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1. Allen MD, Grummitt CG, Hilcenko C, Min SY, Tonkin LM, Johnson CM, Freund SM, Bycroft M, Warren AJ: Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase. EMBO J; 2006 Oct 04;25(19):4503-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase.
  • The mixed-lineage leukaemia (MLL) CXXC domain selectively binds nonmethyl-CpG DNA, and is required for transformation by MLL fusion proteins that commonly arise from recurrent chromosomal translocations in infant and secondary treatment-related acute leukaemias.
  • To elucidate the molecular basis of nonmethyl-CpG DNA recognition, we determined the structure of the human MLL CXXC domain by multidimensional NMR spectroscopy.
  • These data provide a template for the design of specifically targeted therapeutics for poor prognosis MLL-associated leukaemias.
  • [MeSH-major] CpG Islands / genetics. Histone-Lysine N-Methyltransferase / chemistry. Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / chemistry. Neoplasm Proteins / chemistry

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  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16990798.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105161083; United Kingdom / Medical Research Council / / MC/ U105459896
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Solutions; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1589984
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2. 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
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  • [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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3. 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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4. Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML: Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus. J Clin Pathol; 2007 May;60(5):562-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
  • Myeloid sarcomas are tumour masses of myeloid leukaemic cells at extramedullary sites.
  • These tumours can, on occasion, occur without concurrent or antecedent leukaemia.
  • Myeloid sarcomas have been described at unusual locations including the female genital tract.
  • An unusual case of therapy-related acute myeloid leukaemia (t-AML) presenting as isolated monoblastic myeloid sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
  • Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a mixed-lineage leukaemia (MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
  • This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these myeloid sarcomas can be useful for risk assessment and guiding definitive therapy.

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  • (PMID = 17513515.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994540
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5. 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


6. Cleary ML: Regulating the leukaemia stem cell. Best Pract Res Clin Haematol; 2009 Dec;22(4):483-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulating the leukaemia stem cell.
  • Leukaemia stem cells (LSCs) are responsible for sustaining and propagating malignant disease, and, as such, are promising targets for therapy.
  • LSCs in acute myeloid leukaemia (AML) have recently been studied using mouse syngeneic models of leukaemia induced by MLL oncogenes.

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  • (PMID = 19959097.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 16
  • [Other-IDs] NLM/ NIHMS157679; NLM/ PMC2802107
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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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8. Beesley AH, Rampellini JL, Palmer ML, Heng JY, Samuels AL, Firth MJ, Ford J, Kees UR: Influence of wild-type MLL on glucocorticoid sensitivity and response to DNA-damage in pediatric acute lymphoblastic leukemia. Mol Cancer; 2010;9:284
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  • [Title] Influence of wild-type MLL on glucocorticoid sensitivity and response to DNA-damage in pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Rearrangement of the mixed-lineage leukemia gene (MLL) is found in 80% of infant acute lymphoblastic leukemia (ALL) and is associated with poor prognosis and resistance to glucocorticoids (GCs).
  • We have recently observed that GC resistance in T-ALL cell lines is associated with a proliferative metabolism and reduced expression of MLL.
  • In this study we have further explored the relationship between MLL status and GC sensitivity.
  • RESULTS: Negative correlation of MLL expression with GC resistance in 15 T-ALL cell lines was confirmed by quantitative RT-PCR.
  • The absence of MLL-rearrangements suggested that this relationship represented expression of wild-type MLL.
  • Analysis of MLL expression patterns revealed a negative relationship with cellular metabolism, proliferation and anti-apoptotic transcriptional networks.
  • In silico analysis of published data demonstrated that reduced levels of MLL mRNA are associated with relapse and prednisolone resistance in T-ALL patients and adverse clinical outcome in children with MLL-rearranged ALL.
  • RNAi knockdown of MLL expression in T-ALL cell lines significantly increased resistance to dexamethasone and gamma irradiation indicating an important role for wild-type MLL in the control of cellular apoptosis.
  • CONCLUSIONS: The data suggests that reduced expression of wild-type MLL can contribute to GC resistance in ALL patients both with and without MLL-translocations.
  • [MeSH-major] DNA Damage / genetics. Drug Resistance, Neoplasm / genetics. Glucocorticoids / pharmacology. Lymphocytes / drug effects. Myeloid-Lymphoid Leukemia Protein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20979663.001).
  • [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 / Glucocorticoids; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2987983
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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. 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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  • [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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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. 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
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  • [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.

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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 / / G0600914; United Kingdom / Medical Research Council / / 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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14. Krivtsov AV, Armstrong SA: MLL translocations, histone modifications and leukaemia stem-cell development. Nat Rev Cancer; 2007 Nov;7(11):823-33
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  • [Title] MLL translocations, histone modifications and leukaemia stem-cell development.
  • Translocations that involve the mixed lineage leukaemia (MLL) gene identify a unique group of acute leukaemias, and often predict a poor prognosis.
  • The MLL gene encodes a DNA-binding protein that methylates histone H3 lysine 4 (H3K4), and positively regulates gene expression including multiple Hox genes.
  • Leukaemogenic MLL translocations encode MLL fusion proteins that have lost H3K4 methyltransferase activity.
  • A key feature of MLL fusion proteins is their ability to efficiently transform haematopoietic cells into leukaemia stem cells.
  • The link between a chromatin modulator and leukaemia stem cells provides support for epigenetic landscapes as an important part of leukaemia and normal stem-cell development.
  • [MeSH-major] Epigenesis, Genetic / physiology. Gene Expression Regulation. Histone-Lysine N-Methyltransferase / physiology. Histones / metabolism. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / physiology

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  • (PMID = 17957188.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; 0 / Histones; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
  • [Number-of-references] 121
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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. Knapper S: FLT3 inhibition in acute myeloid leukaemia. Br J Haematol; 2007 Sep;138(6):687-99
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  • [Title] FLT3 inhibition in acute myeloid leukaemia.
  • Activating mutations of FLT3 are present in approximately one-third of acute myeloid leukaemia patients and are associated with adverse clinical outcome, while many non-mutated cases also show evidence of FLT3 activation.
  • FLT3 inhibition may also be effective used in combination with other molecularly targeted agents, in postchemotherapy stem-cell-directed maintenance therapy and in MLL-rearranged infant acute lymphoblastic leukaemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid / drug therapy. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Remission Induction / methods

