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1. Whitman SP, Hackanson B, Liyanarachchi S, Liu S, Rush LJ, Maharry K, Margeson D, Davuluri R, Wen J, Witte T, Yu L, Liu C, Bloomfield CD, Marcucci G, Plass C, Caligiuri MA: DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. Blood; 2008 Sep 1;112(5):2013-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication.
  • We report that acute myeloid leukemia (AML) with an aberrant histone methyltransferase, the mixed lineage leukemia partial tandem duplication (MLL-PTD), exhibits increased global DNA methylation versus AML with MLL-wildtype (MLL-WT; P = .02).
  • In MLL-PTD(+) cell lines having SLC5A8 promoter hypermethylation, incubation with decitabine activated SLC5A8 expression.
  • In addition, enhanced cell death was observed in SMCT1-expressing MLL-PTD(+) AML cells treated with valproate.
  • Within the majority of MLL-PTD AML is a mechanism in which DNA hypermethylation silences a TSG that, together with MLL-PTD, can contribute further to aberrant chromatin remodeling and altered gene expression.

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  • (PMID = 18566324.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA101956; United States / NCI NIH HHS / CA / CA016058; United States / NCI NIH HHS / CA / P01 CA101956; United States / NCI NIH HHS / CA / CA089341; United States / NCI NIH HHS / CA / CA089317; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / CA077658; United States / NCI NIH HHS / CA / U24 CA114725; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA114725; United States / NCI NIH HHS / CA / K08 CA089317; 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 / Cation Transport Proteins; 0 / DNA, Neoplasm; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / SLC5A8 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 614OI1Z5WI / Valproic Acid; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC2518901
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2. 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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  • (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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3. Liu H, Cheng EH, Hsieh JJ: MLL fusions: pathways to leukemia. Cancer Biol Ther; 2009 Jul;8(13):1204-11
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  • [Title] MLL fusions: pathways to leukemia.
  • Human leukemias with chromosomal band 11q23 aberrations that disrupt the MLL/HRX/ALL-1 gene portend poor prognosis.
  • MLL associated leukemias account for the majority of infant leukemia, approximately 10% of adult de novo leukemia and approximately 33% of therapy related acute leukemia with a balanced chromosome translocation.
  • The 500 kD MLL precursor is processed by Taspase1 to generate mature MLL(N320/C180), which orchestrates many aspects of biology such as embryogenesis, cell cycle, cell fate and stem cell maintenance.
  • Leukemogenic MLL translocations fuse the common MLL N-terminus (approximately 1,400 aa) in frame with more than 60 translocation partner genes (TPGs).
  • Recent studies on MLL and MLL leukemia have greatly advanced our knowledge concerning the normal function of MLL and its deregulation in leukemogenesis.
  • Here, we summarize the critical biological and pathological activities of MLL and MLL fusions, and discuss available models and potential therapeutic targets of MLL associated leukemias.
  • [MeSH-major] Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 19729989.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein
  • [Number-of-references] 119
  • [Other-IDs] NLM/ PMC3289713
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4. Zeisig BB, Cheung N, Yeung J, So CW: Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia. Cancer Cell; 2008 Nov 4;14(5):345-7
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia.
  • The lack of a proper animal model has impeded understanding of the molecular mechanism of leukemia associated with the MLL-AF4 fusion.
  • In this issue of Cancer Cell, Krivtsov et al. report a much-improved murine Mll-AF4 model and propose a molecular link with H3K79 methylation mediated by the histone methyltransferase DOT1L.
  • [MeSH-major] Disease Models, Animal. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Methylation. Myeloid-Lymphoid Leukemia Protein / physiology. Oncogene Proteins, Fusion / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentOn] Cancer Cell. 2008 Nov 4;14(5):355-68 [18977325.001]
  • (PMID = 18977321.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Dot1l protein, mouse; EC 2.1.1.- / Methyltransferases
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5. Cerveira N, Santos J, Bizarro S, Costa V, Ribeiro FR, Lisboa S, Correia C, Torres L, Vieira J, Snijder S, Mariz JM, Norton L, Mellink CH, Buijs A, Teixeira MR: Both SEPT2 and MLL are down-regulated in MLL-SEPT2 therapy-related myeloid neoplasia. BMC Cancer; 2009;9:147
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  • [Title] Both SEPT2 and MLL are down-regulated in MLL-SEPT2 therapy-related myeloid neoplasia.
  • BACKGROUND: A relevant role of septins in leukemogenesis has been uncovered by their involvement as fusion partners in MLL-related leukemia.
  • Recently, we have established the MLL-SEPT2 gene fusion as the molecular abnormality subjacent to the translocation t(2;11)(q37;q23) in therapy-related acute myeloid leukemia.
  • In this work we quantified MLL and SEPT2 gene expression in 58 acute myeloid leukemia patients selected to represent the major AML genetic subgroups, as well as in all three cases of MLL-SEPT2-associated myeloid neoplasms so far described in the literature.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH) and molecular studies (RT-PCR, qRT-PCR and qMSP) were used to characterize 58 acute myeloid leukemia patients (AML) at diagnosis selected to represent the major AML genetic subgroups: CBFB-MYH11 (n = 13), PML-RARA (n = 12); RUNX1-RUNX1T1 (n = 12), normal karyotype (n = 11), and MLL gene fusions other than MLL-SEPT2 (n = 10).
  • We also studied all three MLL-SEPT2 myeloid neoplasia cases reported in the literature, namely two AML patients and a t-MDS patient.
  • RESULTS: When compared with normal controls, we found a 12.8-fold reduction of wild-type SEPT2 and MLL-SEPT2 combined expression in cases with the MLL-SEPT2 gene fusion (p = 0.007), which is accompanied by a 12.4-fold down-regulation of wild-type MLL and MLL-SEPT2 combined expression (p = 0.028).
  • The down-regulation of SEPT2 in MLL-SEPT2 myeloid neoplasias was statistically significant when compared with all other leukemia genetic subgroups (including those with other MLL gene fusions).
  • In addition, MLL expression was also down-regulated in the group of MLL fusions other than MLL-SEPT2, when compared with the normal control group (p = 0.023) CONCLUSION: We found a significant down-regulation of both SEPT2 and MLL in MLL-SEPT2 myeloid neoplasias.
  • In addition, we also found that MLL is under-expressed in AML patients with MLL fusions other than MLL-SEPT2.
  • [MeSH-major] Down-Regulation. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Phosphoric Monoester Hydrolases / genetics

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  • (PMID = 19445675.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Other-IDs] NLM/ PMC2689242
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6. Cerveira N, Micci F, Santos J, Pinheiro M, Correia C, Lisboa S, Bizarro S, Norton L, Glomstein A, Asberg AE, Heim S, Teixeira MR: Molecular characterization of the MLL-SEPT6 fusion gene in acute myeloid leukemia: identification of novel fusion transcripts and cloning of genomic breakpoint junctions. Haematologica; 2008 Jul;93(7):1076-80
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  • [Title] Molecular characterization of the MLL-SEPT6 fusion gene in acute myeloid leukemia: identification of novel fusion transcripts and cloning of genomic breakpoint junctions.
  • One of the MLL fusion partners in leukemia is the SEPT6 gene, which belongs to the evolutionarily conserved family of genes of septins.
  • In this work we aimed to characterize at both the RNA and DNA levels three acute myeloid leukemias with cytogenetic evidence of a rearrangement between 11q23 and Xq24.
  • Molecular analysis led to the identification of several MLL-SEPT6 fusion transcripts in all cases, including a novel MLL-SEPT6 rearrangement (MLL exon 6 fused with SEPT6 exon 2).
  • Genomic DNA breakpoints were found inside or near Alu or LINE repeats in the MLL breakpoint cluster region, whereas the breakpoint junctions in the SEPT6 intron 1 mapped to the vicinity of GC-rich low-complexity repeats, Alu repeats, and a topoisomerase II consensus cleavage site.
  • These data suggest that a non-homologous end-joining repair mechanism may be involved in the generation of MLL-SEPT6 rearrangements in acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 18492691.001).
  • [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 / MLL-SEPT6 fusion protein, human; 0 / Oncogene Proteins, Fusion
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7. Röhrs S, Dirks WG, Meyer C, Marschalek R, Scherr M, Slany R, Wallace A, Drexler HG, Quentmeier H: Hypomethylation and expression of BEX2, IGSF4 and TIMP3 indicative of MLL translocations in acute myeloid leukemia. Mol Cancer; 2009;8:86
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  • [Title] Hypomethylation and expression of BEX2, IGSF4 and TIMP3 indicative of MLL translocations in acute myeloid leukemia.
  • BACKGROUND: Translocations of the Mixed Lineage Leukemia (MLL) gene occur in a subset (5%) of acute myeloid leukemias (AML), and in mixed phenotype acute leukemias in infancy - a disease with extremely poor prognosis.
  • Animal model systems show that MLL gain of function mutations may contribute to leukemogenesis.
  • Wild-type (wt) MLL possesses histone methyltransferase activity and functions at the level of chromatin organization by affecting the expression of specific target genes.
  • While numerous MLL fusion proteins exert a diverse array of functions, they ultimately serve to induce transcription of specific genes.
  • Hence, acute lymphoblastic leukemias (ALL) with MLL mutations (MLLmu) exhibit characteristic gene expression profiles including high-level expression of HOXA cluster genes.
  • Here, we aimed to relate MLL mutational status and tumor suppressor gene (TSG) methylation/expression in acute leukemia cell lines.
  • RESULTS: Using MS-MLPA (methylation-specific multiplex ligation-dependent probe amplification assay), methylation of 24 different TSG was analyzed in 28 MLLmu and MLLwt acute leukemia cell lines.
  • The positive correlation between MLL translocation, TSG hypomethylation and expression suggested that MLL fusion proteins were responsible for dysregulation of TSG expression in MLLmu cells.
  • This concept was supported by our observation that Bex2 mRNA levels in MLL-ENL transgenic mouse cell lines required expression of the MLL fusion gene.
  • CONCLUSION: These results suggest that the conspicuous expression of the TSG BEX2, IGSF4 and TIMP3 in MLLmu AML cell lines is the consequence of altered epigenetic properties of MLL fusion proteins.
  • [MeSH-major] Immunoglobulins / metabolism. Leukemia, Myeloid, Acute / genetics. Membrane Proteins / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Nerve Tissue Proteins / metabolism. Tissue Inhibitor of Metalloproteinase-3 / metabolism. Translocation, Genetic. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19835597.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BEX2 protein, human; 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Histones; 0 / Hydroxamic Acids; 0 / Immunoglobulins; 0 / MLL-ENL oncoprotein, human; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor beta; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3X2S926L3Z / trichostatin A; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2770485
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8. Worcester HD, Vasef MA: Therapy-related acute myeloid leukemia with 11q23 abnormality coexisting with refractory metastatic Ewing sarcoma: report of a case and review of the literature. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):50-4
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  • [Title] Therapy-related acute myeloid leukemia with 11q23 abnormality coexisting with refractory metastatic Ewing sarcoma: report of a case and review of the literature.
  • The patient's Ewing sarcoma remained refractory to treatment despite continuous intensified chemotherapy and was complicated by a therapy-related acute myeloid leukemia with 11q23 abnormality.
  • Examination of bone marrow at the last clinical follow up demonstrated both acute myeloid leukemia and residual metastatic Ewing sarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Neoplasms / drug therapy. Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / chemically induced. Lung Neoplasms / drug therapy. Sarcoma, Ewing / drug therapy. Translocation, Genetic


9. Saito M, Mori A, Irie T, Tanaka M, Morioka M: [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer]. Rinsho Ketsueki; 2009 Mar;50(3):192-6
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  • [Title] [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer].
  • Among cases of therapy-related acute myeloid leukemia (t-AML) due to DNA topoisomerase II inhibitors, 11q23 abnormality is often detected.
  • The usefulness of paclitaxel as a key drug in chemotherapy for breast cancer has been demonstrated.
  • In this study, we report a patient who developed t-AML with 11q23 abnormality and bone marrow metastasis after breast cancer treatment with paclitaxel.
  • Bone marrow aspiration suggested AML (M4) with (11;19)(q23;p13) chromosome abnormalities.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Bone Marrow Neoplasms / secondary. Breast Neoplasms / pathology. Chromosome Aberrations / drug effects. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Neoplasms, Second Primary. Paclitaxel / adverse effects


10. 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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11. DiMartino JF, Lacayo NJ, Varadi M, Li L, Saraiya C, Ravindranath Y, Yu R, Sikic BI, Raimondi SC, Dahl GV: Low or absent SPARC expression in acute myeloid leukemia with MLL rearrangements is associated with sensitivity to growth inhibition by exogenous SPARC protein. Leukemia; 2006 Mar;20(3):426-32
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  • [Title] Low or absent SPARC expression in acute myeloid leukemia with MLL rearrangements is associated with sensitivity to growth inhibition by exogenous SPARC protein.
  • Although SPARC has been implicated as a tumor suppressor in humans, its function in normal or malignant hematopoiesis has not previously been studied.
  • We found that the leukemic cells of AML patients with MLL gene rearrangements express low to undetectable amounts of SPARC whereas normal hematopoietic progenitors and most AML patients express this gene.
  • SPARC RNA and protein levels were also low or undetectable in AML cell lines with MLL translocations.
  • Consistent with its tumor suppressive effects in various solid tumor models, exogenous SPARC protein selectively reduced the growth of cell lines with MLL rearrangements by inhibiting cell cycle progression from G1 to S phase.
  • The lack of SPARC expression in MLL-rearranged cell lines was associated with dense promoter methylation.
  • Our results suggest that low or absent SPARC expression is a consistent feature of AML cells with MLL rearrangements and that SPARC may function as a tumor suppressor in this subset of patients.
  • A potential role of exogenous SPARC in the therapy of MLL-rearranged AML warrants further investigation.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid / metabolism. Myeloid-Lymphoid Leukemia Protein / genetics. Osteonectin / metabolism
  • [MeSH-minor] Acute Disease. Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16424866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / K08 CA818818; United States / NCRR NIH HHS / RR / M01 RR 00070; United States / NCI NIH HHS / CA / R01 CA90916; United States / NCI NIH HHS / CA / R01 CA92474
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MLL protein, human; 0 / Osteonectin; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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12. Cerveira N, Correia C, Bizarro S, Pinto C, Lisboa S, Mariz JM, Marques M, Teixeira MR: SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23). Oncogene; 2006 Oct 5;25(45):6147-52
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  • [Title] SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23).
  • We have identified a new mixed lineage leukemia (MLL) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality.
  • Fluorescence in situ hybridization demonstrated a rearrangement of the MLL gene and molecular genetic analyses identified a septin family gene, SEPT2, located on chromosome 2q37, as the fusion partner of MLL.
  • RNA and DNA analyses showed the existence of an in-frame fusion of MLL exon 7 with SEPT2 exon 3, with the genomic breakpoints located in intron 7 and 2 of MLL and SEPT2, respectively.
  • Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in MLL intron 7 and SEPT2 intron 2.
  • SEPT2 is the fifth septin family gene fused with MLL, making this gene family the most frequently involved in MLL-related AML (about 10% of all known fusion partners).
  • Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of MLL-associated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

