Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l. - Wikidata - wikimedia - TriplyDB

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.

http://www.wikidata.org/entity/Q36730426

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Epimutational profile of hematologic malignancies as attractive target for new epigenetic therapies Epigenetic regulators and their impact on therapy in acute myeloid leukemia Pediatric AML: From Biology to Clinical Management Recent progress toward epigenetic therapies: the example of mixed lineage leukemia Potent inhibition of DOT1L as treatment of MLL-fusion leukemia Next generation sequencing of acute myeloid leukemia: influencing prognosis.Unique genomic profile of fibrolamellar hepatocellular carcinoma.DOT1L inhibition sensitizes MLL-rearranged AML to chemotherapy Murine models of acute leukemia: important tools in current pediatric leukemia research.AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.Two decades of leukemia oncoprotein epistasis: the MLL1 paradigm for epigenetic deregulation in leukemia.Selective inhibitors of protein methyltransferases Novel agents for the treatment of childhood acute leukemia.DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.Structure-guided DOT1L probe optimization by label-free ligand displacement.Targeting DOT1L and HOX gene expression in MLL-rearranged leukemia and beyond The histone methyltransferase DOT1L: regulatory functions and a cancer therapy target.AF4 uses the SL1 components of RNAP1 machinery to initiate MLL fusion- and AEP-dependent transcription.Treatment of infant leukemias: challenge and promise.Digging deep into "dirty" drugs - modulation of the methylation machinery.MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia Targeted drug discovery for pediatric leukemia.DOT1L as a therapeutic target for the treatment of DNMT3A-mutant acute myeloid leukemia Differential regulation of the c-Myc/Lin28 axis discriminates subclasses of rearranged MLL leukemia Epigenetics of hematopoiesis and hematological malignancies.The Role of Histone Protein Modifications and Mutations in Histone Modifiers in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia.Smyd2 is a Myc-regulated gene critical for MLL-AF9 induced leukemogenesis.Cooperation between AlphavBeta3 integrin and the fibroblast growth factor receptor enhances proliferation of Hox-overexpressing acute myeloid leukemia cells.The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle.In focus: MLL-rearranged leukemia.Targeting the histone orthography of cancer: drugs for writers, erasers and readers.DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.Targeted therapy of acute myeloid leukemia.Molecular mechanisms of MLL-associated leukemia.Epigenetic modifiers in normal and malignant hematopoiesis.Emerging therapeutic drugs for AML.The upstreams and downstreams of H3K79 methylation by DOT1L.Targeting epigenetic regulators for cancer therapy: modulation of bromodomain proteins, methyltransferases, demethylases, and microRNAs.Inhibitors of Protein Methyltransferases and Demethylases.Copy-number variation and protein expression of DOT1L in pancreatic adenocarcinoma as a potential drug target

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Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.

http://www.wikidata.org/entity/Q36730426

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Leukemic transformation by the ...... H3K79 methyltransferase Dot1l.

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Leukemic transformation by the ...... H3K79 methyltransferase Dot1l.

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BLOOD-2012-11-465120

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Leukemic transformation by the ...... H3K79 methyltransferase Dot1l.

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Amit U Sinha

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Aniruddha J Deshpande

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Deepti Banka

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Edward J Olhava

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Jenny Chang

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Kathrin M Bernt

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Liying Chen

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Maurizio Fazio

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Roy M Pollock

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Scott A Armstrong

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P2860

A higher-order complex containing AF4 and ENL family proteins with P-TEFb facilitates oncogenic and physiologic MLL-dependent transcription

Linking H3K79 trimethylation to Wnt signaling through a novel Dot1-containing complex (DotCom)

Afadin: A novel actin filament-binding protein with one PDZ domain localized at cadherin-based cell-to-cell adherens junction

Selective Inhibitors of Histone Methyltransferase DOT1L: Design, Synthesis, and Crystallographic Studies

hDOT1L links histone methylation to leukemogenesis.

GenePattern 2.0

MLL translocations, histone modifications and leukaemia stem-cell development

Chromatin modifications as therapeutic targets in MLL-rearranged leukemia.

Selective killing of mixed lineage leukemia cells by a potent small-molecule DOT1L inhibitor.

AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia.

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