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  • (PMID = 17655729.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HSP90 Heat-Shock Proteins; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 89
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17. Krivtsov AV, Twomey D, Feng Z, Stubbs MC, Wang Y, Faber J, Levine JE, Wang J, Hahn WC, Gilliland DG, Golub TR, Armstrong SA: Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature; 2006 Aug 17;442(7104):818-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.
  • Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme.
  • We isolated LSC from leukaemias initiated in committed granulocyte macrophage progenitors through introduction of the MLL-AF9 fusion protein encoded by the t(9;11)(p22;q23).
  • The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors.
  • LSC can thus be generated from committed progenitors without widespread reprogramming of gene expression, and a leukaemia self-renewal-associated signature is activated in the process.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cell Line. Cell Lineage. Granulocytes / cytology. Granulocytes / pathology. Humans. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Macrophages / cytology. Macrophages / pathology. Mice. Neoplasm Transplantation. Survival Rate


18. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis

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  • (PMID = 18264136.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 111
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19. Balgobind BV, Hollink IH, Reinhardt D, van Wering ER, de Graaf SS, Baruchel A, Stary J, Beverloo HB, de Greef GE, Pieters R, Zwaan CM, van den Heuvel-Eibrink MM: Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique. Eur J Cancer; 2010 Jul;46(10):1892-9
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  • [Title] Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique.
  • Mixed-lineage leukaemia (MLL)-partial tandem duplications (PTDs) are found in 3-5% of adult acute myeloid leukaemia (AML), and are associated with poor prognosis.
  • In adult AML, MLL-PTD is only detected in patients with trisomy 11 or internal tandem duplications of FLT3 (FLT3-ITD).
  • To date, studies in paediatric AML are scarce, and reported large differences in the frequency of MLL-PTD, frequently utilising mRNA RT-PCR only to detect MLL-PTDs.
  • We studied the frequency of MLL-PTD in a large cohort of paediatric AML (n=276) and the results from two different methods, i.e. mRNA RT-PCR, and multiplex ligation-dependent probe amplification (MLPA), a method designed to detect copy number differences of specific DNA sequences.
  • In some patients with an MLL-rearrangement, MLL-PTD transcripts were detected, but were not confirmed by DNA-MLPA, indicating that DNA-MLPA can more accurately detect MLL-PTD compared to mRNA RT-PCR.
  • In paediatric AML, MLL-PTD was detected in 7/276 patients (2.5%).
  • One case had a trisomy 11, while the others had normal cytogenetics.
  • In conclusion, using DNA-MLPA as a novel screenings technique in combination with mRNA RT-PCR a low frequency of MLL-PTD in paediatric AML was found.
  • Larger prospective studies are needed to further define the prognostic relevance of MLL-PTD in paediatric AML.
  • [MeSH-major] Gene Duplication. Genetic Testing / methods. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20233657.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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20. Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC: The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice. Leukemia; 2006 Oct;20(10):1829-39
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  • [Title] The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
  • Rearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia.
  • Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property.
  • We also generated Mll(Een/+) chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
  • Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations.
  • We observed differential regulation of Hox genes between myeloid cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease.
  • We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myeloid Cells / pathology. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 16888613.001).
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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21. 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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22. Daser A, Rabbitts TH: The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis. Semin Cancer Biol; 2005 Jun;15(3):175-88
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  • [Title] The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.
  • The marked association of abnormalities of chromosome 11 long arm, band q23, with human leukaemia led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).
  • MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia).
  • The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.
  • These studies have defined MLL-fusion proteins as regulators of gene expression, controlling such elements as HOX genes, and have indicated a variety of mechanisms by which MLL-fusion proteins contribute to leukaemogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism

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  • (PMID = 15826832.001).
  • [ISSN] 1044-579X
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 123
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23. Brassesco MS, Montaldi AP, Gras DE, Camparoto ML, Martinez-Rossi NM, Scrideli CA, Tone LG, Sakamoto-Hojo ET: Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors. Mutagenesis; 2009 Mar;24(2):153-60
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  • [Title] Cytogenetic and molecular analysis of MLL rearrangements in acute lymphoblastic leukaemia survivors.
  • The successful treatment of paediatric malignancies by multimodal therapy has improved outcomes for children with cancer, especially those with acute lymphoblastic leukaemia (ALL).
  • Depending on dosage, 2-12% of patients treated with topoisomerase II inhibitors and/or alkylating agents develop treatment-related acute myeloid leukaemia characterized by translocations at 11q23.
  • Our goal was to study MLL rearrangements in peripheral lymphocytes using cytogenetic and molecular methods in order to evaluate the late effects of cancer therapy in patients previously treated for childhood ALL.
  • Chromosomal rearrangements at 11q23 were analysed in cytogenetic preparations from 49 long-term ALL survivors and 49 control individuals.
  • Several MLL translocations were detected and identified by inverse polymerase chain reaction, followed by cloning and sequencing.
  • Thirty-five patients (81%) presented putative translocations; among those, 91% corresponded with t(4;11) (q21;q23), while the other 9% corresponded with t(11;X), t(8;11)(q23;q23) and t(11;16).
  • Our results indicate an increase in MLL aberrations in childhood ALL survivors years after completion of therapy.
  • [MeSH-major] Cytogenetic Analysis. Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Survivors
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Case-Control Studies. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Etoposide / therapeutic use. Humans. Molecular Sequence Data. Polymerase Chain Reaction. Teniposide / therapeutic use. Translocation, Genetic

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  • (PMID = 19028982.001).
  • [ISSN] 1464-3804
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; 957E6438QA / Teniposide
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24. Hayashi M, Kondoh K, Nakata Y, Kinoshita A, Mori T, Takahashi T, Sakamoto MI, Yamada T: Establishment of a novel childhood acute myeloid leukaemia cell line, KOPM-88, containing partial tandem duplication of the MLL gene and an in vivo model for childhood acute myeloid leukaemia using NOD/SCID mice. Br J Haematol; 2007 May;137(3):221-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment of a novel childhood acute myeloid leukaemia cell line, KOPM-88, containing partial tandem duplication of the MLL gene and an in vivo model for childhood acute myeloid leukaemia using NOD/SCID mice.
  • MLL gene rearrangement is common in both adult and childhood acute myeloid leukaemia (AML), and its role in oncogenesis has been investigated.
  • While over 50 translocated-partner genes have been identified so far, few studies have detailed the molecular mechanism of partial tandem duplication (PTD) of the MLL gene.
  • The prognostic impact and contribution to leukaemogenesis of MLL-PTD, especially in childhood cases, remain unknown.
  • We have established a novel cell line containing MLL-PTD derived from an 11-year-old patient with AML and designated as KOPM-88.
  • KOPM-88 cells exhibited certain characteristics associated with the myeloid lineage including abundant primary granules in the cytoplasm and the expression of myeloperoxidase.
  • MLL-PTD of exon 2 to exon 6 and exon 2 to exon 8 was revealed using Southern blotting, fluorescence in situ hybridisation, and reverse transcription polymerase chain reaction/DNA sequencing.
  • This is the first report of an in vivo animal model exhibiting the systemic involvement of childhood AML containing MLL-PTD.
  • KOPM-88 cells and our murine model may be useful for investigating the pathogenesis of childhood AML associated with MLL gene rearrangement.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences / genetics

