336-47 [16989659.001]
  • [Cites] Int J Cancer. 2007 Mar 1;120(5):953-60 [17163415.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):233-45 [17361217.001]
  • [Cites] Leukemia. 2007 May;21(5):912-6 [17330104.001]
  • [Cites] Trends Genet. 2007 May;23(5):243-9 [17368621.001]
  • [Cites] Oncogene. 2007 Jun 14;26(28):4148-57 [17260024.001]
  • [Cites] Nat Cell Biol. 2007 Jul;9(7):775-87 [17589498.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):457-66 [17996649.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19971-6 [18056805.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):153-61 [18173753.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S84-5 [15124687.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3087-95 [15126345.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4238-48 [15156179.001]
  • [Cites] Nat Rev Genet. 2004 Jul;5(7):522-31 [15211354.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1827-31 [1542678.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Ann Hematol. 1999 Jun;78(6):251-64 [10422627.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] PLoS Biol. 2004 Nov;2(11):e363 [15502875.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Cell. 2005 Jan 14;120(1):15-20 [15652477.001]
  • [Cites] Nat Genet. 2005 May;37(5):495-500 [15806104.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • (PMID = 18832181.001).
  • [ISSN] 1091-6490
  • [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 / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA127277; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA104509; United States / NCI NIH HHS / CA / R01 CA127277; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA014599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 0 / MIRN126 microRNA, human; 0 / MicroRNAs; EC 2.7.11.- / PLK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2563085
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83. Pui CH: Neonatal leukemia: a nemesis for pediatric oncologists? Pediatr Blood Cancer; 2006 Sep;47(3):234-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neonatal leukemia: a nemesis for pediatric oncologists?
  • [MeSH-major] Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Follow-Up Studies. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Medical Oncology. Myeloid-Lymphoid Leukemia Protein / genetics. Treatment Outcome

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  • [CommentOn] Pediatr Blood Cancer. 2006 Sep;47(3):268-72 [16333820.001]
  • (PMID = 16206196.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comment; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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84. Tauchi H, Tomizawa D, Eguchi M, Eguchi-Ishimae M, Koh K, Hirayama M, Miyamura N, Kinukawa N, Hayashi Y, Horibe K, Ishii E: Clinical features and outcome of MLL gene rearranged acute lymphoblastic leukemia in infants with additional chromosomal abnormalities other than 11q23 translocation. Leuk Res; 2008 Oct;32(10):1523-9
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  • [Title] Clinical features and outcome of MLL gene rearranged acute lymphoblastic leukemia in infants with additional chromosomal abnormalities other than 11q23 translocation.
  • The treatment outcome for infant acute lymphoblastic leukemia (ALL) with positive MLL gene rearrangements remains poor.
  • We analyzed whether additional chromosomal abnormalities (ACA) other than 11q23 translocation could affect the disease behavior and its prognosis.
  • Eighteen of seventy-four patients with infant acute lymphoblastic leukemia showed ACA, including three-way translocations in four, other novel translocations in four, and complex structural chromosomal changes in four.
  • Only age less than 6 months and positive central nervous system leukemia were significant prognostic factors by multivariate analysis.
  • Genetic alterations induced by additional chromosomal changes may be associated with disease progression and poorer overall survival rates in infants with MLL-rearranged ALL.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Chromosomes, Human, Pair 11. Disease-Free Survival. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Survival Rate. Translocation, Genetic. Treatment Outcome

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  • (PMID = 18448165.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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85. Shih LY, Liang DC, Fu JF, Wu JH, Wang PN, Lin TL, Dunn P, Kuo MC, Tang TC, Lin TH, Lai CL: Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement. Leukemia; 2006 Feb;20(2):218-23
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  • [Title] Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement.
  • The fusion transcripts of MLL rearrangement [MLL(+)] in acute myeloid leukemia (AML) and their clinicohematologic correlation have not be well characterized in the previous studies.
  • We used Southern blot analysis to screen MLL(+) in de novo AML.
  • Reverse transcriptase-polymerase chain reaction was used to detect the common MLL fusion transcripts. cDNA panhandle PCR was used to identify infrequent or unknown MLL partner genes.
