Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo. - Wikidata - wikimedia - TriplyDB

Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo.

Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo.

http://www.wikidata.org/entity/Q35557914

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Systematic Classification of Mixed-Lineage Leukemia Fusion Partners Predicts Additional Cancer Pathways Modulation of Protein-Protein Interactions for the Development of Novel Therapeutics Property Focused Structure-Based Optimization of Small Molecule Inhibitors of the Protein-Protein Interaction between Menin and Mixed Lineage Leukemia (MLL)The molecular mechanics of mixed lineage leukemia.Successful strategies in the discovery of small-molecule epigenetic modulators with anticancer potential.Targeting DOT1L and HOX gene expression in MLL-rearranged leukemia and beyond CCI-007, a novel small molecule with cytotoxic activity against infant leukemia with MLL rearrangements.MLL1 is essential for the senescence-associated secretory phenotype Menin-MLL inhibitors block oncogenic transformation by MLL-fusion proteins in a fusion partner-independent manner.Epigenetics of hematopoiesis and hematological malignancies.Targeting Mll1 H3K4 methyltransferase activity to guide cardiac lineage specific reprogramming of fibroblasts.Kmt2a cooperates with menin to suppress tumorigenesis in mouse pancreatic islets.Tumorigenicity of Ewing sarcoma is critically dependent on the trithorax proteins MLL1 and menin.Diagnosis and Therapy of Acute Myeloid Leukemia in the Era of Molecular Risk Stratification.Drugging Chromatin in Cancer: Recent Advances and Novel Approaches.Inhibitors of protein methyltransferases as chemical tools.The upstreams and downstreams of H3K79 methylation by DOT1L.Reprogramming of histone methylation controls the differentiation of monocytes into macrophages.Inhibitors of Protein Methyltransferases and Demethylases.The emerging role of PI3K/AKT-mediated epigenetic regulation in cancer.SON and Its Alternatively Spliced Isoforms Control MLL Complex-Mediated H3K4me3 and Transcription of Leukemia-Associated Genes.Epigenetic balance of gene expression by Polycomb and COMPASS families.Deregulation of the HOXA9/MEIS1 axis in acute leukemia.Targeting the MLL complex in castration-resistant prostate cancer.Targeting human SET1/MLL family of proteins.DNMT3A in Leukemia.NUP98 Fusion Proteins Interact with the NSL and MLL1 Complexes to Drive Leukemogenesis.Recent progress in developing selective inhibitors of protein methyltransferases.PI3K/AKT Signaling Regulates H3K4 Methylation in Breast Cancer Development and Use of Assay Conditions Suited to Screening for and Profiling of SET-Domain-Targeted Inhibitors of the MLL/SET1 Family of Lysine Methyltransferases.Targeting Chromatin Regulators Inhibits Leukemogenic Gene Expression in NPM1 Mutant Leukemia.MLL-AF4 Spreading Identifies Binding Sites that Are Distinct from Super-Enhancers and that Govern Sensitivity to DOT1L Inhibition in Leukemia.Pharmacologic Targeting of Chromatin Modulators As Therapeutics of Acute Myeloid Leukemia Trithorax group genes in hematopoiesis.LEDGF/p75 is dispensable for hematopoiesis but essential for MLL-rearranged leukemogenesis.Targeting multiple nodes of MLL complexes to improve leukemia therapy.Design of the First-in-Class, Highly Potent Irreversible Inhibitor Targeting the Menin-MLL Protein-Protein Interaction.Pharmacologic Inhibition of the Menin-MLL Interaction Leads to Transcriptional Repression of PEG10 and Blocks Hepatocellular Carcinoma.MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia.Fate mapping of human glioblastoma reveals an invariant stem cell hierarchy.

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Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo.

http://www.wikidata.org/entity/Q35557914

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Gwenn Danet-Desnoyers

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Hongliang Zong

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Jay L Hess

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P2860

Structural insights into inhibition of the bivalent menin-MLL interaction by small molecules in leukemia.

Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

High-Affinity Small-Molecule Inhibitors of the Menin-Mixed Lineage Leukemia (MLL) Interaction Closely Mimic a Natural Protein–Protein Interaction

MLL translocations, histone modifications and leukaemia stem-cell development

RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia

Menin-MLL inhibitors reverse oncogenic activity of MLL fusion proteins in leukemia

Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias.

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

Mll rearrangements in haematological malignancies: lessons from clinical and biological studies.

A selective inhibitor of EZH2 blocks H3K27 methylation and kills mutant lymphoma cells.

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