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  • (PMID = 17408461.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Cytokines; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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25. Stam RW, den Boer ML, Pieters R: Towards targeted therapy for infant acute lymphoblastic leukaemia. Br J Haematol; 2006 Mar;132(5):539-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Towards targeted therapy for infant acute lymphoblastic leukaemia.
  • Despite the greatly improved treatment regimes for childhood acute lymphoblastic leukaemia (ALL) in general, resulting in long-term survival in approximately 80% of cases, current therapies still fail in >50% of ALL cases diagnosed within the first year of life (i.e. in infants).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Age of Onset. Forecasting. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics. Prognosis. Remission Induction. Translocation, Genetic

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  • (PMID = 16445826.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [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
  • [Number-of-references] 139
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26. Baldus CD, Mrózek K, Marcucci G, Bloomfield CD: Clinical outcome of de novo acute myeloid leukaemia patients with normal cytogenetics is affected by molecular genetic alterations: a concise review. Br J Haematol; 2007 Jun;137(5):387-400
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical outcome of de novo acute myeloid leukaemia patients with normal cytogenetics is affected by molecular genetic alterations: a concise review.
  • Normal cytogenetics are detected pretreatment in approximately 45% of patients with de novo acute myeloid leukaemia (AML); thus this constitutes the single largest cytogenetic group of AML.
  • They include internal tandem duplication of the FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEBPA and NPM1 genes and aberrant expression of the BAALC, ERG and MN1 genes.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 17488484.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 101140; United States / NCI NIH HHS / CA / CA 16058; United States / NCI NIH HHS / CA / CA 77658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins
  • [Number-of-references] 92
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27. 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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  • [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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28. Palle J, Frost BM, Forestier E, Gustafsson G, Nygren P, Hellebostad M, Jonsson OG, Kanerva J, Schmiegelow K, Larsson R, Lönnerholm G, Nordic Society for Paediatric Haematology and Oncology: Cellular drug sensitivity in MLL-rearranged childhood acute leukaemia is correlated to partner genes and cell lineage. Br J Haematol; 2005 Apr;129(2):189-98
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  • [Title] Cellular drug sensitivity in MLL-rearranged childhood acute leukaemia is correlated to partner genes and cell lineage.
  • Rearrangements in the 11q23 region, the site of the mixed lineage leukaemia (MLL) gene, are found in both childhood acute myeloid (AML) and lymphoblastic (ALL) leukaemia.
  • In AML, children with t(9;11) (n = 10) were significantly more sensitive to cytarabine (P < 0.001) and doxorubicin (P = 0.005) than non-11q23 rearranged patients (n = 108).
  • Children with other 11q23 rearrangements (n = 14) differed less from non-rearranged children.
  • In ALL, children with 11q23 rearrangement (n = 22) were significantly more sensitive to cytarabine (P = 0.026) than children without 11q23 rearrangement (n = 156), also after stratification for white blood cell count.
  • In conclusion, the findings indicate that the cellular drug resistance is correlated to both the cell lineage and the type of 11q23 rearrangement.
  • High cellular sensitivity to cytarabine and doxorubicin might explain the excellent treatment results in children with AML and t(9;11).
  • The present study supports the strategy of contemporary protocols to include high-dose cytarabine in the treatment of 11q23-positive patients both in AML and ALL.
  • [MeSH-major] DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Agents / pharmacology. Cell Lineage. Child. Child, Preschool. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Cytarabine / pharmacology. Cytotoxicity Tests, Immunologic. Doxorubicin / pharmacology. Female. Fluorometry. Glucocorticoids / pharmacology. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein. Prospective Studies. Statistics, Nonparametric. Translocation, Genetic

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  • (PMID = 15813846.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Glucocorticoids; 0 / MLL protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 80168379AG / Doxorubicin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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29. 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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30. Scharf S, Zech J, Bursen A, Schraets D, Oliver PL, Kliem S, Pfitzner E, Gillert E, Dingermann T, Marschalek R: Transcription linked to recombination: a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene. Oncogene; 2007 Mar 1;26(10):1361-71
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  • [Title] Transcription linked to recombination: a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene.
  • The MLL gene is frequently involved in chromosomal translocations associated with high-risk acute leukaemia.
  • Infant and therapy-related acute leukaemia patients display chromosomal breakpoints preferentially clustered in the telomeric portion of the MLL breakpoint cluster region (SCII).
  • Here, we demonstrate that SCII colocalizes with a gene-internal promoter element in the mouse and human MLL gene, respectively.
  • The mRNA generated encodes an N-terminally truncated version of MLL that still exhibits many functional regions, including the C-terminal SET-domain.
  • Etoposide-induced DNA double-strand breaks colocalize with the binding site of RNA polymerase II and the transcription initiation region, but not with a nearby Topo II consensus sequence.
  • Thus, the observed genomic instability of the human MLL gene is presumably linked to transcriptional processes.
  • The consequences of this novel finding for the creation of chromosomal translocations, the biology of the MLL protein and for MLL-mediated acute leukaemia are discussed.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / genetics. Promoter Regions, Genetic. Recombination, Genetic. Transcription, Genetic

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  • (PMID = 16983345.001).
  • [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 / Chromatin; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse; EC 2.7.7.- / RNA Polymerase II
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31. Zuna J, Burjanivova T, Mejstrikova E, Zemanova Z, Muzikova K, Meyer C, Horsley SW, Kearney L, Colman S, Ptoszkova H, Marschalek R, Hrusak O, Stary J, Greaves M, Trka J: Covert preleukemia driven by MLL gene fusion. Genes Chromosomes Cancer; 2009 Jan;48(1):98-107
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  • [Title] Covert preleukemia driven by MLL gene fusion.
  • Acute leukemia is considered to be a two- or multiple-step process.
  • Although there is a considerable knowledge regarding the character of the "first hit," the nature of the "second hit" remains unanswered in most of the cases including leukemias with MLL gene rearrangement.
  • We demonstrate here a striking sequence of events, which include a covert, protracted preleukemic phase characterized by a dominant MLL/FOXO3A clone with intact myeloid differentiation and the subsequent acquisition of a secondary genetic abnormality, leading to overt lymphoblastic leukemia.
  • Backtracking of the secondary acute lymphoblastic leukemia (sALL) with the MLL rearrangement showed no blasts in the bone marrow (BM) during the protracted preleukemic phase.
  • However, at the same time (more than 1 year before the sALL diagnosis) the MLL/FOXO3A was present in up to 90% of BM cells including myeloid lineage, suggesting that the fusion arose in a multipotent progenitor.
  • These data provide insight into the dynamics of leukemogenesis in secondary leukemia with MLL rearrangement.
  • [MeSH-major] Gene Fusion. Leukemia, Promyelocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 19 / genetics. Cytogenetic Analysis. Female. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / metabolism. Gene Expression Regulation, Leukemic. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Myeloid Cells / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Polymorphism, Single Nucleotide