  • MLL(+) was identified in 114 (98 adults) of 988 AML patients.
  • MLL fusion transcripts comprised of 63 partial tandem duplication of MLL (MLL-PTD), 14 MLL-AF9, 9 MLL-AF10, 9 MLL-ELL, 8 MLL-AF6, 4 MLL-ENL and one each of MLL-AF1, MLL-AF4, MLL-MSF, MLL-LCX, MLL-LARG, MLL-SEPT6 and MLL-CBL.
  • The frequency of MLL-PTD was 7.1% in adults and 0.9% in children (P<0.001).
  • 11q23 abnormalities were detected in 64% of MLL/t11q23 and in none of MLL-PTD by conventional cytogenetics.
  • There were no differences in remission rate, event-free survival and overall survival between adult MLL-PTD and MLL/t11q23 groups.
  • The present study showed that cDNA panhandle PCR can identify all rare or novel MLL partner genes.
  • MLL-PTD was rare in childhood AML.
  • MLL(+) adults had a poor outcome with no difference in survival between MLL-PTD and MLL/t11q23 groups.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child, Preschool. Female. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 16341046.001).
  • [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 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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86. Kalina T, Vaskova M, Mejstrikova E, Madzo J, Trka J, Stary J, Hrusak O: Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens. BMC Cancer; 2005;5:38
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  • [Title] Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens.
  • BACKGROUND: Aberrant expression of myeloid antigens (MyAgs) on acute lymphoblastic leukemia (ALL) cells is a well-documented phenomenon, although its regulating mechanisms are unclear.
  • Granulocytic marker CD66c -- Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is aberrantly expressed on ALL with strong correlation to genotype (negative in TEL/AML1 and MLL/AF4, positive in BCR/ABL and hyperdiploid cases).
  • Our data show that different myeloid antigens often differ in biological importance, which may be obscured by combining them into "MyAg positive ALL".
  • CONCLUSION: In contrast to general notion we show that different MyAgs in lymphoblastic leukemia represent different biological circumstances.
  • [MeSH-major] Antigens, CD / biosynthesis. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • [Cites] Crit Rev Oncol Hematol. 1999 Dec;32(3):175-85 [10633847.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1092-4 [15830012.001]
  • [Cites] Cancer Res. 2000 Jul 1;60(13):3419-24 [10910050.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):794-9 [11564065.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1952-8 [11877265.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Mar;15(1):1-19 [11987913.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1233-58 [12094248.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):105-13 [12491511.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3638-46 [14512395.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):465-73 [14724575.001]
  • [Cites] Biochem Biophys Res Commun. 2004 May 7;317(3):837-43 [15081416.001]
  • [Cites] Oncogene. 2004 Jul 29;23(34):5834-42 [15208677.001]
  • [Cites] Cancer Res. 1968 Sep;28(9):1908-14 [5676741.001]
  • [Cites] Science. 1986 Nov 7;234(4777):697-704 [3535067.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3305-14 [8205554.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2127-33 [7808000.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1233-9 [7543176.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] J Leukoc Biol. 1996 Jul;60(1):106-17 [8699114.001]
  • [Cites] Infect Immun. 1996 Nov;64(11):4574-9 [8890209.001]
  • [Cites] Leukemia. 1998 Jul;12(7):1064-70 [9665191.001]
  • [Cites] Blood. 1998 Aug 1;92(3):795-801 [9680347.001]
  • [Cites] Tissue Antigens. 1998 Jul;52(1):1-8 [9714468.001]
  • [Cites] Leukemia. 1999 May;13(5):779-85 [10374883.001]
  • [Cites] Cytometry. 1999 Aug 15;38(4):139-52 [10440852.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):595-605 [10666389.001]
  • (PMID = 15826304.001).