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  • (PMID = 16682951.001).
  • [ISSN] 0950-9232
  • [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 / DNA, Neoplasm; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
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13. Mikulásová Z, Ilencíková D, Slamka T, Durovcíková D: [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)]. Klin Onkol; 2010;23(6):401-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)].
  • [Transliterated title] Akútna myeloblastová leukémia s alteráciami MLL protoonkogénu (11q23/MLL+ AML).
  • One of the most common chromosomal breakpoint regions in acute myeloid leukaemia is the chromosome band 11q23.
  • The analysis of this region led to the discovery of the extremely promiscuous MLL gene, in which more than 60 MLL translocation partner genes have been described.
  • Among the most frequent are t(9;11)(p21-22;q23)/MLL-AF9, t(10; 11)(p13; q23)/MLL-AF10, t(11;19)(q23;p13)/MLL-ELL, ENL and t(6;11)(q27;q23)/MLL-AF6.
  • The presented work provides an overview of the molecular mechanisms by means of which MLL proto-oncogene can be converted into oncogene.
  • Genetic alternations of the MLL Proto-Oncogene Protein besides translocation are also represented by complex chromosomal rearrangements, deletions, insertions, partial tandem duplications, amplifications and gains.
  • Abnormalities of the MLL ProtoOncogene Protein are usually connected with bad prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 11 / genetics. Humans. Translocation, Genetic

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  • (PMID = 21351416.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] slo
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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14. Klymenko SV, Bink K, Trott KR, Bebeshko VG, Bazyka DA, Dmytrenko IV, Abramenko IV, Bilous NI, Zitzelsberger H, Misurin AV, Atkinson MJ, Rosemann M: MLL gene alterations in radiation-associated acute myeloid leukemia. Exp Oncol; 2005 Mar;27(1):71-5
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  • [Title] MLL gene alterations in radiation-associated acute myeloid leukemia.
  • AIM: Although acute myelogenous leukemia (AML) arising after radiation exposure is considered to be secondary, little is known about the molecular mechanisms by which the radiation induces the leukemogenic phenotype.
  • The aim of the study was to analyze whether the MLL translocations are as frequent in radiation-associated AML as in spontaneous AML cases.
  • METHODS: Sixty one AML samples obtained at diagnosis were analyzed for the presence of MLL abnormalities using fluorescent in situ hybridization and/or reverse transcription polymerase chain reaction.
  • RESULTS: MLL gene translocations were detected in both groups of spontaneous and therapy-related AML (1/32 and 1/2 cases respectively).
  • The sole MLL rearrangement found in the group of radiation-associated AML patients was a duplication of the gene.
  • CONCLUSION: Our data preclude the involvement of MLL gene translocations in radiation-induced leukemogenesis, but support the assumption that loss and gain of chromosomal material could be crucial in the leukemogenesis of AML patients with the history of radiation exposure due to the Chernobyl accident.
  • [MeSH-major] Chernobyl Nuclear Accident. Chromosome Aberrations / radiation effects. DNA, Neoplasm / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15812362.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 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
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15. Pardee TS, Zuber J, Lowe SW: Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia.
  • : 7060 Background: Acute myeloid leukemia (AML) is an aggressive, genetically heterogeneous malignancy.
  • The Flt3 receptor tyrosine kinase containing an internal tandem duplication (Flt3 ITD) is a common mutation in AML and associated with a poor prognosis; however, its effect on chemotherapy response is currently unknown.
  • METHODS: Murine AML was generated by retroviral transduction of an MLL-ENL fusion protein into fetal liver cells and subsequent transplantation into syngeneic mice.
  • Blasts were harvested from moribund animals and myeloid lineage confirmed by immunophenotyping.

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  • (PMID = 27961434.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Rubnitz J, Inaba H, Ribeiro R, Pounds S, Pui C, Leung W: Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10034

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.
  • We hypothesized that the transplantation of purified haploidentical NK cells may be a safe and effective form of consolidation therapy that will reduce the risk of relapse among children with acute myeloid leukemia (AML) who are not treated with HSCT.
  • Leukemic cell genetic abnormalities included CBFβ-MYH11in 4 cases, RBM15-MKL1in 2 cases, MLL-ENL and MLL-AF9 in 1 case each; 2 cases had no detectable abnormalities.
  • With a median follow-up time of 637 days, all patients remain in remission.

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  • (PMID = 27962581.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Schwind S, Marcucci G, Maharry K, Radmacher MD, Whitman SP, Paschka P, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML). J Clin Oncol; 2009 May 20;27(15_suppl):7001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML).
  • FLT3, NPM1, CEBPA, MLL, and WT1 mutations, and ERG and BAALC expression were analyzed centrally. miR-181a expression was measured in pretherapy marrow using OSUCCC v3.0 arrays.
  • The mean of 2 miR-181a probe log intensities was used as a continuous variable for analyses.

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  • (PMID = 27961373.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Sait SN, Claydon MA, Conroy JM, Nowak NJ, Barcos M, Baer MR: Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):143-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia.
  • Reciprocal chromosomal translocations involving the MLL gene at chromosome region 11q23 are recurring cytogenetic abnormalities in both de novo and therapy-related acute myeloid leukemia (AML) and in acute lymphoblastic leukemia.
  • We report a t(4;11)(p12;q23) with rearrangement of MLL and FRYL (also known as AF4p12), a human homolog to the furry gene of Drosophila, in an adult patient with therapy-related AML after fludarabine and rituximab therapy for small lymphocytic lymphoma and radiation therapy for breast carcinoma.
  • To our knowledge, t(4;11)(p12;q23) has been reported in two previous patients, and MLL and FRYL rearrangement was demonstrated in one of them.
  • Thus, t(4;11)(p12;q23) with MLL and FRYL involvement represents a new recurring 11q23 translocation, to date seen only in therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17854671.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 4F4X42SYQ6 / Rituximab; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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19. Morerio C, Rapella A, Tassano E, Rosanda C, Panarello C: MLL-MLLT10 fusion gene in pediatric acute megakaryoblastic leukemia. Leuk Res; 2005 Oct;29(10):1223-6
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  • [Title] MLL-MLLT10 fusion gene in pediatric acute megakaryoblastic leukemia.
  • The occurrence of MLL gene rearrangement in acute megakaryoblastic leukemia (AML-M7, acute myeloid leukemia, French-American-British type M7) is very rare and limited to pediatric age: in particular, MLL-MLLT10 fusion, previously reported as characteristic of monocytic leukemia, has been reported in only one case of pediatric megakaryoblastic leukemia.
  • We describe the second case with this association in light of the few reported cases of AML-M7 with MLL and/or 11q23 involvement.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein. Translocation, Genetic

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  • (PMID = 16111539.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 15
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20. Kakihana K, Kubo F, Wakabayashi S, Kurosu T, Miki T, Murakami N, Miura O: A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jul 15;184(2):109-12
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  • [Title] A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia.
  • MLL located at 11q23 is fused with a variety of partner genes by recurrent chromosomal translocations in acute leukemias.
  • ELL, the MLL partner gene located on chromosome 19p13.1, encodes an RNA polymerase II transcriptional elongation factor, which also possesses the N-terminal region involved in the inhibition of transcription initiation.
  • Here we report a case of chronic myelomonocytic leukemia (CMML) with a 46,XY,t(11;19)(q23;p13.1) karyotype that transformed to acute myeloid leukemia (AML) without showing any karyotypic evolution.
  • Interphase fluorescent in situ hybridization analysis showed the split MLL signals in 95% of bone marrow cells when the diagnosis of CMML was made and the percentage of blasts was 1.2%.
  • Sequence analysis of reverse-transcriptional polymerase chain reaction product revealed a novel variant form of MLL-ELL transcript in which MLL exon 10 was fused to ELL exon 3.
  • MLL has been fused to ELL exon 2 in all the previously reported MLL-ELL transcripts, which have always been associated with AML.
  • It is deduced that the variant form of MLL-ELL may be defective not only in inhibition of transcription initiation, but also in transcriptional elongation.
  • Thus, a possibility is raised that the unique clinical presentation of the present case with t(11;19)(q23;p13.1) might be related to the variant form of MLL-ELL.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic


21. Basecke J, Whelan JT, Griesinger F, Bertrand FE: The MLL partial tandem duplication in acute myeloid leukaemia. Br J Haematol; 2006 Nov;135(4):438-49

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  • [Title] The MLL partial tandem duplication in acute myeloid leukaemia.
  • Mixed lineage leukaemia gene-partial tandem duplications (MLL-PTD) characterise acute myeloid leukaemia (AML) with trisomy 11 and AML with a normal karyotype.
  • MLL-PTD confer a worse prognosis with shortened overall and event free survival in childhood and adult AML.
  • This review summarises clinical studies on MLL-PTD positive AML and recent experimental findings on the putative leukaemogenic role of MLL-PTD.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences
  • [MeSH-minor] Acute Disease. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 11 / genetics. DNA, Neoplasm / genetics. Genetic Predisposition to Disease. Histone-Lysine N-Methyltransferase. Humans. Prognosis. Trisomy

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  • (PMID = 16965385.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 81
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22. Pajuelo-Gámez JC, Cervera J, García-Casado Z, Mena-Durán AV, Valencia A, Barragán E, Such E, Bolufer P, Sanz MA: MLL amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Apr 15;174(2):127-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL amplification in acute myeloid leukemia.
  • The chromosomal alterations at 11q23 that involve the mixed-lineage leukemia gene (MLL, HTRX1, HRX, ALL1) are one of the most common cytogenetic abnormalities in acute leukemia and have been associated with a poor prognosis.
  • Given that not all MLL alterations are seen under conventional cytogenetics or fluorescence in situ hybridization (FISH), it is very important to use molecular techniques to determine the cause of alteration.
  • In this study, we describe two cases of AML in which FISH analysis showed a high-level 11q23 amplification, to confirm if this overexpression may be accompanied by partial tandem duplication of the MLL gene (MLL-PTD).
  • The 11q23 region characterization included conventional cytogenetics, FISH, and comparative genomic hybridization analysis to study the expression patterns of several oncogenes located within the amplified region and detection of partial tandem duplication of the MLL gene by reverse-transcription polymerase chain reaction (RT-PCR) and sequencing.
  • MLL-PTD were detected in the two patients.
  • Moreover, patient 1 showed amplification of the MLL flanking region.
  • Our data suggest that molecular methods such as RT-PCR or sequencing should be used to detect MLL alterations, and that amplification of MLL locus may be extended to its flanking region.
  • [MeSH-major] Gene Amplification. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Aged. Aneuploidy. Base Sequence. Chromosome Banding. Chromosome Deletion. Female. Genome, Human. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization / methods. Sequence Analysis, DNA

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  • (PMID = 17452254.001).
  • [ISSN] 0165-4608
  • [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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23. Eguchi M, Eguchi-Ishimae M, Greaves M: Molecular pathogenesis of MLL-associated leukemias. Int J Hematol; 2005 Jul;82(1):9-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular pathogenesis of MLL-associated leukemias.
  • Chromosome translocations disrupting the MLL gene are associated with various hematologic malignancies but are particularly common in infant and secondary therapy-related acute leukemias.
  • The normal MLL-encoded protein is an essential component of a supercomplex with chromatin-modulating activity conferred by histone acetylase and methyltransferase activities, and the protein plays a key role in the developmental regulation of gene expression, including Hox gene expression.
  • In leukemia, this function is subverted by breakage, recombination, and the formation of chimeric fusion with one of many alternative partners.
  • Such MLL translocations result in the replacement of the C-terminal functional domains of MLL with those of a fusion partner, yielding a newly formed MLL chimeric protein with an altered function that endows hematopoietic progenitors with self-renewing and leukemogenic activity.
  • This potent impact of the MLL chimera can be attributed to one of 2 kinds of activity of the fusion partner: direct transcriptional transactivation or dimerization/oligomerization.
  • Key unresolved issues currently being addressed include the set of target genes for MLL fusions, the stem cell of origin for the leukemias, the role of additional secondary mutations, and the origins or etiology of the MLL gene fusions themselves.
  • Further elaboration of the biology of MLL gene-associated leukemia should lead to novel and specific therapeutic strategies.
  • [MeSH-major] Leukemia / genetics. Leukemia / physiopathology. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / physiology. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Hematopoiesis / physiology. Hematopoietic Stem Cells / physiology. Histone-Lysine N-Methyltransferase. Humans. Oncogene Proteins, Fusion / physiology

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  • (PMID = 16105754.001).
  • [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] 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] 165
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24. Horton SJ, Walf-Vorderwülbecke V, Chatters SJ, Sebire NJ, de Boer J, Williams O: Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities. Blood; 2009 May 14;113(20):4922-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities.
  • Chromosomal translocations involving 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL fusion genes.
  • However, the dependence of acute leukemia on MLL fusion activity in vivo and the efficacy of targeting this activity to eliminate disease have not been established.
  • We have developed a model for conditional expression of MLL-ENL in hematopoietic progenitor cells, in which expression of the fusion oncogene is turned off by doxycycline.
  • Conditionally immortalized myeloblast cells derived from these progenitors were found to induce leukemia in vivo.
  • Leukemic cells isolated from primary recipient mice were shown to have acquired additional genetic abnormalities and, when transplanted into secondary recipients, induced leukemia with shortened latencies.
  • However, the leukemic cells remained dependent on MLL-ENL expression in vitro and in vivo, and its ablation resulted in regression of established leukemias.
  • This study demonstrates that even genetically complex leukemias can be reversed on inactivation of the initiating MLL fusion and has important implications for the design of novel leukemia therapies.
  • [MeSH-major] Chromosome Aberrations. Genetic Therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / antagonists & inhibitors