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  • (PMID = 18932267.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / FOXO3 protein, human; 0 / Forkhead Transcription Factors; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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32. Olesen LH, Aggerholm A, Andersen BL, Nyvold CG, Guldberg P, Nørgaard JM, Hokland P: Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling. Br J Haematol; 2005 Nov;131(4):457-67
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  • [Title] Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling.
  • Although a number of molecular aberrations have been described in acute myeloid leukaemia (AML), no study has yet determined their relative prognostic importance.
  • Internal tandem duplication (ITD) of the FLT3 gene and partial tandem duplication of the MLL gene were found in 24% and 4%, respectively.
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid / genetics. Tandem Repeat Sequences / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA, Neoplasm / genetics. Gene Expression Profiling. Genes, MDR. Humans. Middle Aged. Neoplasm Proteins / genetics. Promoter Regions, Genetic / genetics. Proportional Hazards Models. Retrospective Studies. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16281935.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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33. Martino V, Tonelli R, Montemurro L, Franzoni M, Marino F, Fazzina R, Pession A: Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23). Oncol Rep; 2006 Jan;15(1):207-11
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  • [Title] Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23).
  • The MLL-AF9 oncogene originates from the translocation t(9;11)(p22;q23), which is mainly associated with monocytic acute myeloid leukaemia (AML-M5; FAB-classification).
  • In AML-M5 THP-1 cells carrying t(9;11) (p22;q23) and expressing MLL-AF9, we previously showed that MLL-AF9 expression is down-regulated during monocyte-macrophage maturation.
  • We have subsequently observed that in a 'rapid-growing' variant of the THP-1 cell line (THP-1-R) MLL-AF9 down-regulation does not occur.
  • MLL fusion proteins (including MLL-AF9) deregulate MYC transactivation activity, and both presence and absence of MYC down-regulation have been reported during monocyte-macrophage maturation in THP-1 cells.
  • In the present study, we analyze the expression patterns of MLL-AF9, MLL wild-type and MYC after induction of monocyte-macrophage terminal differentiation in the AML-M5 cell lines, THP-1, THP-1-R, Mono-Mac-6 (MM6) and MOLM-13, all of which carry t(9;11)(p22;q23) and express MLL-AF9.
  • RT-PCR analysis indicated that down-regulation of MLL-AF9, MLL or MYC is not necessary to abolish malignant phenotypes by induction of terminal monocyte-macrophage differentiation in leukaemic cells carrying t(9;11)(p22;q23).
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Macrophages / cytology. Monocytes / cytology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Cell Differentiation / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 9 / genetics. Down-Regulation. Histone-Lysine N-Methyltransferase. Humans. Translocation, Genetic

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  • (PMID = 16328057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MYC protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-myc; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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34. Eden T: Aetiology of childhood leukaemia. Cancer Treat Rev; 2010 Jun;36(4):286-97
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  • [Title] Aetiology of childhood leukaemia.
  • The acute leukaemias account for about 30% of all malignancy seen in childhood across the Western world.
  • For some leukaemias (e.g. infant MLL positive ALL) the first event appears adequate to create a malignant clone but for the majority of ALL and AML further 'genetic' changes are required, probably postnatal.
  • Many environmental factors have been proposed as causative for leukaemia but only ionising irradiation and certain chemicals, e.g. benzene and cytotoxics (alkylators and topoisomerase II inhibitors) have been confirmed and then principally for acute myeloid leukaemia.
  • It appears increasingly likely that delayed, dysregulated responses to 'common' infectious agents play a major part in the conversion of pre-leukaemic clones into overt precursor B cell ALL, the most common form of childhood leukaemia.
  • There is no single cause for childhood leukaemia and for most individuals a combination of factors appears to be necessary; all involving gene-environment interactions.
  • [MeSH-major] Leukemia / etiology

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  • [Copyright] 2010. Published by Elsevier Ltd.
  • (PMID = 20223594.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid
  • [Number-of-references] 141
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35. Shapiro S, Hughes G, Al-Obaidi MJ, O'Reilly E, Ramesh S, Smith J, Ahmad R, Dawson C, Riddle P, Sekhar M: Acute myeloid leukaemia secondary to treatment with capecitabine for metastatic colorectal cancer. Eur J Haematol; 2007 Jun;78(6):543-4
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  • [Title] Acute myeloid leukaemia secondary to treatment with capecitabine for metastatic colorectal cancer.
  • A 63-year-old woman was diagnosed with acute myelo-monocytic leukaemia, associated with MLL gene rearrangement, 16 months after completion of oral capecitabine for metastatic colon cancer.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Colorectal Neoplasms / secondary. Deoxycytidine / analogs & derivatives. Fluorouracil / analogs & derivatives. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Capecitabine. Humans

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  • (PMID = 17509107.001).
  • [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 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
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36. Escobar PA, Smith MT, Vasishta A, Hubbard AE, Zhang L: Leukaemia-specific chromosome damage detected by comet with fluorescence in situ hybridization (comet-FISH). Mutagenesis; 2007 Sep;22(5):321-7
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  • [Title] Leukaemia-specific chromosome damage detected by comet with fluorescence in situ hybridization (comet-FISH).
  • Acute myeloid leukaemia (AML) is associated with exposure to benzene and treatment with chemotherapeutic agents.
  • Translocations of the MLL gene at 11q23 are frequently observed in AML arising from treatment with topoisomerase II inhibitors, such as etoposide.
  • Our goal was to determine whether or not breakage at 5q31 and 11q23 is selectively induced by these chemical agents.
  • HQ, melphalan and etoposide induced DNA breaks at both 5q31 and 11q23 chromosome regions in a dose-dependant manner.
  • However, HQ produced significantly more DNA damage at 5q31 than at 11q23.
  • Etoposide produce slightly more DNA damage at 11q23 and melphalan had a somewhat greater effect at 5q31, but not significantly so.
  • [MeSH-major] Alkylating Agents / toxicity. Chromosomes, Human, Pair 11 / drug effects. Chromosomes, Human, Pair 5 / drug effects. Comet Assay / methods. DNA Damage. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Cell Line, Tumor. Histone-Lysine N-Methyltransferase. Humans. Lymphocytes / drug effects. Lymphocytes / ultrastructure. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic

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  • (PMID = 17575318.001).
  • [ISSN] 0267-8357
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES01896; United States / NIEHS NIH HHS / ES / P42 ES04705
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 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. Kokandakar HR, Tembhare PR, Mamoon A, Mulay VM, Bhople KS: Acute basophilic leukaemia: a case report. Indian J Pathol Microbiol; 2007 Apr;50(2):443-6

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  • [Title] Acute basophilic leukaemia: a case report.
  • Acute basophilic leukaemia is an uncommon form of acute leukaemia, rarely occurring as de novo disease.
  • We present a case of acute basophilic leukaemia with (11q23)-MLL gene rearrangement, in an 18-year-old male with review of literature and discussion of diagnostic criteria.
  • [MeSH-major] Leukemia, Basophilic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Coloring Agents. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Staining and Labeling. Tolonium Chloride

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  • (PMID = 17883105.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 15XUH0X66N / Tolonium Chloride; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 11
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38. Harrison CJ, Moorman AV, Barber KE, Broadfield ZJ, Cheung KL, Harris RL, Jalali GR, Robinson HM, Strefford JC, Stewart A, Wright S, Griffiths M, Ross FM, Harewood L, Martineau M: Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study. Br J Haematol; 2005 May;129(4):520-30
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  • [Title] Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study.
  • Summary Interphase fluorescence in situ hybridization (iFISH) was used independently to reveal chromosomal abnormalities of prognostic importance in a large, consecutive series of children (n = 2367) with acute lymphoblastic leukaemia (ALL).
  • The fusions, TEL/AML1 and BCR/ABL, and rearrangements of the MLL gene occurred at frequencies of 22% (n = 447/2027) (25% in B-lineage ALL), 2% (n = 43/2027) and 2% (n = 47/2016) respectively.
  • We were thus able to define amplification of AML1 as a new recurrent abnormality in ALL, associated with a poor prognosis.
  • Amplification involving the ABL gene, a rare recurrent abnormality confined to T ALL patients, was identified for the first time.
  • The iFISH contributed significantly to the high success rate of 91% (n = 2114/2323) and the remarkable abnormality detection rate of 89% (n = 1879/2114).
  • This study highlights the importance of iFISH as a complementary tool to cytogenetics in routine screening for significant chromosomal abnormalities in ALL.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Cytogenetic Analysis. DNA-Binding Proteins / genetics. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Gene Rearrangement. Genes, abl. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Interphase. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogenes / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics

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  • (PMID = 15877734.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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39. Luciani M, Rana I, Pansini V, Caniglia M, Coletti V, Maraschini A, Lombardi A, De Rossi G: Infant leukaemia: clinical, biological and therapeutic advances. Acta Paediatr Suppl; 2006 Jul;95(452):47-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infant leukaemia: clinical, biological and therapeutic advances.
  • Infant acute lymphoid leukaemia (IALL) represents a distinct subset with an extremely poor response to therapy, despite major progress in the treatment of childhood leukaemia.
  • The outcome of IALL patients with ALL-1/MLL rearrangements at the 11q23 cytogenetic band, early pre-B immunophenotype, high WBC count and age below 6 mo is significantly worse than in patients without these characteristics, and current therapies appear inadequate in a significant number of cases.
  • Therefore, an international protocol (Interfant 99) was recently started, using a more aggressive approach, which included lymphoid- and myeloid-specific drugs, and indications for stem-cell transplantation.
  • We reviewed the clinical characteristics of the disease, the results of several recent international clinical trials, and our experience with 16 infants with acute lymphoid leukaemia diagnosed and treated at our institution.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 16801167.001).
  • [ISSN] 0803-5326
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992). Supplement
  • [ISO-abbreviation] Acta Paediatr Suppl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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40. Kuchenbauer F, Schnittger S, Look T, Gilliland G, Tenen D, Haferlach T, Hiddemann W, Buske C, Schoch C: Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO. Br J Haematol; 2006 Sep;134(6):616-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO.
  • AML1-ETO collaborates with further genetic abnormalities to induce acute myeloid leukaemia (AML).
  • Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56.5%) and del(9)(q22) (24/99, 24.2%).
  • Further molecular abnormalities were FLT3 mutations (3/87, 3.4%), AML1 (1/26, 3.8%) and PU1 (1/14, 7.1%).
  • MLL-PTD, KRAS and CEBPA mutations were not found.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid. Male. Middle Aged

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  • (PMID = 16938118.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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41. Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG: A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial. Lancet; 2007 Jul 21;370(9583):240-50
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  • [Title] A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
  • BACKGROUND: Acute lymphoblastic leukaemia in infants younger than 1 year is rare, and infants with the disease have worse outcomes than do older children.
  • We initiated an international study to investigate the effects of a new hybrid treatment protocol with elements designed to treat both acute lymphoblastic leukaemia and acute myeloid leukaemia, and to identify any prognostic factors for outcome in infants.
  • Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given a hybrid regimen based on the standard protocol for acute lymphoblastic leukaemia, with some elements designed for treatment of acute myeloid leukaemia.
  • All types of rearrangements in the (mixed lineage leukaemia) MLL gene, very high white blood cell count, age of younger than 6 months, and a poor response to the prednisone prophase were independently associated with inferior outcomes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [CommentIn] Lancet. 2007 Jul 21;370(9583):198-200 [17658376.001]
  • (PMID = 17658395.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
  • [Grant] United Kingdom / Medical Research Council / / G0300130
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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42. Rujkijyanont P, Beyene J, Wei K, Khan F, Dror Y: Leukaemia-related gene expression in bone marrow cells from patients with the preleukaemic disorder Shwachman-Diamond syndrome. Br J Haematol; 2007 Jun;137(6):537-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukaemia-related gene expression in bone marrow cells from patients with the preleukaemic disorder Shwachman-Diamond syndrome.
  • Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure disorder with cytopenia and a high propensity for myelodysplastic syndrome (MDS) and leukaemia, particularly acute myeloid leukaemia.
  • In accordance to the multi-hit theory of carcinogenesis, it is likely that several molecular and cellular hits occur before MDS/leukaemia become apparent.
  • Among 154 known leukaemia-related genes, several oncogenes were found to be upregulated, including LARG, TAL1 and MLL, and of several tumour suppressor genes were downregulated, including DLEU1, RUNX1, FANCD2 and DKC1.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / genetics. Male. Reverse Transcriptase Polymerase Chain Reaction. Syndrome