  • [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 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD65s antigen, human; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 63231-63-0 / RNA; EC 3.4.11.2 / Antigens, CD13
  • [Other-IDs] NLM/ PMC1112585
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87. Luciani M, Rana I, Pansini V, Caniglia M, Coletti V, Maraschini A, Lombardi A, De Rossi G: Infant leukaemia: clinical, biological and therapeutic advances. Acta Paediatr Suppl; 2006 Jul;95(452):47-51
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  • [Title] Infant leukaemia: clinical, biological and therapeutic advances.
  • Infant acute lymphoid leukaemia (IALL) represents a distinct subset with an extremely poor response to therapy, despite major progress in the treatment of childhood leukaemia.
  • The outcome of IALL patients with ALL-1/MLL rearrangements at the 11q23 cytogenetic band, early pre-B immunophenotype, high WBC count and age below 6 mo is significantly worse than in patients without these characteristics, and current therapies appear inadequate in a significant number of cases.
  • Therefore, an international protocol (Interfant 99) was recently started, using a more aggressive approach, which included lymphoid- and myeloid-specific drugs, and indications for stem-cell transplantation.
  • We reviewed the clinical characteristics of the disease, the results of several recent international clinical trials, and our experience with 16 infants with acute lymphoid leukaemia diagnosed and treated at our institution.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 16801167.001).
  • [ISSN] 0803-5326
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992). Supplement
  • [ISO-abbreviation] Acta Paediatr Suppl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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88. Stam RW, Hubeek I, den Boer ML, Buijs-Gladdines JG, Creutzig U, Kaspers GJ, Pieters R: MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia. Leukemia; 2006 Jan;20(1):179-82
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  • [Title] MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia.
  • [MeSH-major] Cytarabine / therapeutic use. Drug Resistance, Neoplasm / genetics. Gene Rearrangement. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


89. Kuriyama K: [Classification of myeloid leukemias]. Nihon Rinsho; 2009 Oct;67(10):1853-62
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  • [Title] [Classification of myeloid leukemias].
  • Myeloid leukemia in this series corresponds to the myeloid neoplasms of the 4th WHO classification of pathology and genetics of tumor of haematopoietic and lymphoid tissue.
  • The myeloid neoplasms are composed of six categories, which are 1) myeloproliferative neoplasms (MPN), a new category of 2) myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1, 3) myelodysplastic syndrome (MDS)/MPN, 4) MDS, 5) acute myeloid leukemia (AML) and related precursor neoplasms, and 6) acute leukemias of ambiguous lineage.
  • In MPNs without chronic myelogenous leukemia, the genetic marker of JAK2 V617F is added to the diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis.
  • AML with t(9;.
  • 11) (p22;q23); MLLT3-MLL, AML with t(6;9) (p23; q34); DEK-NUP214, AML with inv(3) (q21q26.2) or t(3;.
  • 3) (q21 ; q26.2); RPN1-EVI1 and AML (megakaryoblastic) with t(1;.
  • 22) (p13; q13); RBM15-MKL1 are added to the subtype of AML with recurrent genetic abnormalities, and AML with gene mutations of NPM1 and CEBPA are also added as provisional entities of it.
  • The myeloid neoplasms of the 4th WHO classification are comprehensive and seem to be dynamic by incorporating the results of leukemia researches.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Eosinophilia. Humans. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. World Health Organization

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  • (PMID = 19860179.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Number-of-references] 14
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90. Lin C, Smith ER, Takahashi H, Lai KC, Martin-Brown S, Florens L, Washburn MP, Conaway JW, Conaway RC, Shilatifard A: AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia. Mol Cell; 2010 Feb 12;37(3):429-37
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  • [Title] AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia.
  • Chromosomal translocations involving the MLL gene are associated with infant acute lymphoblastic and mixed lineage leukemia.
  • There are a large number of translocation partners of MLL that share very little sequence or seemingly functional similarities; however, their translocations into MLL result in the pathogenesis of leukemia.
  • To define the molecular reason why these translocations result in the pathogenesis of leukemia, we purified several of the commonly occurring MLL chimeras.
  • Knockdown of AFF4 in leukemic cells shows reduction in MLL chimera target gene expression, suggesting that AFF4/SEC could be a key regulator in the pathogenesis of leukemia through many of the MLL partners.