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  • (PMID = 19029444.001).
  • [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 / DNA-Binding Proteins; 0 / Mllt1 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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25. Maitta RW, Cannizzaro LA, Ramesh KH: Association of MLL amplification with poor outcome in acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):40-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of MLL amplification with poor outcome in acute myeloid leukemia.
  • Chromosomal rearrangements and amplification of the MLL gene at 11q23 are common abnormalities found in patients with severe myelodysplastic disorders and lymphoid and acute myeloid leukemias.
  • MLL rearrangements are associated with aggressive disease in both children and adults, with current evidence suggesting that MLL alterations are associated with a poor prognosis.
  • We report the clinical, cytogenetic and histologic findings of a patient who presented with a de novo diagnosis of AML-M4 and who fits the profile of patients presenting with MLL alterations, such as old age at presentation, rapid progression, therapeutic refractoriness, and poor outcome.
  • Two bone marrow specimens taken 1 month apart show the rapid deterioration of the patient's cytogenetic abnormalities at the 11q23 locus, with amplification of MLL that was originally seen as a homogeneously staining region (hsr) on chromosome 11.
  • In the second biopsy the hsr and MLL amplification appears as nonreciprocal translocation of multiple copies in the form of marked amplification of MLL on chromosome 16 in a background of increasing chromosomal aberrations.
  • This case suggests that either the MLL amplification and translocation alone or in conjunction with other flanking oncogenes may have played an important role in poor patient outcome.
  • [MeSH-major] Gene Amplification / physiology. Leukemia, Myeloid, Acute / diagnosis. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19480936.001).
  • [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
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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26. Jin S, Zhao H, Yi Y, Nakata Y, Kalota A, Gewirtz AM: c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis. J Clin Invest; 2010 Feb;120(2):593-606
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis.
  • Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia.
  • These chromosomal translocations commonly result in MLL fusion proteins that dysregulate transcription.
  • Recent data suggest that the MYB proto-oncogene, which is an important regulator of hematopoietic cell development, has a role in leukemogenesis driven by the MLL-ENL fusion protein, but exactly how is unclear.
  • Here we have demonstrated that c-Myb is recruited to the MLL histone methyl transferase complex by menin, a protein important for MLL-associated leukemic transformation, and that it contributes substantially to MLL-mediated methylation of histone H3 at lysine 4 (H3K4).
  • Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus.
  • This decreased occupancy was associated with a diminished ability of an MLL-ENL fusion protein to transform normal mouse hematopoietic cells.
  • The finding that c-Myb has the ability to direct epigenetic marks, along with its participation in an autoregulatory feedback loop with genes known to transform hematopoietic cells, lends mechanistic and translationally relevant insight into its role in MLL-associated leukemogenesis.
  • [MeSH-major] Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myb / metabolism

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  • (PMID = 20093773.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA072765; United States / NCI NIH HHS / CA / 2P01CA072765-11
  • [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 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myb; 0 / Recombinant Fusion Proteins; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2810070
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27. Whitman SP, Liu S, Vukosavljevic T, Rush LJ, Yu L, Liu C, Klisovic MI, Maharry K, Guimond M, Strout MP, Becknell B, Dorrance A, Klisovic RB, Plass C, Bloomfield CD, Marcucci G, Caligiuri MA: The MLL partial tandem duplication: evidence for recessive gain-of-function in acute myeloid leukemia identifies a novel patient subgroup for molecular-targeted therapy. Blood; 2005 Jul 1;106(1):345-52
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  • [Title] The MLL partial tandem duplication: evidence for recessive gain-of-function in acute myeloid leukemia identifies a novel patient subgroup for molecular-targeted therapy.
  • MLL (ALL-1) chimeric fusions and MLL partial tandem duplications (PTD) may have mechanistically distinct contributions to leukemogenesis.
  • Acute myeloid leukemia (AML) blasts with the t(9;11)(p22;.
  • q23) express MLL-AF9 and MLL wild-type (WT) transcripts, while normal karyotype AML blasts with the MLL(PTD/WT) genotype express MLL PTD but not the MLL WT.
  • Silencing of MLL WT in MLL(PTD/WT) blasts was reversed by DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors, and MLL WT induction was associated with selective sensitivity to cell death.
  • Reduction of MLL PTD expression induced MLL WT and reduced blast colony-forming units, supporting opposing functions for MLL PTD and MLL WT whereby the MLL PTD contributes to the leukemic phenotype via a recessive gain-of-function.
  • The coincident suppression of the MLL WT allele with the expression of the MLL PTD allele, along with the functional data presented here, supports the hypothesis that loss of WT MLL function via monoallelic repression contributes to the leukemic phenotype by the remaining mutant allele.
  • These data from primary AML and the pharmacologic reversal of MLL WT silencing associated with a favorable alteration in the threshold for apoptosis suggest that these patients with poor prognosis may benefit from demethylating or histone deacetylase inhibitor therapy, or both.

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  • (PMID = 15774615.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA93548; United States / NCI NIH HHS / CA / CA089317; United States / NCI NIH HHS / CA / R01 CA89341; United States / NCI NIH HHS / CA / P30 CA16058; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA09338; United States / NCI NIH HHS / CA / R01 CA102031
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / MLL protein, human; 0 / Oligodeoxyribonucleotides; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1895129
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28. Yamamoto S, Nishi M, Taniguchi K, Imayoshi M, Ogata Y, Iwanaga M, Sakai N, Hamasaki Y, Ishii E: Partial tandem duplication of MLL gene in acute myeloid leukemia with translocation (11;17)(q23;q12-21). Am J Hematol; 2005 Sep;80(1):46-9
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  • [Title] Partial tandem duplication of MLL gene in acute myeloid leukemia with translocation (11;17)(q23;q12-21).
  • Translocation 11q23 and MLL gene rearrangements are commonly observed in acute myeloid leukemia (AML) in association with the myelomonocytic or monocytic feature.
  • We describe a case involving a 15-year-old patient with AML characterized by leukemic cells exhibiting translocation (11;17)(q23;q12-21) and MLL gene rearrangement.
  • No fusion partner gene of the MLL gene was identified, including RARalpha(17q12) or AF17 (17q21); however, a partial tandem duplication of the MLL exon 11/exon 10 was detected in leukemic cells via a 3'RACE method for detection of unknown partner genes.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Base Sequence. Chromosome Mapping. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Myeloid-Lymphoid Leukemia Protein

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138343.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [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
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29. Spector LG, Xie Y, Robison LL, Heerema NA, Hilden JM, Lange B, Felix CA, Davies SM, Slavin J, Potter JD, Blair CK, Reaman GH, Ross JA: Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group. Cancer Epidemiol Biomarkers Prev; 2005 Mar;14(3):651-5
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  • [Title] Maternal diet and infant leukemia: the DNA topoisomerase II inhibitor hypothesis: a report from the children's oncology group.
  • BACKGROUND: The MLL 11q23 translocation arises in utero and is present in 75% of infant leukemias.
  • That MLL+ acute myeloid leukemia (AML) can arise following chemotherapy with DNA topoisomerase II (DNAt2) inhibitors suggests that these substances, which also occur naturally in foods, may contribute toward infant leukemia.
  • We hypothesized that maternal consumption of dietary DNAt2 inhibitors during pregnancy would increase the risk of infant leukemia, particularly AML(MLL+).
  • METHODS: This Children's Oncology Group case-control study consisted of 240 incident cases of infant acute leukemia [AML and acute lymphoblastic leukemia (ALL)] diagnosed during 1996 to 2002 and 255 random digit dialed controls.
  • RESULTS: There was little evidence of an association between the specific DNAt2 index and leukemia overall and by subtype.
  • An exception was AML(MLL+); odds ratios (95% confidence intervals) comparing the second to fourth quartiles to the first were 1.9 (0.5-7.0), 2.1 (0.6-7.7), and 3.2 (0.9-11.9), respectively (P for trend = 0.10).
  • For the vegetable and fruit index, there were significant or near-significant inverse linear trends for all leukemias combined, ALL(MLL+), and AML(MLL-).
  • CONCLUSION: Overall, maternal consumption of fresh vegetables and fruits during pregnancy was associated with a decreased risk of infant leukemia, particularly MLL+.
  • However, for AML(MLL+) cases, maternal consumption of specific DNAt2 inhibitors seemed to increase risk.
  • Although based on small numbers, these data provide some support for distinct etiologic pathways in infant leukemia.

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  • (PMID = 15767345.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA079940; United States / NCI NIH HHS / CA / CA79940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
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30. Bizarro S, Cerveira N, Correia C, Lisboa S, Peixoto A, Norton L, Teixeira MR: Molecular characterization of a rare MLL-AF4 (MLL-AFF1) fusion rearrangement in infant leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):61-4
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  • [Title] Molecular characterization of a rare MLL-AF4 (MLL-AFF1) fusion rearrangement in infant leukemia.
  • The t(4;11)(q21;q23) involving the genes MLL and AF4 (alias for AFF1) is detected in 50-70% of infant leukemia.
  • We characterize at both the DNA and RNA level a rare MLL-AF4 fusion transcript identified in a 15-month-old girl with acute lymphoblastic leukemia.
  • Direct sequence analysis of the reverse transcriptase-polymerase chain reaction product showed an in-frame fusion between MLL exon 9 and AF4 exon 6.
  • We further demonstrated that the genomic breakpoints were located 1,553 bp downstream of MLL exon 9 and 1,239 bp upstream of AF4 exon 6.
  • Four Alu repeats were detected in MLL intron 9 and two Alu repeats and one LINE1 repetitive element were identified downstream of AF4 exon 5.
  • Finally, a 9-bp polypurine (A) tract and an 8-bp polypyrimidine (T) tract were found flanking the translocation breakpoint.
  • In summary, we have characterized at both the RNA and the DNA level a rare MLL-AF4 fusion variant that was presumably mediated by Alu repeats or polypurine and polypyrimidine tracts located in the vicinity of genomic breakpoints.
  • [MeSH-major] DNA-Binding Proteins / genetics. DNA-Binding Proteins / physiology. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / physiology. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Oncogene Proteins, Fusion / genetics

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  • (PMID = 17889710.001).
  • [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
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Purines; 0 / Pyrimidines; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 63231-63-0 / RNA; 9007-49-2 / DNA; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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31. Mi S, Li Z, Chen P, He C, Cao D, Elkahloun A, Lu J, Pelloso LA, Wunderlich M, Huang H, Luo RT, Sun M, He M, Neilly MB, Zeleznik-Le NJ, Thirman MJ, Mulloy JC, Liu PP, Rowley JD, Chen J: Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia. Proc Natl Acad Sci U S A; 2010 Feb 23;107(8):3710-5
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  • [Title] Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia.
  • We have found that it is also frequently amplified and the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias.
  • Furthermore, we show that MLL fusions exhibit a much stronger direct binding to the locus of this miRNA cluster than does wild-type MLL; these changes are associated with elevated levels of histone H3 acetylation and H3K4 trimethylation and an up-regulation of these miRNAs.
  • More importantly, we show that this miRNA cluster can significantly increase colony-forming capacity of normal mouse bone marrow progenitor cells alone and, particularly, in cooperation with MLL fusions.
  • Finally, through combinatorial analysis of miRNA and mRNA arrays of mouse bone marrow progenitor cells transfected with this miRNA cluster and/or MLL fusion gene, we identified 363 potential miR-17-92 target genes that exhibited a significant inverse correlation of expression with the miRNAs.
  • Taken together, our studies suggest that overexpression of miR-17-92 cluster in MLL-rearranged leukemias is likely attributed to both DNA copy number amplification and direct up-regulation by MLL fusions, and that the miRNAs in this cluster may play an essential role in the development of MLL-associated leukemias through inhibiting cell differentiation and apoptosis, while promoting cell proliferation, by regulating relevant target genes.

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  • (PMID = 20133587.001).
  • [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 / R01 CA118319; United States / NCI NIH HHS / CA / CA127277; United States / NCI NIH HHS / CA / R01 CA127277; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / P01CA105049; United States / NCI NIH HHS / CA / P01 CA105049; United States / NCI NIH HHS / CA / CA118319
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN17 microRNA, human; 0 / MIRN92 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2840429
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32. Gao C, Zhao W, Liu Y, Gong WY, Li WJ, Li ZG, Wu MY: [Characteristics of fusion gene and immunophenotype in MLL gene rearrangement positive childhood acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1283-8
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  • [Title] [Characteristics of fusion gene and immunophenotype in MLL gene rearrangement positive childhood acute lymphoblastic leukemia].
  • The study was aimed to investigate the fusion gene transcript and immunophenotypic characteristics of the mixed linage leukemia (MLL)-rearranged positive childhood acute lymphoblastic leukemia (ALL).
  • The incidence of MLL rearrangement in 601 cases of ALL patients was detected by the multiple-nested polymerase chain reaction (PCR); the subtypes and features of the fusion gene transcript were analyzed by PCR products sequencing; the immunophenotypic characteristics at diagnosis were compared between the 22 MLL rearrangement positive of ALL patient, 30 negative control which selected randomly from the patients whose fusion gene could not be detected in the same term and 43 pro-B-ALL patients.
  • The results showed that the incidence of MLL positive ALL was 3.66%, constituted 29.9% of the pro-B-ALL.
  • The MLL rearrangement positive 20 B-ALL patients were all CD10 negative; the number of patients who carried CD13, CD33 and CD34 was lower than that of pro-B-ALL who had no fusion gene, whereas the expression of CD20, CD22, CD2, CD5, CD7 showed no difference.
  • 4 kind partner genes of MLL-AF4, AF9, AF10 and ENL were detected.
  • The fusion loci of MLL gene were mainly located at the exon 6, 7, 8 and many kind of fusion loci of MLL may exist in one patient; whereas its partner gene fusion loci were relatively single.
  • A transcript contains a random insert sequence existed in a transcript of one MLL-AF10+ patient.
  • It is concluded that though incidence of MLL rearrangement is low, but it has a variety of fusion transcripts, the ALL patients has unique biological characteristics at immunophenotype and fusion transcript.