43. Dai Y, Guzman ML, Chen S, Wang L, Yeung SK, Pei XY, Dent P, Jordan CT, Grant S: The NF (Nuclear factor)-κB inhibitor parthenolide interacts with histone deacetylase inhibitors to induce MKK7/JNK1-dependent apoptosis in human acute myeloid leukaemia cells. Br J Haematol; 2010 Oct;151(1):70-83
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  • [Title] The NF (Nuclear factor)-κB inhibitor parthenolide interacts with histone deacetylase inhibitors to induce MKK7/JNK1-dependent apoptosis in human acute myeloid leukaemia cells.
  • Interactions between the nuclear factor (NF)-κB inhibitor parthenolide and the pan-histone deacetylase inhibitors (HDACIs) vorinostat and LBH589 were investigated in human acute myeloid leukaemia (AML) cells, including primary AML blasts.
  • U937, HL-60, NB4, MV-4-11, and MOLM-13).
  • Significantly, parthenolide also increased HDACI-mediated cell death in haematopoietic cells transduced with the MLL-MLLT1 fusion gene, which exhibit certain leukaemia-initiating cell characteristics, as well as primary AML blasts.

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
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  • (PMID = 20701602.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / R01 CA141703; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / CA 93738; United States / NCI NIH HHS / CA / 1 P50 CA130805-01; United States / NCI NIH HHS / CA / R01 CA150214
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / NF-kappa B; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS225049; NLM/ PMC2950247
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44. Olde Nordkamp L, Mellink C, van der Schoot E, van den Berg H: Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics? J Pediatr Hematol Oncol; 2009 Dec;31(12):930-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Karyotyping, FISH, and PCR in acute lymphoblastic leukemia: competing or complementary diagnostics?
  • BACKGROUND: Chromosomal abnormalities, such as t(9;22)(q34;q11) (ABL/BCR), t(12;21)(p13;q22) (TEL/AML1), and t(11q23) (MLL) are independent prognostic indicators in childhood acute lymphoblastic leukemia resulting in risk adapted therapy.
  • Accurate and rapid detection of these abnormalities is mandatory, which is achieved by karyotyping, fluorescence in situ hybridization, and real time quantitative reverse transcriptase polymerase chain reaction (RQ-PCR).
  • All consecutive patients under 18 years with acute lymphoblastic leukaemia were included.
  • However, the sensitivity of karyotyping for detecting the TEL-AML1 fusion gene and the sensitivity of RQ-PCR for detecting MLL-rearrangements was rather low.
  • CONCLUSIONS: Diagnostic accuracy of tests for detecting t(9;22), t(12;21), and t(11q23) is generally high, although sensitivity is not optimal for all anomalies.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Rearrangement. Humans. Infant. Infant, Newborn. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Retrospective Studies. Translocation, Genetic / genetics

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  • (PMID = 19875970.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. Jo A, Tsukimoto I, Ishii E, Asou N, Mitani S, Shimada A, Igarashi T, Hayashi Y, Ichikawa H: Age-associated difference in gene expression of paediatric acute myelomonocytic lineage leukaemia (FAB M4 and M5 subtypes) and its correlation with prognosis. Br J Haematol; 2009 Mar;144(6):917-29

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age-associated difference in gene expression of paediatric acute myelomonocytic lineage leukaemia (FAB M4 and M5 subtypes) and its correlation with prognosis.
  • Acute myeloid leukaemia, French-American-British M4 and M5 subtypes (AML-M4/M5) is frequently associated with MLL gene rearrangement and its incidence is relatively high among infants.
  • All subgroups included patients with MLL gene rearrangement as well as normal and other karyotypes.
  • Surprisingly, gene expression signatures of MLL gene rearrangement differed substantially among these subgroups.
  • In addition, subgroup C presented extremely poor outcome (3-year event-free survival 28%) whilst eight patients with MLL gene rearrangement in subgroup C had all relapsed within 18 months.
  • [MeSH-major] Gene Expression Profiling. Gene Rearrangement. Leukemia, Myelomonocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19120366.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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47. Burjanivova T, Madzo J, Muzikova K, Meyer C, Schneider B, Votava F, Marschalek R, Stary J, Trka J, Zuna J: Prenatal origin of childhood AML occurs less frequently than in childhood ALL. BMC Cancer; 2006;6:100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive.
  • In AML patients (n = 13, age 1-14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers.
  • [MeSH-major] Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Fetal Blood / chemistry. Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte. Leukemia, Myeloid / embryology. Oncogene Proteins, Fusion / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / embryology
  • [MeSH-minor] Bone Marrow Cells / chemistry. Child. Child, Preschool. Clone Cells / chemistry. Cohort Studies. Core Binding Factor Alpha 2 Subunit / blood. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Humans. Infant. Infant, Newborn. Male. Myeloid-Lymphoid Leukemia Protein / blood. Myeloid-Lymphoid Leukemia Protein / genetics. Neonatal Screening. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / blood. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16630339.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF6 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1463004
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48. Joannides M, Grimwade D: Molecular biology of therapy-related leukaemias. Clin Transl Oncol; 2010 Jan;12(1):8-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The nature of the causative agent has an important bearing upon the characteristics, biology, time to onset and prognosis of the resultant leukaemia.
  • Agents targeting topoisomerase II induce acute leukaemias with balanced translocations that generally arise within 3 years, often involving the MLL, RUNX1 and RARA loci at 11q23, 21q22 and 17q21 respectively.
  • Therapy-related acute myeloid leukaemias occurring after exposure to antimetabolites and/or alkylating agents are biologically distinct with a longer latency period, being characterised by more complex karyotypes and loss of p53.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics

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  • (PMID = 20080465.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Number-of-references] 62
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49. Okada Y, Jiang Q, Lemieux M, Jeannotte L, Su L, Zhang Y: Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L. Nat Cell Biol; 2006 Sep;8(9):1017-24
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  • Chromosomal translocation is a common cause of leukaemia and the most common chromosome translocations found in leukaemia patients involve the mixed lineage leukaemia (MLL) gene.
  • AF10 is one of more than 30 MLL fusion partners in leukaemia.
  • We have recently demonstrated that the H3K79 methyltransferase hDOT1L contributes to MLL-AF10-mediated leukaemogenesis through its interaction with AF10 (ref. 5).
  • In addition to MLL, AF10 has also been reported to fuse to CALM (clathrin-assembly protein-like lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML).
  • Thus, our study establishes CALM-AF10 fusion as a cause of leukaemia and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind leukaemia caused by CALM-AF10 fusion.