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  • (PMID = 19840468.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. Somervaille TC, Cleary ML: Grist for the MLL: how do MLL oncogenic fusion proteins generate leukemia stem cells? Int J Hematol; 2010 Jun;91(5):735-41
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  • [Title] Grist for the MLL: how do MLL oncogenic fusion proteins generate leukemia stem cells?
  • MLL fusion oncogenes are pathogenically associated with 5-10% of human acute leukemias.
  • Through multiple interactions with chromatin regulatory factors, they convert a normal hematopoietic hierarchy into a leukemia cell hierarchy sustained at its apex by a population of inappropriately self-renewing myeloid cells termed leukemia stem cells (LSCs).
  • Initiation of the aberrant leukemia cell hierarchy is associated with an abnormal epigenetic state at Hoxa and Meis1 loci, with concomitant high level Hoxa and Meis1 expression.
  • In contrast, differentiation-mediated exit of LSCs from the self-renewing compartment of the leukemia clone depends on the prevailing levels of the transcription factor Myb, which functions as part of an LSC maintenance program influenced, but not directly controlled, by Hoxa and Meis1.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Hematopoietic Stem Cells / pathology. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20454944.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C147/A6058
  • [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 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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35. Bursen A, Schwabe K, Rüster B, Henschler R, Ruthardt M, Dingermann T, Marschalek R: The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4. Blood; 2010 Apr 29;115(17):3570-9
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  • [Title] The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4.
  • The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).
  • To elucidate the leukemogenic potential of the fusion proteins MLL.AF4 and AF4.MLL, Lin(-)/Sca1(+) purified cells (LSPCs) were retrovirally transduced with either both fusion genes or with MLL.AF4 or AF4.MLL alone.
  • Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia.
  • Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months.
  • These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein.
  • In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20194896.001).
  • [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 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
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36. Hudecek M, Bartsch K, Jäkel N, Heyn S, Pfannes R, Al-Ali HK, Cross M, Pönisch W, Gerecke U, Edelmann J, Ittel T, Niederwieser D: Spontaneous remission of acute myeloid leukemia relapse after hematopoietic cell transplantation in a high-risk patient with 11q23/MLL abnormality. Acta Haematol; 2008;119(2):111-4
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  • [Title] Spontaneous remission of acute myeloid leukemia relapse after hematopoietic cell transplantation in a high-risk patient with 11q23/MLL abnormality.
  • A 35-year-old female patient was diagnosed with acute myeloid leukemia with multiple genetic aberrations [48 XX, del(3)(q21), +6, t(11;15)(q23;q15), +21] including an 11q23/MLL abnormality.
  • A bone marrow aspirate revealed 55% leukemic blasts carrying the unfavorable genetic aberrations seen at initial diagnosis (11q23/MLL).
  • Molecular analysis of the 11q23/MLL rearrangement was used to evaluate minimal residual disease, which became undetectable in repetitive FISH analyses.
  • This is the first report of spontaneous remission in a patient with initially a multiaberrant leukemic cell clone and a proven 11q23/MLL abnormality at relapse after HCT.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / pathology. Myeloid-Lymphoid Leukemia Protein / genetics

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  • [Copyright] 2008 S. Karger AG, Basel
  • (PMID = 18367831.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [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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37. He J, Chen ZX, Xue YQ, Pan JL, He HL, Li JQ, Wu YF, Huang YP, Zhu LL: [Study on clinical and biological characteristics of childhood acute leukemia with MLL gene rearrangements]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):477-80
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  • [Title] [Study on clinical and biological characteristics of childhood acute leukemia with MLL gene rearrangements].
  • OBJECTIVE: To study the clinical and laboratory features of childhood acute leukemia (AL) with MLL gene rearrangements.
  • METHODS: Sixteen of 298 cases of childhood AL with MLL rearrangements were studied by using MLL dual-color FISH, multiplex RT-PCR with 13 pairs of primers in combination with R banding karyotype analysis and cell immunophenotyping by flow cytometry.
  • RESULTS: Sixteen cases of childhood AL with MLL rearrangements accounted for 5.4% of 298 AL patients, and 56.3% of infant ALs.
  • Among 106 cases analyzed by multiplex RT-PCR, MLL gene rearrangements were found in 11 cases, including MLL/AF4 fusion gene in 2, MLL/AF6 fusion gene in 1, MLL/AF6 and MLL/ELL combined with MLL/ AFX or HOX11 in one case each, MLL/AF9 in 2, MLL/AF10 in 1, MLL/ELL in 2.
  • MLL partial tandem duplication in 1 and activated HOX11 in 1.
  • In 27 cases assayed by FISH, 9 cases (36.0%) were demonstrated MLL gene rearrangements.
  • In 16 patients with MLL gene rearrangements, 14 (87.5%) exhibited clonal chromosome abnormalities involved chromosome 11 in 11 cases: being t(4;11) in 2, t(6;11), t(8;11), t(7;8;11), t(9;11) in each trisomy 11 in 2 and 11q--in 3 cases.
  • Among these 16 patients, 11 were B-ALL, and 5 AML-M5, 3 of the latter were CD7+ and CD2+.
  • CONCLUSION: Multiplex RT-PCR combined with FISH provided a more accurate and sensitive method for detection of MLL gene rearrangements.
  • Finding out MLL gene rearrangement is of most importance in guiding therapy and predicting prognosis in childhood AL.
  • [MeSH-major] Gene Rearrangement. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 16383239.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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38. Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Morice P, Bourquard P, Banzakour S, Le Calvez G, Marion V, Berthou C, De Braekeleer M: Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations. Cancer Genet Cytogenet; 2005 Mar;157(2):169-74
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  • [Title] Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations.
  • Band 11q23 is known to be involved in translocations and insertions with a variety of partner chromosomes.
  • They lead to MLL rearrangement, resulting in a fusion with numerous genes.
  • We report here 2 male adults in whom a diagnosis of acute myelomonoblastic leukemia (FAB M4) and acute monoblastic leukemia (FAB M5) was made.
  • Conventional cytogenetic techniques showed a 45,XY,t(1;11)(p32;q23),-7 karyotype in the first case and a 46,XY, t(11;17)(q23;q21) in the second case.
  • Fluorescent in situ hybridization (FISH) with a specific MLL probe showed the gene to be disrupted, the 3' region being translocated on the derivative chromosomes 1 and 17, respectively.
  • Fourteen and 24 patients, including ours, with acute myeloblastic leukemia associated with a t(1;11)(p32;q23) and a t(11;17)(q23;q21), respectively have been reported in the literature.
  • Several patients with the latter translocation have also been identified to have acute lymphoblastic leukemia (ALL).
  • Although both translocations are preferentially associated with monocytic differentiation, the t(11;17)(q23;q21) is more common in adults and has been reported in many patients with ALL, compared to the t(1;11)(p32;q23).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15721641.001).
  • [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 / 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
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39. Muntean AG, Hess JL: MLL-AF9 leukemia stem cells: hardwired or taking cues from the microenvironment? Cancer Cell; 2008 Jun;13(6):465-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL-AF9 leukemia stem cells: hardwired or taking cues from the microenvironment?
  • MLL rearrangements in humans lead to both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL).
  • In this issue of Cancer Cell, Wei et al. (2008) describe generation of AML, ALL, and biphenotypic leukemia by manipulating the cytokine milieu of human progenitor cells expressing MLL-AF9.
  • They demonstrate that both multipotent and lineage-restricted progenitors are targeted by MLL-AF9 fusion proteins and that Rac signaling is crucial for survival.
  • This study demonstrates the heterogeneity of MLL-AF9 leukemic stem cells and the importance of the microenvironment in determining lineage outcome.
  • [MeSH-major] Cell Lineage. Cell Transformation, Neoplastic / pathology. Fetal Stem Cells / pathology. Leukemia, Myeloid, Acute / pathology. Multipotent Stem Cells / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [CommentOn] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]
  • (PMID = 18538728.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 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
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40. Dou Y, Hess JL: Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia. Int J Hematol; 2008 Jan;87(1):10-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia.
  • Fusion of the mixed lineage leukemia protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic oncoprotein.
  • Considerable progress has been made in delineating the differences between normal Hox gene regulation by MLL and deregulated transcription in MLL-induced leukemias.
  • Some MLL translocation partners dimerize the truncated MLL molecule.
  • These enzymatic activities, including RNA polymerase II phosphorylation as well as histone H3 lysine 79 methylation present attractive targets for the development of future MLL-directed therapy.
  • [MeSH-major] Leukemia / genetics. Leukopoiesis / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Transcription, Genetic / genetics

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  • (PMID = 18224408.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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41. Libura J, Slater DJ, Felix CA, Richardson C: Therapy-related acute myeloid leukemia-like MLL rearrangements are induced by etoposide in primary human CD34+ cells and remain stable after clonal expansion. Blood; 2005 Mar 1;105(5):2124-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myeloid leukemia-like MLL rearrangements are induced by etoposide in primary human CD34+ cells and remain stable after clonal expansion.
  • Rearrangements involving the MLL gene on chromosome band 11q23 are a hallmark of therapy-related acute myeloid leukemias following treatment with topoisomerase II poisons including etoposide.
  • Therapy-related and de novo genomic translocation breakpoints cluster within a well-characterized 8.3-kb fragment of MLL.
  • Repair of etoposide-stabilized DNA topoisomerase II covalent complexes may initiate MLL rearrangements observed in patients.
  • We used a culture system of primary human hematopoietic CD34+ cells and inverse polymerase chain reaction to characterize the spectrum of stable genomic rearrangements promoted by etoposide exposure originating within an MLL translocation hotspot in therapy-related leukemia.
  • Illegitimate repair events after minimal repair included MLL tandem duplications and translocations, with minor populations of deletions or insertions.
  • In stably repaired cells that proliferated for 10 to 14 days, the significant majority of illegitimate events were MLL tandem duplications, and several deletions, inversions, insertions, and translocations.
  • Thus, etoposide promotes specific rearrangements of MLL consistent with the full spectrum of oncogenic events identified in leukemic samples.
  • [MeSH-major] DNA-Binding Proteins / genetics. Etoposide / adverse effects. Gene Rearrangement / drug effects. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid / chemically induced. Neoplasms, Second Primary / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Antigens, CD34. Cell Proliferation. Cells, Cultured. Clone Cells. Fetal Blood. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein. Translocation, Genetic

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  • [CommentIn] Blood. 2005 Mar 1;105(5):1843-4 [15747400.001]
  • (PMID = 15528316.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA100159; United States / NCI NIH HHS / CA / R01CA77683; United States / NCI NIH HHS / CA / R01CA85469
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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42. Kowarz E, Burmeister T, Lo Nigro L, Jansen MW, Delabesse E, Klingebiel T, Dingermann T, Meyer C, Marschalek R: Complex MLL rearrangements in t(4;11) leukemia patients with absent AF4.MLL fusion allele. Leukemia; 2007 Jun;21(6):1232-8
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  • [Title] Complex MLL rearrangements in t(4;11) leukemia patients with absent AF4.MLL fusion allele.
  • The human mixed lineage leukemia (MLL) gene is frequently involved in genetic rearrangements with more than 55 different translocation partner genes, all associated with acute leukemia.
  • Reciprocal chromosomal translocations generate two MLL fusion alleles, where 5'- and 3'-portions of MLL are fused to gene segments of given fusion partners.
  • In case of t(4;11) patients, about 80% of all patients exhibit both reciprocal fusion alleles, MLL.AF4 and AF4.MLL, respectively.
  • By contrast, 20% of all t(4;11) patients seem to encode only the MLL.AF4 fusion allele.
  • Here, we analyzed these 'MLL.AF4(+)/AF4.MLL(-)' patients at the genomic DNA level to unravel their genetic situation.
  • Cryptic translocations and three-way translocations were found in this group of t(4;11) patients.
  • Reciprocal MLL fusions with novel translocation partner genes, for example NF-KB1 and RABGAP1L, were identified and actively transcribed in leukemic cells.
  • In other patients, the reciprocal 3'-MLL gene segment was fused out-of-frame to PBX1, ELF2, DSCAML1 and FXYD6.
  • Finally, patients were identified that encode only solitary 3'-MLL gene segments on the reciprocal allele.
  • Based on these data, we propose that all t(4;11) patients exhibit reciprocal MLL alleles, but due to the individual recombination events, provide different pathological disease mechanisms.
  • [MeSH-major] Gene Rearrangement. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Alleles. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Humans. Oncogene Proteins, Fusion / analysis

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  • (PMID = 17410185.001).
  • [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-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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43. Takei N, Suzukawa K, Mukai HY, Itoh T, Okoshi Y, Yoda Y, Nagasawa T: Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement. Int J Hematol; 2006 Apr;83(3):247-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement.
  • Results of recent studies with animal models suggest that expression of MLL fusion proteins promotes acute leukemogenesis.
  • However, the most potent MLL fusion proteins are not sufficient for the development of acute myeloid leukemia (AML).
  • The clinical data on the pathogenesis of this type of leukemia are limited.
  • We analyzed the case of a patient with therapy-related AML with MLL rearrangement.
  • The patient initially developed AML with t(8;21).
  • Although the patient achieved complete remission with chemotherapy, an abnormal karyotype, inv(11)(q21q23), was detected.
  • After 6-year persistence of a clone with the inversion 11 karyotype in the bone marrow, secondary AML developed.
  • Results of fluorescence in situ hybridization analysis combined with magnet-activated cell sorting analysis showed that MLL rearrangement was detected in CD34+ and CD13+ fractions but not in a CD3+ fraction of the bone marrow.
  • One was that MLL rearrangement was not sufficient for the development of leukemia.
  • The other was that MLL rearrangement targets specific lineages.
  • [MeSH-major] Chromosome Inversion / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Antigens, CD13 / biosynthesis. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Female. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 16720556.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.11.2 / Antigens, CD13
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44. Kaltenbach S, Soler G, Barin C, Gervais C, Bernard OA, Penard-Lacronique V, Romana SP: NUP98-MLL fusion in human acute myeloblastic leukemia. Blood; 2010 Sep 30;116(13):2332-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NUP98-MLL fusion in human acute myeloblastic leukemia.
  • H3K4 (histone H3 lysine 4) methylation by the SET domain of the trithorax-group protein MLL (mixed-lineage leukemia) is important for the control of homeobox (HOX) gene expression during development.
  • MLL is tethered to the HOXA locus through interaction of its amino-terminus with menin.
  • MLL fusion proteins associated with human leukemia contain the menin interaction peptide and frequently recruit H3K79 (histone H3 lysine 79) methylation activity.
  • We have characterized a novel recurrent chromosomal aberration, inv(11)(p15q23), as an isolated chromosomal abnormality in 2 patients with acute myeloid leukemia.
  • This aberration is predicted to result in the expression of an NUP98 (nucleoporin 98 kDa)-MLL fusion protein that is unable to interact with menin.
  • This fusion protein is predicted to participate in cellular transformation by activating MLL targets other than HOXA genes.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Aged. Base Sequence. Cell Transformation, Neoplastic / genetics. Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Gene Expression. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Histones / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Oncogene Fusion. Proto-Oncogene Proteins / metabolism

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  • (PMID = 20558618.001).
  • [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 / DNA Primers; 0 / DNA, Neoplasm; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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45. Li ZY, Liu DP, Liang CC: New insight into the molecular mechanisms of MLL-associated leukemia. Leukemia; 2005 Feb;19(2):183-90
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insight into the molecular mechanisms of MLL-associated leukemia.
  • Rearrangements of the MLL gene (ALL1, HRX, and Hrtx) located at chromosome band 11q23 are commonly involved in adult and pediatric cases of primary acute leukemias and also found in cases of therapy-related secondary leukemias.
  • Studies on mouse models of MLL translocation and cell lines containing MLL rearrangements showed that the MLL gene linked chromosomal rearrangements to cellular differentiation and tumor tropism.
  • Moreover, recent structural/functional studies on MLL and aberrant MLL proteins provided new clues and suggested that different mechanisms might be included in leukemogenesis by MLL rearrangements.
  • The connection between these different mechanisms will help us understand globally how aberrant MLL oncogenes affect the normal cellular processes at molecular level.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Mutation. Myeloid-Lymphoid Leukemia Protein. Zinc Fingers / genetics

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  • (PMID = 15618964.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 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] 89
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46. Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ: The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression. Proc Natl Acad Sci U S A; 2005 Sep 27;102(39):14028-33
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  • [Title] The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression.
  • MLL, involved in many chromosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with which it is able to form in-frame fusions.
  • Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated leukemia.
  • We explored downstream target genes of the most prevalent MLL fusion protein, MLL-AF4.
  • To this end, we developed inducible MLL-AF4 fusion cell lines in different backgrounds.
  • Overexpression of MLL-AF4 does not lead to increased proliferation in either cell line, but rather, cell growth was slowed compared with similar cell lines inducibly expressing truncated MLL.
  • We found that in the MLL-AF4-induced cell lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
  • To explore whether CDKN1B might be a direct target of MLL and of MLL-AF4, we used chromatin immunoprecipitation (ChIP) assays and luciferase reporter gene assays.
  • MLL-AF4 binds to the CDKN1B promoter in vivo and regulates CDKN1B promoter activity.
  • Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9 leukemia cell lines.
  • Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background cell type, MLL-AF4 inhibits or activates CDKN1B expression.
  • This finding may have implications in terms of leukemia stem cell resistance to chemotherapy in MLL-AF4 leukemias.