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  • [ErratumIn] Nat Cell Biol. 2006 Oct;8(10):1178
  • (PMID = 16921363.001).
  • [ISSN] 1465-7392
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI48407; United States / NIAID NIH HHS / AI / R56 AI048407; United States / NHLBI NIH HHS / HL / R21 HL072240; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIGMS NIH HHS / GM / R01 GM068804; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIGMS NIH HHS / GM / GM68804; United States / NHLBI NIH HHS / HL / HL72240; United States / NIAID NIH HHS / AI / R01 AI048407
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / MLLT10 protein, human; 0 / Mllt10 protein, mouse; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Phosphoproteins; 0 / Transcription Factors; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Methyltransferases
  • [Other-IDs] NLM/ NIHMS684864; NLM/ PMC4425349
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50. 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 .

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  • [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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51. Basecke J, Podleschny M, Becker A, Seiffert E, Schwiers I, Schwiers R, Haase D, Glass B, Schmitz N, Trumper L, Griesinger F: Therapy-associated genetic aberrations in patients treated for non-Hodgkin lymphoma. Br J Haematol; 2008 Apr;141(1):52-9
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  • Therapy-associated myelodysplastic syndromes and acute myeloid leukaemia (t-AML/MDS) following high dose chemotherapy are significant problems, with a cumulative incidence of 20% or more in myeloablative treatment regimen.
  • Molecular aberrations (RUNX1/RUNX1T1, PML-RARA, CBFB-MYH11, MLL-MLLT1, BCR-ABL1) were observed in 33.3% (Arm A) and 55.4% (Arm B) of patients and in 14.9% and 28.7% of respective samples.
  • None of these patients developed a t-AML/MDS during a 3-year clinical follow up period.
  • We concluded that the high incidence of genetic aberrations reflected a dose-dependent, transient therapy-induced genetic damage which is not predictive of a t-AML/MDS.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Follow-Up Studies. Humans. Leukemia, Myeloid, Acute / chemically induced. Middle Aged. Prednisolone / therapeutic use. Prognosis. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic. Vincristine / therapeutic use

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  • (PMID = 18324966.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; CHOEP protocol
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52. Basso G, Case C, Dell'Orto MC: Diagnosis and genetic subtypes of leukemia combining gene expression and flow cytometry. Blood Cells Mol Dis; 2007 Sep-Oct;39(2):164-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and genetic subtypes of leukemia combining gene expression and flow cytometry.
  • Acute leukemia, defined as a genetic disease, is the most common cancer in children representing about one half of all cancers among persons younger than 15 years.
  • Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) each represents a heterogeneous complex of disorders, with genetic abnormalities presenting in more than 80% of ALLs and more than 90% of AMLs.
  • The diagnostic gold standard and classification of leukaemia involves various methods including morphology, cytochemistry, cytogenetics and molecular genetics, immunophenotyping, and molecular biology.
  • These diagnostic methods are a prerequisite for individual treatment strategies and for the evaluation of treatment response especially considering that many distinct types of acute leukemia are known to carry predictable prognoses and warrant specific therapy.
  • Microarray technology offers the possibility of quantifying thousands of genes in a single analysis, thus potentially becoming an essential tool for molecular classification to be used in routine leukaemia diagnostics.
  • MLL+ leukaemia is a perfect example as to the exact correspondence between gene expression and protein expression evaluated by flow cytometry.
  • Applying computational analysis to flow cytometry results, it is possible to distinguish the MLL+ acute leukemia from MLL- acute leukemia using as the top ranked antigen some top ranked genes described in the Microarray evaluation.
  • Key markers discriminating different leukemia phenotypes can be identified by univariate hypothesis testing from a data set of immunophenotypic markers described by two variables, one reflecting the intensity of expression (MESF) and the other the pattern of distribution (CV).
  • A current multi center study called Microarray Innovations in Leukemia (MILE Study) uses higher density gene chips providing nearly complete coverage of the human genome.
  • The study which has analyzed thus far 1837 retrospective cases shows that each important leukemia subtype has a specific genetic fingerprint, meaning that different combinations of genes whose expression is linked to each subtype can be identified allowing for patient tailored therapy.
  • [MeSH-major] Flow Cytometry. Gene Expression Profiling. Leukemia / diagnosis