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  • (PMID = 16169901.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC1236570
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47. Jiang F, Ai J, Xiao W, Wang Z: FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity. Cancer Lett; 2007 Aug 18;253(2):265-72
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.
  • U19/EAF2 has also been identified as ELL-associated factor 2 (EAF2) based on its binding to ELL, a fusion partner of MLL in acute myeloid leukemia.
  • U19/EAF2 is a putative transcription factor with a transactivation domain and capability of sequence-specific DNA binding.
  • RESULTS: FB1, an E2A fusion partner in childhood leukemia, was identified as a binding-partner of U19/EAF2.

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  • (PMID = 17395368.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK051193; United States / NIDDK NIH HHS / DK / R37 DK051193-12; United States / NIDDK NIH HHS / DK / R37 DK051193; United States / NCI NIH HHS / CA / CA090386-020002; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / P50 CA090386-020002; United States / NCI NIH HHS / CA / P50 CA90386; United States / NIDDK NIH HHS / DK / R01 DK51193; United States / NIDDK NIH HHS / DK / DK051193-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / EAF1 protein, human; 0 / EAF2 protein, human; 0 / ELL protein, human; 0 / TFPT protein, human; 0 / Transcription Factors; 0 / Transcriptional Elongation Factors
  • [Other-IDs] NLM/ NIHMS27735; NLM/ PMC1989770
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48. Stevens SJ, Meers LE, Albrechts JC, Mebis-Verhees K, Bos GM, Engelen JJ, Janssen JW: A translocation in acute lymphoblastic leukemia that cytogenetically mimics the recurrent MLL-AFF1 translocation and fuses SEPT11 to MLL. Cancer Genet Cytogenet; 2010 Aug;201(1):48-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A translocation in acute lymphoblastic leukemia that cytogenetically mimics the recurrent MLL-AFF1 translocation and fuses SEPT11 to MLL.
  • A 55-year-old man sought care for aggressive acute lymphoblastic leukemia (ALL), which developed 8 years after he had received chemotherapeutic treatment for nephrotic syndrome.
  • The sole cytogenetic abnormality observed in bone marrow-derived metaphases was a t(4;11)(q21;q23), which is a frequently occurring translocation in ALL.
  • However, subsequent reverse transcriptase-polymerase chain reaction for the expected mixed lineage leukemia [trithorax homolog, Drosophila] (MLL)-AFF1 fusion transcript was negative.
  • Reverse transcriptase-polymerase chain reaction revealed expression of a chimeric MLL-SEPT11 transcript, thus identifying what is to our knowledge a hitherto undescribed translocation in ALL.
  • Sequence analysis of cDNA showed in-frame fusion of MLL exon 11 to SEPT11 exon 2.
  • This MLL-SEPT11 fusion is cytogenetically indistinguishable from the recurrent t(4;11)(q21;q23).
  • Thus, it is crucial to characterize cytogenetic aberrations in leukemia by molecular methods, even in cases where a known recurrent translocation is presumed.
  • This report expands the spectrum of ALL-related translocations and hypothesizes on the mechanism leading to the MLL-SEPT11 fusion.
  • Five septins have been identified thus far as MLL fusion partners in leukemia.
  • Their putative oncogenic role may be related to forced MLL dimerization by the septin coiled coil and GTP-binding domains, which could convert MLL to an oncogene.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Gene Fusion. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Base Sequence. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Septins

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633769.001).
  • [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
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.1.- / SEPT11 protein, human; EC 3.6.1.- / Septins
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49. Zhao J, Yin YM, Zhao YL, Sun Y, Wang JB, Zhong J, Zhang X, Fei XH, Shan FX, Liu HX, Wang T, Wang H, Tong CR, Wu T, Lu DP: [Clinical and molecular biologic characteristics of 36 cases of leukemia with 11q23/mll]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1381-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical and molecular biologic characteristics of 36 cases of leukemia with 11q23/mll].
  • This study was aimed to analyze the clinical and cytogenetic characteristics of acute leukemia with 11q23/mll rearrangement and explore the reasonable therapeutic principles.
  • Characteristics in general situation, morphology, immunology, molecular biology, cytogenetics, treatment and overall survival of 36 cases of acute leukemias with mll gene rearrangement were studied and analyzed.
  • The results showed that 36 cases with mll gene rearrangement were found positive (7.2%) in 494 patients with acute leukemia.
  • Among the 36 cases of mll rearrangement positive, 32 cases were diagnosed as acute myeloid leukemia (AML) with myeloid antigen expression, of which 5 cases expressed lymphoblastic differentiation antigen; 4 cases were classified as B-lineage acute lymphoblastic leukemia (ALL), of which non-lineage myeloid expression pattern were found in 3 cases.
  • In 29 out of 36 cases (80%) the clonal chromosomal aberration were detected, of which chromosome 11 aberration were observed in 22 cases.
  • All patients received chemotherapy with a total response rate of 47.2%.
  • Of the responded patients, 10 cases relapsed within 6 months, with a recurrence rate of 40%; 9 cases received hematopoietic stem cell transplantation (HSCT), 7 cases of which survived after transplantation.
  • It is concluded that acute leukemia patients with mll gene rearrangement show poor response to chemotherapy, high recurrence rate and poor prognosis.

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  • (PMID = 21176334.001).
  • [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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50. Jansen MW, Corral L, van der Velden VH, Panzer-Grümayer R, Schrappe M, Schrauder A, Marschalek R, Meyer C, den Boer ML, Hop WJ, Valsecchi MG, Basso G, Biondi A, Pieters R, van Dongen JJ: Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement. Leukemia; 2007 Apr;21(4):633-41
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  • [Title] Immunobiological diversity in infant acute lymphoblastic leukemia is related to the occurrence and type of MLL gene rearrangement.
  • The aim of this study was to identify immunobiological subgroups in 133 infant acute lymphoblastic leukemia (ALL) cases as assessed by their immunophenotype, immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangement pattern, and the presence of mixed lineage leukemia (MLL) rearrangements.
  • MLL translocations were found in 79% of infants, involving MLL-AF4 (41%), MLL-ENL (18%), MLL-AF9 (11%) or another MLL partner gene (10%).
  • MLL-AF4 and MLL-ENL-positive infants demonstrated immature rearrangements, whereas in MLL-AF9-positive leukemias more mature rearrangements predominated.
  • The immature Ig/TCR pattern in infant ALL correlated with young age at diagnosis, CD10 negativity and predominantly with the presence and the type of MLL translocation.
  • The high frequency of immature and oligoclonal Ig/TCR rearrangements is probably caused by early (prenatal) oncogenic transformation in immature B-lineage progenitor cells with germline Ig/TCR genes combined with a short latency period.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17268512.001).
  • [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 / Receptors, Antigen, T-Cell; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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51. Millot F, Brizard F, Sorel N, Preudhomme C, Cividin M, Guilhot F, Brizard A: Therapy-related acute lymphoblastic leukemia with MLL rearrangement following treatment of Burkitt's leukemia. Leuk Lymphoma; 2005 Jun;46(6):925-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute lymphoblastic leukemia with MLL rearrangement following treatment of Burkitt's leukemia.
  • The occurrence of therapy-related acute lymphoblastic leukemia (ALL) is rare and, to our knowledge, is not reported in patients treated for Burkitt's leukemia.
  • We report on a child with ALL with translocation t(4;11)(q21;q23) involving the MLL gene, 13 months after chemotherapy for Burkitt's leukemia.
  • [MeSH-major] Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / immunology. Chromosomes, Human, Pair 4. Gene Expression Regulation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Translocation, Genetic

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  • (PMID = 16019540.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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52. Soler G, Radford I, Meyer C, Marschalek R, Brouzes C, Ghez D, Romana S, Berger R: MLL insertion with MLL-MLLT3 gene fusion in acute leukemia: case report and review of the literature. Cancer Genet Cytogenet; 2008 May;183(1):53-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL insertion with MLL-MLLT3 gene fusion in acute leukemia: case report and review of the literature.
  • A new chromosomal insertion involving the MLL gene was detected by fluorescence in situ hybridization in a patient with acute myeloblastic leukemia (AML) and a t(9;11)(p21;q13).
  • Genomic polymerase chain reaction confirmed the MLL-MLLT3 gene fusion.
  • A review of the literature on MLL insertions shows that the opposite orientation of the genes involved in the fusion plays a role in the genesis of the rearrangement in most of the cases reported.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutagenesis, Insertional. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 18474298.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-MLLT3 fusion protein, human; 0 / MLLT3 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 51
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53. Tashiro H, Mizutani-Noguchi M, Shirasaki R, Shirafuji N: Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts. Biochem Biophys Res Commun; 2010 Jan 1;391(1):592-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.
  • We show in this paper that non-adherent leukemia blasts can change into myofibroblasts.
  • When myeloblasts from two cases of acute myelogenous leukemia with a fusion product comprising mixed lineage leukemia and RNA polymerase II elongation factor, were cultured long term, their morphology changed to that of myofibroblasts with similar molecular characteristics to the parental myeloblasts.
  • The original leukemia blasts, when cultured on the leukemia blast-derived myofibroblasts, grew extensively.
  • Leukemia blasts can create their own microenvironment for proliferation.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Fibroblasts / pathology. Leukemia, Myeloid, Acute / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Myoblasts / pathology. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 19932689.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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54. Aplan PD: Chromosomal translocations involving the MLL gene: molecular mechanisms. DNA Repair (Amst); 2006 Sep 8;5(9-10):1265-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal translocations involving the MLL gene: molecular mechanisms.
  • Translocations involving the MLL gene are among the most common of these non-random translocations.
  • Leukemias with MLL translocations have been the topic of intense interest because of the unusual, biphenotypic immunophenotype of these leukemias, because of the unique clinical presentation of some MLL translocations (infant leukemia and therapy-related leukemia), and because of the large number of different chromosomal loci that partner with MLL in these translocations.
  • This review is focused on the potential mechanisms that lead to MLL translocations, and will discuss aberrant VDJ recombination, Alu-mediated recombination, non-homologous end joining, as well as the effect of DNA topoisomerase II poisons and chromatin structure.

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  • (PMID = 16797254.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromatin; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS13506; NLM/ PMC1635494
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55. Suzukawa K, Shimizu S, Nemoto N, Takei N, Taki T, Nagasawa T: Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21). Int J Hematol; 2005 Jul;82(1):38-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21).
  • More than 40 genes have been reported as translocation partners of the mixed lineage leukemia gene (MLL) in hematologic malignancies.
  • AF17 was identified earlier than most other MLL translocation partners.
  • On the other hand, there is only 1 report of an MLL-AF17 fusion transcript in acute myeloid leukemia (AML).
  • Here we describe a 40-year-old man with a diagnosis of AML involving t(11;17)(q23;q21).
  • We identified a chromosomal breakpoint for t(11;17)(q23;q21) at MLL intron 6 and AF17 intron 8.
  • Although the previously reported form of the MLL-AF17 fusion transcript was not detected by reverse transcriptase-polymerase chain reaction (PCR) analysis, a novel form of an MLL-AF17 fusion transcript joining MLL exon 6 to AF17 exon 9 was detected by complementary DNA panhandle PCR.
  • The fact that 2 forms of MLL-AF17 retain the leucine zipper domain of AF17 suggests that the dimerization domain of AF17 is critical for leukemogenesis by the MLL-AF17 fusion gene.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16105757.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLL-AF17 fusion protein, human; 0 / MLLT6 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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56. Cavazzini F, Bardi A, Tammiso E, Ciccone M, Russo-Rossi A, Divona D, Lo Coco F, Hernandez JM, Wlodarska I, Hagemeijer A, Castoldi G, Cuneo A: Validation of an interphase fluorescence in situ hybridization approach for the detection of MLL gene rearrangements and of the MLL/AF9 fusion in acute myeloid leukemia. Haematologica; 2006 Mar;91(3):381-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Validation of an interphase fluorescence in situ hybridization approach for the detection of MLL gene rearrangements and of the MLL/AF9 fusion in acute myeloid leukemia.
  • To validate a 2-step FISH assay for the identification of the t(9;11)(p22;q23), 96 acute myeloid leukemias were studied by cytogenetic analysis, FISH and molecular biology.
  • After a first FISH step using an MLL probe, 24/27 cases with 11q23 break showed MLL rearrangement.
  • In the second step, 24 cases with MLL rearrangement were studied using MLL and AF9 probes: 17/18 cases with t(9;11) showed MLL/AF9 fusion.
  • In 6 patients with 11q23/MLL rearrangements other than t(9;11), FISH confirmed MLL involvement and excluded AF9 involvement.
  • This is a reliable method for the identification of MLL/AF9 fusion in interphase cells, allowing for a reclassification of cases with suboptimal chromosome morphology.
  • The frequency of deletion surrounding MLL and AF9 breakpoint is low.
  • [MeSH-major] Gene Rearrangement / genetics. In Situ Hybridization, Fluorescence / methods. Interphase / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16503549.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / MLLT3 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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57. 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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58. Olesen LH, Nyvold CG, Aggerholm A, Nørgaard JM, Guldberg P, Hokland P: Delineation and molecular characterization of acute myeloid leukemia patients with coduplication of FLT3 and MLL. Eur J Haematol; 2005 Sep;75(3):185-92
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  • [Title] Delineation and molecular characterization of acute myeloid leukemia patients with coduplication of FLT3 and MLL.
  • Partial tandem (PTD) and internal tandem duplications (ITD) of the MLL or FLT3 genes respectively, have been demonstrated in acute myeloid leukemia (AML).
  • We analyzed blast cells from 250 adult patients treated at the same institution during a 15-year period for FLT3 ITD and MLL PTD and the duplications were found in 24% and 4%, respectively.
  • Two of the patients had a normal karyotypic analysis, while the remaining two showed aberrations in chromosome 11, one with trisomy 11 and the other with a der (11).
  • The extensive molecular characterization of FLT3/MLL coduplicated patients presented here indicates that, even though they do not differ molecularly from the groups of patients with single ITDs, their prognosis and overall survival is universally poor.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Duplication. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogenes / genetics. Receptor Protein-Tyrosine Kinases / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Base Sequence. DNA Methylation. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Mutation. Myeloid-Lymphoid Leukemia Protein. Promoter Regions, Genetic. fms-Like Tyrosine Kinase 3

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  • (PMID = 16104873.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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59. Somervaille TC, Matheny CJ, Spencer GJ, Iwasaki M, Rinn JL, Witten DM, Chang HY, Shurtleff SA, Downing JR, Cleary ML: Hierarchical maintenance of MLL myeloid leukemia stem cells employs a transcriptional program shared with embryonic rather than adult stem cells. Cell Stem Cell; 2009 Feb 6;4(2):129-40
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  • [Title] Hierarchical maintenance of MLL myeloid leukemia stem cells employs a transcriptional program shared with embryonic rather than adult stem cells.
  • The genetic programs that promote retention of self-renewing leukemia stem cells (LSCs) at the apex of cellular hierarchies in acute myeloid leukemia (AML) are not known.
  • In a mouse model of human AML, LSCs exhibit variable frequencies that correlate with the initiating MLL oncogene and are maintained in a self-renewing state by a transcriptional subprogram more akin to that of embryonic stem cells (ESCs) than to that of adult stem cells.
  • The transcription/chromatin regulatory factors Myb, Hmgb3, and Cbx5 are critical components of the program and suffice for Hoxa/Meis-independent immortalization of myeloid progenitors when coexpressed, establishing the cooperative and essential role of an ESC-like LSC maintenance program ancillary to the leukemia-initiating MLL/Hox/Meis program.
  • Enriched expression of LSC maintenance and ESC-like program genes in normal myeloid progenitors and poor-prognosis human malignancies links the frequency of aberrantly self-renewing progenitor-like cancer stem cells (CSCs) to prognosis in human cancer.

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  • [CommentIn] Cell Stem Cell. 2009 Feb 6;4(2):97-8 [19200795.001]
  • (PMID = 19200802.001).
  • [ISSN] 1875-9777
  • [Journal-full-title] Cell stem cell
  • [ISO-abbreviation] Cell Stem Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116606-04; United States / NCI NIH HHS / CA / T32 CA009151; United Kingdom / Cancer Research UK / / C147/A6058; United States / NCI NIH HHS / CA / CA116606-04; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NCI NIH HHS / CA / CA 116606; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / T32 CA 09151; United States / NCI NIH HHS / CA / CA 55029; United States / NCI NIH HHS / CA / CA055029-18
  • [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 / Chromosomal Proteins, Non-Histone; 0 / HMGB3 Protein; 0 / Oncogene Proteins v-myb; 0 / Oncogene Proteins, Fusion; 107283-02-3 / heterochromatin-specific nonhistone chromosomal protein HP-1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS102286; NLM/ PMC2670853
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60. Eguchi M, Eguchi-Ishimae M, Knight D, Kearney L, Slany R, Greaves M: MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia. Genes Chromosomes Cancer; 2006 Aug;45(8):754-60
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  • [Title] MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia.
  • MLL fusion genes are a predominant feature of acute leukemias in infants and in secondary acute myeloid leukemia (AML) associated with prior chemotherapy with topo-II poisons.
  • We have suggested that these coupled features might be explained if MLL fusion gene encoded proteins rendered cells more vulnerable to further DNA damage and mutation in the presence of chronic exposure to the agent(s) that induced the MLL fusion itself.
  • We have tested this idea by exploiting a hormone regulated MLL-ENL (MLLT1) activation system and show that MLL-ENL function in normal murine progenitor cells substantially increases the incidence of chromosomal abnormalities in proliferating cells that survive exposure to etoposide VP-16.
  • [MeSH-major] Chromosome Aberrations. DNA Damage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 16688745.001).
  • [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 / Estrogen Antagonists; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 094ZI81Y45 / Tamoxifen; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 17197F0KYM / afimoxifene
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61. Faller BA, Robu VG, Borghaei H: Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer. Clin Lung Cancer; 2009 Nov;10(6):438-40
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  • [Title] Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer.
  • We present a case of acute myelogenous leukemia with an 11q23/MLL rearrangement diagnosed 1 year after the completion of 4 cycles of cisplatin and vinorelbine for resected NSCLC.
  • To our knowledge, this is the first case of therapy-related acute myelogenous leukemia (t-AML) associated with this chemotherapy combination.
  • The literature on t-AML with the 11q23/MLL rearrangement is reviewed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Translocation, Genetic / drug effects
  • [MeSH-minor] Aged. Carcinoma, Non-Small-Cell Lung / drug therapy. Chromosomes, Human, Pair 11. Cisplatin / administration & dosage. Follow-Up Studies. Histone-Lysine N-Methyltransferase. Humans. Lung Neoplasms / drug therapy. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives


62. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
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  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • CEBPalpha mutations only occurred in patients with intermediate cytogenetics and not in 56 children with AML1-ETO, CBFbeta-MYH11, PML-RARalpha or MLL rearrangements.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 15618961.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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63. Saito H, Otsubo K, Kakimoto A, Komatsu N, Ohsaka A: Emergence of two unrelated clones in acute myeloid leukemia with MLL-SEPT9 fusion transcript. Cancer Genet Cytogenet; 2010 Sep;201(2):111-5
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  • [Title] Emergence of two unrelated clones in acute myeloid leukemia with MLL-SEPT9 fusion transcript.
  • We report a case of acute myeloid leukemia (AML) with two unrelated clones, one of which was t(11;17)(q23;q25) carrying MLL-SEPT9 fusion transcripts.
  • Although the karyotype of bone marrow cells at the initial diagnosis was normal, two unrelated chromosomal aberrations concurrently appeared during the course of the disease, suggestive of t(11;17)(q23;q25) and add(1)(p36.1),del(6)(q?
  • Spectral karyotyping analysis identified a reciprocal translocation between chromosomes 11 and 17, and a translocation of the q arm of chromosome 6 to chromosome 1.
  • Dual-color fluorescence in situ hybridization analysis that used probes specific for MLL in combination with tel 1p and tel 1q revealed a translocation of 1p-->pter to chromosome 6 and a translocation of 11q23-->qter to chromosome 17.
  • Reverse transcriptase-polymerase chain reaction and sequencing analyses demonstrated MLL-SEPT9 fusion transcripts with the breakpoint of MLL exon 8/SEPT9 exon 2 and MLL exon 9/SEPT9 exon 2.
  • Thus, the karyotype was defined as 46,XY,t(11;17)(q23;q25)/46,XY,t(1;6)(p36.3;q23).
  • Our case represents an additional MLL-SEPT9-positive AML that was considered to be related to therapy.
  • [MeSH-major] Chromosome Aberrations. Cytoskeletal Proteins / genetics. GTP-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682395.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytoskeletal Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.1.- / SEPT9 protein, human; EC 3.6.1.- / Septins
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64. Meyer C, Schneider B, Jakob S, Strehl S, Attarbaschi A, Schnittger S, Schoch C, Jansen MW, van Dongen JJ, den Boer ML, Pieters R, Ennas MG, Angelucci E, Koehl U, Greil J, Griesinger F, Zur Stadt U, Eckert C, Szczepański T, Niggli FK, Schäfer BW, Kempski H, Brady HJ, Zuna J, Trka J, Nigro LL, Biondi A, Delabesse E, Macintyre E, Stanulla M, Schrappe M, Haas OA, Burmeister T, Dingermann T, Klingebiel T, Marschalek R: The MLL recombinome of acute leukemias. Leukemia; 2006 May;20(5):777-84
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  • [Title] The MLL recombinome of acute leukemias.
  • Chromosomal rearrangements of the human MLL gene are a hallmark for aggressive (high-risk) pediatric, adult and therapy-associated acute leukemias.
  • A recently developed long-distance inverse PCR method was applied to genomic DNA isolated from individual acute leukemia patients in order to identify chromosomal rearrangements of the human MLL gene.
  • We present data of the molecular characterization of 414 samples obtained from 272 pediatric and 142 adult leukemia patients.
  • The precise localization of genomic breakpoints within the MLL gene and the involved translocation partner genes (TPGs) was determined and several new TPGs were identified.
  • The combined data of our study and published data revealed a total of 87 different MLL rearrangements of which 51 TPGs are now characterized at the molecular level.
  • Thus, translocations of the MLL gene, by itself coding for a histone H3K4 methyltransferase, are presumably not randomly chosen, rather functionally selected.
  • [MeSH-major] Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Child. Chromosome Aberrations. Chromosome Mapping. DNA / genetics. DNA / isolation & purification. Histone-Lysine N-Methyltransferase. Histones / metabolism. Humans. Methylation


65. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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66. Pan JL, Xue YQ, Jiang HY, He J, Wang W, Wu YF: [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Aug;22(4):444-6

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  • [Title] [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5].
  • OBJECTIVE: To explore the value of reverse transcription-multiplex nested PCR in detecting MLL rearrangement in lzAML-M4/M5.
  • Five common MLL fusion genes and MLL partial tandem duplication in 40 AML cases, including 12 M4 and 28 M5 were detected by reverse transcription(RT)-multiplex nested PCR.
  • RESULTS: R-banding karyotypic analysis revealed 11q23 translocation including t(6;11)(q27;q23), t(9;11)(p21;q23), t(11;17)(q23;q21) and t(11;19)(q23;p13.1) in 7 cases.
  • MLL rearrangements consisting of MLL/AF6 (1 case), MLL/AF9 (1 case), MLL/AF17 (2 cases), MLL/ELL (2 cases) and MLL partial tandem duplication(2 cases) were detected in 8 cases by RT-multiplex nested PCR.
  • Among 8 cases with MLL rearrangement, 6 were chromosome translocation, 2 were MLL partial tandem duplication.
  • CONCLUSION: RT-multiplex nested PCR is a powerful technique in the detection of MLL rearrangement for tentativelly diagnosed AML-M4/M5.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic

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  • (PMID = 16086288.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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67. Stam RW, Schneider P, Hagelstein JA, van der Linden MH, Stumpel DJ, de Menezes RX, de Lorenzo P, Valsecchi MG, Pieters R: Gene expression profiling-based dissection of MLL translocated and MLL germline acute lymphoblastic leukemia in infants. Blood; 2010 Apr 8;115(14):2835-44
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  • [Title] Gene expression profiling-based dissection of MLL translocated and MLL germline acute lymphoblastic leukemia in infants.
  • Acute lymphoblastic leukemia (ALL) in infants (< 1 year) is characterized by a poor prognosis and a high incidence of MLL translocations.
  • Several studies demonstrated the unique gene expression profile associated with MLL-rearranged ALL, but generally small cohorts were analyzed as uniform patient groups regardless of the type of MLL translocation, whereas the analysis of translocation-negative infant ALL remained unacknowledged.
  • Here we generated and analyzed primary infant ALL expression profiles (n = 73) typified by translocations t(4;11), t(11;19), and t(9;11), or the absence of MLL translocations.
  • Our data show that MLL germline infant ALL specifies a gene expression pattern that is different from both MLL-rearranged infant ALL and pediatric precursor B-ALL.
  • Moreover, we demonstrate that, apart from a fundamental signature shared by all MLL-rearranged infant ALL samples, each type of MLL translocation is associated with a translocation-specific gene expression signature.
  • Finally, we show the existence of 2 distinct subgroups among t(4;11)-positive infant ALL cases characterized by the absence or presence of HOXA expression, and that patients lacking HOXA expression are at extreme high risk of disease relapse.
  • These gene expression profiles should provide important novel insights in the complex biology of MLL-rearranged infant ALL and boost our progress in finding novel therapeutic solutions.
  • [MeSH-major] Chromosomes, Human / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Translocation, Genetic


68. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • The majority of MLL gene rearrangements are associated with infant ALL, and their presence predicts a poor prognosis which worsens with earlier age of presentation.
  • Rearrangements of the MLL gene are found in most cases of infant AML and regardless of age confer an intermediate risk.
  • The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and AML-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.
  • The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.
  • This review considers recent advances in our understanding of the role of MLL gene rearrangements in pediatric clinical practice.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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69. 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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70. 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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71. Liedtke M, Cleary ML: Therapeutic targeting of MLL. Blood; 2009 Jun 11;113(24):6061-8
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  • [Title] Therapeutic targeting of MLL.
  • Treatment of hematologic malignancies is evolving from a uniform approach to targeted therapies directed at the underlying molecular abnormalities of disease.
  • The mixed lineage leukemia (MLL) proto-oncogene is a recurrent site of genetic rearrangements in acute leukemias; and since its discovery in 1992, many advances have been made in understanding its role in leukemogenesis.
  • A variety of MLL translocation partners have been described, and detailed structure/function studies have identified functional domains that are required for transformation.
  • Proteins associated with the MLL core complex or its fusion partners have been isolated and characterized for their critical roles in leukemia pathogenesis.
  • Downstream mediators of MLL transcriptional regulation and multiple collaborating signaling pathways have been described and characterized.
  • These advances in our understanding of MLL-related leukemogenesis provide a foundation for ongoing and future efforts to develop novel therapeutic strategies that will hopefully result in better treatment outcomes.
  • [MeSH-major] Leukemia / therapy. Myeloid-Lymphoid Leukemia Protein / metabolism

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  • (PMID = 19289854.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA120349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [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
  • [Number-of-references] 78
  • [Other-IDs] NLM/ PMC2699228
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72. Ohnishi H, Taki T, Yoshino H, Takita J, Ida K, Ishii M, Nishida K, Hayashi Y, Taniwaki M, Bessho F, Watanabe T: A complex t(1;22;11)(q44;q13;q23) translocation causing MLL-p300 fusion gene in therapy-related acute myeloid leukemia. Eur J Haematol; 2008 Dec;81(6):475-80
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  • [Title] A complex t(1;22;11)(q44;q13;q23) translocation causing MLL-p300 fusion gene in therapy-related acute myeloid leukemia.
  • The authors, herein, report a therapy-related acute myeloid leukemia with MLL-p300 fusion gene.
  • Spectral karyotyping clarified that chromosome 11 is involved in complex t(1;22;11)(q44;q13;q23), and is fused to the chromosome 22, and direct sequencing revealed the fusion of exon 8 of MLL and exon 15 of p300 in this case.
  • This is only the second reported case of leukemia with an MLL-p300 fusion gene, and the other case with MLL-p300 was also a therapy-related leukemia.
  • Considering that the MLL-CBP fusion gene is also found almost exclusively in therapy-related leukemia, the association of MLL-p300 and MLL-CBP with therapy-related leukemia rather than de novo leukemia is thereby suggested.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic. p300-CBP Transcription Factors / genetics

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  • (PMID = 18778367.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [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; EC 2.3.1.48 / p300-CBP Transcription Factors
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73. Somervaille TC, Cleary ML: Identification and characterization of leukemia stem cells in murine MLL-AF9 acute myeloid leukemia. Cancer Cell; 2006 Oct;10(4):257-68
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  • [Title] Identification and characterization of leukemia stem cells in murine MLL-AF9 acute myeloid leukemia.
  • Using a mouse model of human acute myeloid leukemia (AML) induced by the MLL-AF9 oncogene, we demonstrate that colony-forming cells (CFCs) in the bone marrow and spleen of leukemic mice are also leukemia stem cells (LSCs).
  • These self-renewing cells (1) are frequent, accounting for 25%-30% of myeloid lineage cells at late-stage disease;.
  • (2) generate a phenotypic, morphologic, and functional leukemia cell hierarchy;.
  • (3) express mature myeloid lineage-specific antigens; and (4) exhibit altered microenvironmental interactions by comparison with the oncogene-immortalized CFCs that initiated the disease.
  • Therefore, the LSCs responsible for sustaining, expanding, and regenerating MLL-AF9 AML are downstream myeloid lineage cells, which have acquired an aberrant Hox-associated self-renewal program as well as other biologic features of hematopoietic stem cells.