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  • (PMID = 17588788.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
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53. 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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54. Ibrahim K, Daud SS, Seah YL, Yeoh AE, Ariffin H, Malaysia-Singapore Leukemia Study Group: Rapid detection of prognostically important childhood acute lymphoblastic leukemia chimeric transcripts using multiplex SYBR green real-time reverse transcription PCR. Ann Clin Lab Sci; 2008;38(4):338-43
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  • [Title] Rapid detection of prognostically important childhood acute lymphoblastic leukemia chimeric transcripts using multiplex SYBR green real-time reverse transcription PCR.
  • Childhood acute lymphoblastic leukaemia (ALL) is a heterogenous disease in which oncogene fusion transcripts are known to influence the biological behaviour of the different ALL subtypes.
  • We describe a SYBR-Green real-time multiplex PCR assay to screen for transcripts TEL-AML1, E2A-PBX1, MLL-AF4, and the two breakpoints of BCR-ABL (p190 and p210).
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18988926.001).
  • [ISSN] 1550-8080
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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55. Robinson BW, Behling KC, Gupta M, Zhang AY, Moore JS, Bantly AD, Willman CL, Carroll AJ, Adamson PC, Barrett JS, Felix CA: Abundant anti-apoptotic BCL-2 is a molecular target in leukaemias with t(4;11) translocation. Br J Haematol; 2008 Jun;141(6):827-39
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  • [Title] Abundant anti-apoptotic BCL-2 is a molecular target in leukaemias with t(4;11) translocation.
  • Chemotherapy resistance from imbalanced apoptosis regulation may contribute to poor outcome in leukaemias with t(4;11).
  • Anti-apoptotic BCL-2 expression and target modulation were characterized in cell lines with t(4;11) and BCL-2 expression was examined in MLL and non-MLL infant/paediatric leukaemia cases by Western blot analysis and/or real-time polymerase chain reaction.
  • Apoptosis and cell cycle were evaluated by flow cytometry in RS4:11 cells.
  • Primary leukaemias and cell lines with t(4;11) expressed abundant BCL2 mRNA and protein.
  • Variable, sometimes substantial BCL2 mRNA was detected in other leukaemia subtypes.
  • G3139 reduced BCL2 mRNA and protein in RS4:11 cells.
  • The most sensitive cell line to single-agent G3139 was RS4:11.
  • Low G3139 concentrations sensitized RS4:11 and MV4-11 cells to select anti-leukaemia cytotoxic drugs.
  • In RS4:11 cells, combining G3139 with doxorubicin (ADR) increased active caspase 3 and TUNEL staining compared to ADR alone, indicating greater apoptosis, and G3139 increased S-phase progression.
  • The abundant BCL-2 affords a molecular target in leukaemias with t(4;11).
  • G3139 exhibits preclinical activity and synergy with select cytotoxic agents in RS4:11 and MV4-11 cells, and these effects occur through apoptosis.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 18422996.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 80168379AG / Doxorubicin; 85J5ZP6YSL / oblimersen
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56. Starkova J, Zamostna B, Mejstrikova E, Krejci R, Drabkin HA, Trka J: HOX gene expression in phenotypic and genotypic subgroups and low HOXA gene expression as an adverse prognostic factor in pediatric ALL. Pediatr Blood Cancer; 2010 Dec 1;55(6):1072-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, HOX expression patterns in leukemia cells compared to normal lymphoid progenitors have not been systematically studied in acute lymphoblastic leukemia (ALL) subtypes.
  • HOXA3-4, HOXA7, and HOXB3-4 genes were differentially expressed between BCP-ALL and T-ALL subgroups, and among genotypically defined MLL/AF4, TEL/AML1, BCR/ABL, hyperdiploid and normal karyotype subgroups.
  • HOXA7 gene was low expressed at the RNA level in patients with hyperdiploid leukemia, whereas HOXB7 and CDX2 genes were low expressed in TEL/AML1-positive and BCR/ABL-positive cases, respectively.
  • In contrast to previous findings in acute myeloid leukemia, high HOXA RNA expression was associated with an excellent prognosis in Cox's regression model (P = 0.03).
  • In MLL/AF4-positive ALL, lower HOXA RNA expression correlated with the methylation status of their promoters.
  • CONCLUSIONS: HOX gene RNA expression cannot discriminate leukemia subgroups or relative maturity of leukemic cells.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Homeodomain Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 20672366.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / HOXB2 protein, human; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
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57. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • The overexpression of HOXA genes was associated with overexpression of its cofactor MEIS1 in CALM-AF10+ T-ALL, reaching levels of expression similar to those observed in MLL-t AL.
  • Consequently, CALM-AF10+ T-ALL and MLL-t AL share a specific HOXA overexpression, indicating they activate common oncogenic pathways.
  • In addition, BMI1, located close to AF10 breakpoint, was overexpressed only in CALM-AF10+ T-ALL and not in MLL-t AL.
  • This suggests that decreased CDKN2A activity, as a result of BMI1 overexpression, contributes to leukemogenesis in CALM-AF10+ T-ALL.
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis

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  • (PMID = 16107895.001).
  • [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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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58. Bacher U, Kohlmann A, Haferlach T: Perspectives of gene expression profiling for diagnosis and therapy in haematological malignancies. Brief Funct Genomic Proteomic; 2009 May;8(3):184-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • For a decade, gene expression profiling (GEP) has been applied in leukaemia research.
  • Thus, various studies demonstrated worldwide that the majority of genetically defined leukaemia subtypes are accurately predictable by GEP, for example, with respect to reciprocal rearrangements in acute myeloid leukaemia (AML).
  • Treatment-specific sensitivity assays are being developed for targeted drugs such as farnesyl transferase inhibitors in AML or imatinib in BCR-ABL1 positive acute lymphoblastic leukaemia (ALL).
  • Large multicentre studies such as the MILE Study (Microarray Innovations in LEukemia) aim at translating this methodology into clinical routine workflows and to catalyze this process.

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  • (PMID = 19474126.001).
  • [ISSN] 1477-4062
  • [Journal-full-title] Briefings in functional genomics & proteomics
  • [ISO-abbreviation] Brief Funct Genomic Proteomic
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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59. Quentmeier H, Tonelli R, Geffers R, Pession A, Uphoff CC, Drexler HG: Expression of BEX1 in acute myeloid leukemia with MLL rearrangements. Leukemia; 2005 Aug;19(8):1488-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of BEX1 in acute myeloid leukemia with MLL rearrangements.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Nerve Tissue Proteins / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15920485.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BEX1 protein, human; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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60. De Braekeleer E, Douet-Guilbert N, Morel F, Le Bris MJ, Meyer C, Marschalek R, Férec C, De Braekeleer M: FLNA, a new partner gene fused to MLL in a patient with acute myelomonoblastic leukaemia. Br J Haematol; 2009 Sep;146(6):693-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FLNA, a new partner gene fused to MLL in a patient with acute myelomonoblastic leukaemia.
  • [MeSH-major] Chromosomes, Human, Pair 11. Contractile Proteins / genetics. Leukemia, Myeloid / genetics. Microfilament Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19622092.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contractile Proteins; 0 / DNA, Neoplasm; 0 / Filamins; 0 / Microfilament Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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61. Schuster FR, Führer M, Woessmann W, Reiter A, Harbott J, Viehmann S, Borkhardt A: Treatment of relapsed acute myelogeneous leukaemia with MLL/AF 6 fusion after stem cell transplantation by intensive reinduction followed by adoptive immunotherapy. Leukemia; 2005 Jul;19(7):1273-4; author reply 1275-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of relapsed acute myelogeneous leukaemia with MLL/AF 6 fusion after stem cell transplantation by intensive reinduction followed by adoptive immunotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 6 / genetics. Immunotherapy, Adoptive. Leukemia, Myeloid, Acute / drug therapy. Oncogene Proteins, Fusion / genetics. Stem Cell Transplantation
  • [MeSH-minor] Child. Female. Graft vs Host Disease / etiology. Humans. Male. Mycoses / etiology. Myeloid-Lymphoid Leukemia Protein. RNA, Messenger / genetics. Recurrence. Remission Induction

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  • (PMID = 15902291.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF6 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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62. Nigro LL, Sainati L, Leszl A, Mirabile E, Spinelli M, Consarino C, Di Cataldo A, Magro S, Felix CA, Basso G: Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation. Leukemia; 2007 Feb;21(2):360-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation.
  • [MeSH-major] Dendritic Cells / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / immunology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antigens, CD / genetics. Antigens, CD / immunology. Cell Differentiation. Child. Histone-Lysine N-Methyltransferase. Humans

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  • (PMID = 17205059.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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