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  • [CommentIn] Cancer Cell. 2006 Oct;10(4):253-4 [17045202.001]
  • (PMID = 17045204.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009151; United States / NCI NIH HHS / CA / CA116601; United States / NCI NIH HHS / CA / CA55029
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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74. Kern W, Haferlach C, Haferlach T, Schnittger S: Monitoring of minimal residual disease in acute myeloid leukemia. Cancer; 2008 Jan 1;112(1):4-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring of minimal residual disease in acute myeloid leukemia.
  • Two highly sensitive methods, multiparameter flow cytometry (MFC) and real-time quantitative PCR (RQ-PCR), are increasingly used to monitor minimal residual disease (MRD) and to guide risk-adapted management in acute myeloid leukemia (AML).
  • With a sensitivity of 10(-4) (PML-RARA) to 10(-7) (patient-specific primers, FLT3 and NPM1 mutations), RQ-PCR is more sensitive in most cases.
  • [MeSH-major] Flow Cytometry. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Polymerase Chain Reaction

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  • [Copyright] 2007 American Cancer Society
  • (PMID = 18000811.001).
  • [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] 0 / Biomarkers, Tumor
  • [Number-of-references] 83
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75. Kohlmann A, Schoch C, Dugas M, Schnittger S, Hiddemann W, Kern W, Haferlach T: New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes. Leukemia; 2005 Jun;19(6):953-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes.
  • Rearrangements of the MLL gene occur in both acute lymphoblastic and acute myeloid leukemias (ALL, AML).
  • This study addressed the global gene expression pattern of these two leukemia subtypes with respect to common deregulated pathways and lineage-associated differences.
  • We analyzed 73 t(11q23)/MLL leukemias in comparison to 290 other acute leukemias and demonstrate that 11q23 leukemias combined are characterized by a common specific gene expression signature.
  • Additionally, in unsupervised and supervised data analysis algorithms, ALL and AML cases with t(11q23) segregate according to the lineage they are derived from, that is, myeloid or lymphoid, respectively.
  • Through the use of novel biological network analyses, essential regulators of early B cell development, PAX5 and EBF, were shown to be associated with a clear B-lineage commitment in lymphoblastic t(11q23)/MLL leukemias.
  • Also, the influence of the different MLL translocation partners on the transcriptional program was directly assessed.
  • Taken together, the identified molecular expression pattern of MLL fusion gene samples and biological networks revealed new insights into the aberrant transcriptional program in 11q23/MLL leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Cell Lineage / genetics. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Multigene Family. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 15815718.001).
  • [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 / 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
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76. Tamai H, Inokuchi K: 11q23/MLL acute leukemia : update of clinical aspects. J Clin Exp Hematop; 2010;50(2):91-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 11q23/MLL acute leukemia : update of clinical aspects.
  • Rearrangements of the MLL gene located at 11q23 are common chromosomal abnormalities associated with acute leukemia (AL), especially infant and secondary leukemia after previous treatment with DNA topoisomerase II inhibitors.
  • 11q23/MLL abnormalities have been widely recognized as an important prognostic factor in AL.
  • Over 70 chromosome partners of 11q23 have been identified to date, at least 50 of which have been cloned and characterized at the molecular level.
  • Recent studies showed that the prognosis of 11q23/MLL AL varies widely according to the partner gene, the leukemia cell lineage, the age of the patient and the treatment administered.
  • Special strategies are needed to treat 11q23/MLL AL, including allogeneic hematopoietic stem cell transplantation, according to the fusion partner.
  • The development of novel methodologies, including new molecular therapeutic targets, is also needed to improve the prognosis of 11q23/MLL AL.
  • The present article provides an update on the current status of prognosis and treatment of 11q23/MLL AL according to the fusion partner.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 21123966.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [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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77. Ohtake S: [Acute myeloid leukemia]. Gan To Kagaku Ryoho; 2007 Dec;34(13):2175-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute myeloid leukemia].
  • The heterogeneity of acute myeloid leukemia (AML) has been established by many new insights from molecular biological studies.
  • In AML with favorable cytogenetic changes, KIT gene mutation has been known as a worse prognostic marker.
  • Even in AML with normal cytogenetics, numerous molecular genetic alterations have been identified including internal tandem duplication of the FLT3 gene (FLT3-ITD), mutations in the NPM1 gene, mutations in the CEBPA gene, and partial tandem duplication of the MLL gene.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18079616.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
  • [Number-of-references] 20
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78. Mori T, Nishimura N, Hasegawa D, Kawasaki K, Kosaka Y, Uchide K, Yanai T, Hayakawa A, Takeshima Y, Nishio H, Matsuo M: Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia. Leuk Res; 2010 Oct;34(10):1398-401

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia.
  • Most chromosomal rearrangements including the mixed lineage leukemia (MLL) gene are manifested as leukemia and predict a poor prognosis.
  • Although more than 50 MLL-rearrangement partners are characterized, MLL-related leukemogenesis remains to be understood.
  • Here we report a case of a 3-year old boy bearing a novel MLL-rearrangement with the suppressor of actin mutations 1-like (SACM1L) gene in the absence of leukemia.
  • Bone marrow cells harboring the MLL-SACM1L rearrangement appeared during chemotherapy for acute lymphoblastic leukemia with hyperdiploidy and were continuously detected over 7 years without clonal expansion.
  • [MeSH-major] Gene Rearrangement. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child, Preschool. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 3. Histone-Lysine N-Methyltransferase. Humans. Male. Translocation, Genetic

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20553989.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Membrane Proteins; 0 / SACM1L protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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79. Muntean AG, Giannola D, Udager AM, Hess JL: The PHD fingers of MLL block MLL fusion protein-mediated transformation. Blood; 2008 Dec 1;112(12):4690-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PHD fingers of MLL block MLL fusion protein-mediated transformation.
  • Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are associated with aggressive acute lymphoid and myeloid leukemias.
  • These translocations are restricted to an 8.3-kb breakpoint region resulting in fusion of amino terminal MLL sequences in frame to 1 of more than 60 different translocation partners.
  • The translocations consistently delete the plant homeodomain (PHD) fingers and more carboxyl terminal MLL sequences.
  • Here we show that inclusion of the PHD fingers in the MLL fusion protein MLL-AF9 blocked immortalization of hematopoietic progenitors.
  • These data provide an explanation for why MLL translocation breakpoints exclude the PHD fingers and suggest a possible role for these domains in regulating the function of wild-type MLL.

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  • (PMID = 18796627.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007622; United States / NCI NIH HHS / CA / R01 CA078815; United States / NHLBI NIH HHS / HL / T32 HL07622; United States / NCI NIH HHS / CA / R01CA92251; United States / NCI NIH HHS / CA / R01 CA092251; United States / NCI NIH HHS / CA / R01CA78815
  • [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 / Homeodomain Proteins; 0 / MLL protein, human; 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2597135
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80. Faber J, Armstrong SA: Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies. Klin Padiatr; 2007 Nov-Dec;219(6):306-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
  • An important question in the development of novel, less toxic antileukemic strategies specifically targeting leukemia stem cells is how closely leukemia stem cells are related to normal hematopoietic stem cells.
  • It has been recently demonstrated that leukemia stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
  • Introduction of Mixed-lineage leukemia ( MLL)-fusion oncoproteins, frequently found in infant leukemias and therapy-related leukemias, into differentiated hematopoietic progenitor cells results in the generation of leukemias with a high frequency of leukemia stem cells.
  • The progenitor-derived leukemia stem cells ectopically express a limited stem cell program while maintaining the global identity of differentiated myeloid cells.
  • Development of therapeutic strategies that specifically target the leukemia stem cell program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human leukemias with high efficacy yet less side effects.
  • [MeSH-major] Leukemia / therapy. Leukemia, Biphenotypic, Acute. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells

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  • (PMID = 18050039.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [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] 62
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81. Mansur MB, Emerenciano M, Splendore A, Brewer L, Hassan R, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements. Leuk Res; 2010 Apr;34(4):483-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoblastic leukemia in early childhood presents NOTCH1 mutations and MLL rearrangements.
  • T-cell acute lymphoblastic leukemia (T-ALL) may affect children in very early age.
  • Other alterations included MLL(+) (n=4), SIL-TAL1(+) (n=3), FLT3 mutation (n=1) and HOX11L2(+) (n=1).
  • Our results suggest that NOTCH1 and MLL abnormalities are primary leukemogenic hits in early T-ALL.
  • [MeSH-major] Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19631984.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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82. Doubek M, Palasek I, Pospisil Z, Borsky M, Klabusay M, Brychtova Y, Jurcek T, Jeziskova I, Krejci M, Dvorakova D, Mayer J: Detection and treatment of molecular relapse in acute myeloid leukemia with RUNX1 (AML1), CBFB, or MLL gene translocations: frequent quantitative monitoring of molecular markers in different compartments and correlation with WT1 gene expression. Exp Hematol; 2009 Jun;37(6):659-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection and treatment of molecular relapse in acute myeloid leukemia with RUNX1 (AML1), CBFB, or MLL gene translocations: frequent quantitative monitoring of molecular markers in different compartments and correlation with WT1 gene expression.
  • OBJECTIVE: Our objective was to determine the value of frequent minimal residual disease (MRD) monitoring in acute myeloid leukemia (AML) as a robust marker of impending relapse, and whether treatment benefits patients during the MRD-positive phase of their disease.
  • MATERIALS AND METHODS: Frequent MRD monitoring was performed in all AML treatment phases using real-time quantitative polymerase chain reaction for fusion transcripts (CBFB/MYH11; RUNX1/RUNX1T1 fusion transcripts of MLL gene) and for the Wilms' tumor (WT1) gene.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasm Proteins / analysis. Neoplasm, Residual / diagnosis. Translocation, Genetic. WT1 Proteins / analysis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Case-Control Studies. Core Binding Factor Alpha 2 Subunit / analysis. Core Binding Factor beta Subunit / analysis. Female. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / analysis. Recurrence. Young Adult

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  • (PMID = 19463768.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / Neoplasm Proteins; 0 / RUNX1 protein, human; 0 / WT1 Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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83. Cóser VM, Meyer C, Basegio R, Menezes J, Marschalek R, Pombo-de-Oliveira MS: Nebulette is the second member of the nebulin family fused to the MLL gene in infant leukemia. Cancer Genet Cytogenet; 2010 Apr 15;198(2):151-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nebulette is the second member of the nebulin family fused to the MLL gene in infant leukemia.
  • Genetic aberrations involving the mixed lineage leukemia (MLL) gene are frequently diagnosed in infant acute lymphoblastic and acute myeloid leukemia.
  • More than 60 fusion partner genes have been described at the molecular level, 31 of which have been characterized solely in infant leukemia cases.
  • Here we describe a new MLL fusion partner gene, NEBL, which was identified in a case of acute myeloid leukemia in an infant.
  • The chromosomal breakpoints of the MLL-NEBL and NEBL-MLL fusion genes were cloned by long-distance inverse polymerase chain reaction.
  • Therefore, the combination of cytogenetic and independent molecular techniques such as long-distance inverse polymerase chain reaction are indispensable for the rapid identification and characterization of rare MLL rearrangements.
  • [MeSH-major] Carrier Proteins / genetics. Cytoskeletal Proteins / genetics. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362230.001).
  • [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 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / LIM Domain Proteins; 0 / MLL protein, human; 0 / Muscle Proteins; 0 / NEBL protein, human; 0 / Oncogene Proteins, Fusion; 0 / nebulin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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84. Li L, Zhang AH, Liu LB, Bi L, Wang L, Zhao YJ, Zou P: [Effect of down-regulating mll-af9 gene expression on proliferation of acute monocytic leukemia cell line THP-1]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Apr;16(2):254-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of down-regulating mll-af9 gene expression on proliferation of acute monocytic leukemia cell line THP-1].
  • This study was aimed to investigate the effect of small interfering RNA (siRNA) on the expression of mll-af9 oncogene and the proliferation of human acute monocytic leukemia cell line THP-1.
  • One group of siRNA was designed targeting mll-af9 mRNA and finally obtained by chemosynthesis.
  • Then the obtained siRNA was transfected into cultured human acute monocytic leukemia cell line THP-1 by lipofectamine.
  • The level of mll-af9 mRNA expression was analyzed by reverse transcription polymerase chain reaction (RT-PCR).
  • The level of mll-af9 mRNA expression was significantly inhibited in siRNA-transfected cells as compared with the controls. mll-af9-targeted siRNA inhibited the proliferation of THP-1 cells and induced cell apoptosis effectively after transfection.
  • It is concluded that the mll-af9-targeted siRNA can effectively inhibit the proliferation of human acute monocytic leukemia cell line THP-1.

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  • (PMID = 18426643.001).
  • [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-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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85. Cano F, Drynan LF, Pannell R, Rabbitts TH: Leukaemia lineage specification caused by cell-specific Mll-Enl translocations. Oncogene; 2008 Mar 20;27(13):1945-50
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukaemia lineage specification caused by cell-specific Mll-Enl translocations.
  • Chromosomal translocations involving the Mixed-Lineage Leukaemia (MLL) gene underlie many human leukaemias and MLL rearrangements are found in both acute myelogenous and acute lymphoblastic leukaemias.
  • To assess the functionally relevant haematopoietic cell contexts for MLL fusions to be tumorigenic, we have generated different lines of mice in which de novo Mll-associated translocations occur.
  • Translocations between Mll and Enl cause myeloid neoplasias, initiating in stem cells or progenitors while no tumours arose when the translocation was restricted to the B-cell compartment.
  • Despite the absence of tumorigenesis, Mll-Enl translocations did occur and Mll-Enl fusion mRNA was expressed in B-cell-restricted translocators.
  • A permissive cellular environment is therefore required for oncogenicity of Mll-associated translocations since the occurrence of Mll-Enl does not promote unrestricted proliferation in all haematopoietic cellular contexts, consistent with a specific instructive role of the MLL-fusion proteins in leukaemogenesis.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. T-Lymphocytes / pathology. Translocation, Genetic
  • [MeSH-minor] Animals. Antigens, CD19 / genetics. Antigens, CD19 / physiology. Cells, Cultured. Histone-Lysine N-Methyltransferase. Integrases / metabolism. Mice. Myeloid Progenitor Cells / cytology. Myeloid Progenitor Cells / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Phenotype. Recombination, Genetic. Stem Cells / cytology. Stem Cells / metabolism

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  • (PMID = 17906700.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0600914; United Kingdom / Medical Research Council / / MRC/ MC/ U105178807; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Mllt3 protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 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 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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86. Harrison CJ, Griffiths M, Moorman F, Schnittger S, Cayuela JM, Shurtleff S, Gottardi E, Mitterbauer G, Colomer D, Delabesse E, Castéras V, Maroc N: A multicenter evaluation of comprehensive analysis of MLL translocations and fusion gene partners in acute leukemia using the MLL FusionChip device. Cancer Genet Cytogenet; 2007 Feb;173(1):17-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicenter evaluation of comprehensive analysis of MLL translocations and fusion gene partners in acute leukemia using the MLL FusionChip device.
  • Rearrangements of the MLL gene are significant in acute leukemia.
  • Among the most frequent translocations are t(4;11)(q21;q23) and t(9;11)(p22;q23), which give rise to the MLL-AFF1 and MLL-MLLT3 fusion genes (alias MLL-AF4 and MLL-AF9) in acute lymphoblastic and acute myeloid leukemia, respectively.
  • Current evidence suggests that determining the MLL status of acute leukemia, including precise identification of the partner gene, is important in defining appropriate treatment.
  • A novel molecular diagnostic device, the MLL FusionChip, has been successfully used to identify MLL fusion gene translocations in acute leukemia, including the precise breakpoint location.
  • This study evaluated the performance of the MLL FusionChip within a routine clinical environment, comprising nine centers worldwide, in the analysis of 21 control and 136 patient samples.
  • It was shown that the assay allowed accurate detection of the MLL fusion gene, regardless of the breakpoint location, and confirmed that this multiplex approach was robust in a global multicenter trial.
  • The MLL FusionChip was shown to be superior to other detection methods.
  • The type of molecular information provided by MLL FusionChip gave an indication of the appropriate primers to design for disease monitoring of MLL patients following treatment.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Child. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Chromosomes, Human, Pair 9. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Oligonucleotide Array Sequence Analysis / instrumentation. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [ErratumIn] Cancer Genet Cytogenet. 2007 Dec;179(2):167
  • (PMID = 17284365.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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87. Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W: Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10. Leuk Res; 2010 Aug;34(8):1107-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.
  • We report a case of a 6-month-old boy with a mixed phenotype acute leukemia (MPAL), bilineal and biphenotypic immunophenotype (B-lymphoid lineage and combined B-lymphoid and monocytic lineage) with t(10;11)(p12;q23);MLL-MLLT10.
  • He was treated with acute myeloid leukemia protocol and in complete remission at 7-month follow-up.
  • To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as MPAL in an infant.
  • From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing MPAL and monitoring minimal residual disease.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Biphenotypic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20299091.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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88. Amare Kadam PS, Raje GC, Pais AP, Banavali S: Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL. Cancer Genet Cytogenet; 2008 Apr 1;182(1):27-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
  • Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations.
  • One case of der(21) duplication with ETV6/RUNX1 exhibited a novel MLL translocation variant t(6;11)(p21.1p23;q13q25), with translocation of 3' telomeric MLL and deletion of 5' centromeric MLL.
  • Another case of der(21) duplication with ETV6/RUNX1 showed MLL rearrangement upon Southern blotting.
  • The remaining five ETV6/RUNX1-positive cases had MLL allelic deletion.
  • ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events.
  • We conclude that the cases with coexisting ETV6/RUNX1 and MLL aberrations probably exist as a small, hidden group of ETV6/RUNX1-positive BCP-ALL, which invites further investigation, in large series from different populations, to confirm the findings and establish the biological mechanisms and prognostic significance.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18328947.001).
  • [ISSN] 0165-4608
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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89. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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90. 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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  • (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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91. Baldus CD, Bullinger L: Gene expression with prognostic implications in cytogenetically normal acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):356-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression with prognostic implications in cytogenetically normal acute myeloid leukemia.
  • Acute myeloid leukemia (AML) represents a heterogeneous group of leukemia entities that differ with regard to biology, clinical course, and prognosis.
  • In addition to the impact of gene mutations, including the MLL, FLT3, CEBPA, or NPM1 genes in CN-AML, recent analyses have provided evidence that altered gene expression might not only be of biological but also of prognostic relevance in CN-AML patients.
  • Ultimately, a better understanding of gene expression alterations and hence the molecular basis of the disease will contribute to a refined leukemia classification, which will include both previously known CN-AML subgroups and novel classes defined by distinct gene expression clusters with prognostic significance.
  • [MeSH-major] Gene Expression. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 18692686.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 53
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92. Popovic R, Zeleznik-Le NJ: MLL: how complex does it get? J Cell Biochem; 2005 May 15;95(2):234-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL: how complex does it get?
  • The mixed lineage leukemia (MLL) gene encodes a very large nuclear protein homologous to Drosophila trithorax (trx).
  • MLL is required for the proper maintenance of HOX gene expression during development and hematopoiesis.
  • The exact regulatory mechanism of HOX gene expression by MLL is poorly understood, but it is believed that MLL functions at the level of chromatin organization.
  • MLL was identified as a common target of chromosomal translocations associated with human acute leukemias.
  • About 50 different MLL fusion partners have been isolated to date, and while similarities exist between groups of partners, there exists no unifying property shared by all the partners.
  • MLL gene rearrangements are found in leukemias with both lymphoid and myeloid phenotypes and are often associated with infant and secondary leukemias.
  • The immature phenotype of the leukemic blasts suggests an important role for MLL in the early stages of hematopoietic development.
  • Mll homozygous mutant mice are embryonic lethal and exhibit deficiencies in yolk sac hematopoiesis.
  • Recently, two different MLL-containing protein complexes have been isolated.
  • These and other gain- and loss-of-function experiments have provided insight into normal MLL function and altered functions of MLL fusion proteins.
  • This article reviews the progress made toward understanding the function of the wild-type MLL protein.
  • [MeSH-minor] Animals. Gene Expression Regulation, Developmental / physiology. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans. Leukemia, Lymphoid / genetics. Leukemia, Myeloid / genetics. Mice. Myeloid-Lymphoid Leukemia Protein. Phenotype

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  • (PMID = 15779005.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [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 2.1.1.43 / Mll protein, mouse
  • [Number-of-references] 49
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93. 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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94. Wong P, Iwasaki M, Somervaille TC, So CW, Cleary ML: Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. Genes Dev; 2007 Nov 1;21(21):2762-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential.
  • Oncogenic mutations of the MLL histone methyltransferase confer an unusual ability to transform non-self-renewing myeloid progenitors into leukemia stem cells (LSCs) by mechanisms that remain poorly defined.
  • Misregulation of Hox genes is likely to be critical for LSC induction and maintenance but alone it does not recapitulate the phenotype and biology of MLL leukemias, which are clinically heterogeneous--presumably reflecting differences in LSC biology and/or frequency.
  • TALE (three-amino-acid loop extension) class homeodomain proteins of the Pbx and Meis families are also misexpressed in this context, and we thus employed knockout, knockdown, and dominant-negative genetic techniques to investigate the requirements and contributions of these factors in MLL oncoprotein-induced acute myeloid leukemia.
  • Our studies show that induction and maintenance of MLL transformation requires Meis1 and is codependent on the redundant contributions of Pbx2 and Pbx3.
  • Meis1 in particular serves a major role in establishing LSC potential, and determines LSC frequency by quantitatively regulating the extent of self-renewal, differentiation arrest, and cycling, as well as the rate of in vivo LSC generation from myeloid progenitors.
  • Thus, TALE proteins are critical downstream effectors within an essential homeoprotein network that serves a rate-limiting regulatory role in MLL leukemogenesis.

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  • [CommentIn] Genes Dev. 2007 Nov 15;21(22):2845-9 [18006680.001]
  • [ErratumIn] Genes Dev. 2007 Nov 15;21(22):3017. So, Chai Wai Eric [corrected to So, Chi Wai Eric]
  • (PMID = 17942707.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / R37 CA042971; United States / NCI NIH HHS / CA / CA42971; United States / NCI NIH HHS / CA / CA55029
  • [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 / Neoplasm Proteins; 0 / Pbx2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tgif protein, mouse; 0 / myeloid ecotropic viral integration site 1 protein; 146150-81-4 / proto-oncogene protein Pbx3; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2045130
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95. Rice KL, Licht JD: HOX deregulation in acute myeloid leukemia. J Clin Invest; 2007 Apr;117(4):865-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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96. Gué M, Sun JS, Boudier T: Simultaneous localization of MLL, AF4 and ENL genes in interphase nuclei by 3D-FISH: MLL translocation revisited. BMC Cancer; 2006;6:20
MedlinePlus Health Information. consumer health - Genes and Gene Therapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Simultaneous localization of MLL, AF4 and ENL genes in interphase nuclei by 3D-FISH: MLL translocation revisited.
  • MLL translocation in acute leukaemia) and two models have been proposed to explain the origins of recurrent reciprocal translocation.
  • Since the MLL gene involved in 11q23 translocation has more than 40 partners, the study of the relative positions of the MLL gene with both the most frequent partner gene (AF4) and a less frequent partner gene (ENL), should elucidate the MLL translocation mechanism.
  • METHODS: Using triple labeling 3D FISH experiments, we have determined the relative positions of MLL, AF4 and ENL genes, in two lymphoblastic and two myeloid human cell lines.
  • RESULTS: In all cell lines, the ENL gene is significantly closer to the MLL gene than the AF4 gene (with P value < 0.0001).
  • According to the static "contact first" model of the translocation mechanism, a minimal distance between loci would indicate a greater probability of the occurrence of t(11;19)(q23;p13.3) compared to t(4;11)(q21;q23).
  • However this is in contradiction to the epidemiology of 11q23 translocation.
  • [MeSH-major] Cell Nucleus / chemistry. DNA-Binding Proteins / genetics. Genes. Imaging, Three-Dimensional. In Situ Hybridization, Fluorescence / methods. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Transformed / chemistry. Cell Line, Transformed / ultrastructure. Cell Line, Tumor / chemistry. Cell Line, Tumor / ultrastructure. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 19 / ultrastructure. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 4 / ultrastructure. HL-60 Cells / chemistry. HL-60 Cells / ultrastructure. Herpesvirus 4, Human. Histone-Lysine N-Methyltransferase. Humans. Interphase. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Male. Models, Genetic. Multiple Myeloma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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  • (PMID = 16433901.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 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/ PMC1388228
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97. Stumpel DJ, Schneider P, van Roon EH, Boer JM, de Lorenzo P, Valsecchi MG, de Menezes RX, Pieters R, Stam RW: Specific promoter methylation identifies different subgroups of MLL-rearranged infant acute lymphoblastic leukemia, influences clinical outcome, and provides therapeutic options. Blood; 2009 Dec 24;114(27):5490-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific promoter methylation identifies different subgroups of MLL-rearranged infant acute lymphoblastic leukemia, influences clinical outcome, and provides therapeutic options.
  • MLL-rearranged infant acute lymphoblastic leukemia (ALL) remains the most aggressive type of childhood leukemia, displaying a unique gene expression profile.
  • To test this hypothesis, we used differential methylation hybridization to explore the DNA methylation patterns underlying MLL-rearranged ALL in infants.
  • The obtained results were correlated with gene expression data to confirm gene silencing as a result of promoter hypermethylation.
  • Distinct promoter CpG island methylation patterns separated different genetic subtypes of MLL-rearranged ALL in infants.
  • MLL translocations t(4;11) and t(11;19) characterized extensively hypermethylated leukemias, whereas t(9;11)-positive infant ALL and infant ALL carrying wild-type MLL genes epigenetically resembled normal bone marrow.
  • Furthermore, the degree of promoter hypermethylation among infant ALL patients carrying t(4;11) or t(11;19) appeared to influence relapse-free survival, with patients displaying accentuated methylation being at high relapse risk.
  • Finally, we show that the demethylating agent zebularine reverses aberrant DNA methylation and effectively induces apoptosis in MLL-rearranged ALL cells.
  • Collectively these data suggest that aberrant DNA methylation occurs in the majority of MLL-rearranged infant ALL cases and guides clinical outcome.
  • Therefore, inhibition of aberrant DNA methylation may be an important novel therapeutic strategy for MLL-rearranged ALL in infants.
  • [MeSH-major] DNA Methylation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 9 / genetics. Cluster Analysis. CpG Islands / genetics. Cytidine / analogs & derivatives. Cytidine / pharmacology. Dose-Response Relationship, Drug. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Infant. Jurkat Cells. Survival Analysis. Treatment Outcome

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  • (PMID = 19855078.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE18400
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 5CSZ8459RP / Cytidine
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98. 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
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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99. 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
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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  • (PMID = 19965632.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE19143
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / MLL protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; VB0R961HZT / Prednisone
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100. Haferlach T: Molecular genetic pathways as therapeutic targets in acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2008;:400-11
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetic pathways as therapeutic targets in acute myeloid leukemia.
  • The heterogeneity of acute myeloid leukemia (AML) results from a complex network of cytogenetic aberrations and molecular mutations.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
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  • (PMID = 19074117.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Genetic Markers; 0 / Oxides; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 111
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