Distinct pathways affected by menin versus MLL1/MLL2 in MLL-rearranged acute myeloid leukemia.
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M. Meyerson | J. Grembecka | A. Kranz | K. Anastassiadis | P. Ernst | Yufei Chen | A. Stewart | Kenneth L. Jones
[1] Liu Liu,et al. Design of the First-in-Class, Highly Potent Irreversible Inhibitor Targeting the Menin-MLL Protein-Protein Interaction. , 2018, Angewandte Chemie.
[2] Kenneth L. Jones,et al. MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia. , 2017, Cancer cell.
[3] M. Konopleva,et al. MLL-AF4 Spreading Identifies Binding Sites that Are Distinct from Super-Enhancers and that Govern Sensitivity to DOT1L Inhibition in Leukemia , 2017, Cell reports.
[4] F. Nigsch,et al. Complementary activities of DOT1L and Menin inhibitors in MLL-rearranged leukemia , 2017, Leukemia.
[5] R. Majeti,et al. ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. , 2016, Cancer discovery.
[6] Zhaohui S. Qin,et al. MLL1 and MLL1 fusion proteins have distinct functions in regulating leukemic transcription program , 2016, Cell Discovery.
[7] J. Downing,et al. Childhood Acute Lymphoblastic Leukemia: Progress Through Collaboration. , 2015, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[8] Bo Wen,et al. Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo. , 2015, Cancer cell.
[9] J. Hess,et al. The same site on the integrase-binding domain of lens epithelium-derived growth factor is a therapeutic target for MLL leukemia and HIV. , 2014, Blood.
[10] T. Kutateladze,et al. Diverse functions of PHD fingers of the MLL/KMT2 subfamily. , 2014, Biochimica et biophysica acta.
[11] A. H. Smits,et al. Quantitative Dissection and Stoichiometry Determination of the Human SET1/MLL Histone Methyltransferase Complexes , 2013, Molecular and Cellular Biology.
[12] Maksymilian Chruszcz,et al. Structural insights into inhibition of the bivalent menin-MLL interaction by small molecules in leukemia. , 2012, Blood.
[13] Jolanta Grembecka,et al. Menin-MLL inhibitors reverse oncogenic activity of MLL fusion proteins in leukemia. , 2012, Nature chemical biology.
[14] T. Graeber,et al. An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance. , 2011, Genes & development.
[15] Lars Bullinger,et al. MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L. , 2011, Cancer cell.
[16] C. Allis,et al. Multiple interactions recruit MLL1 and MLL1 fusion proteins to the HOXA9 locus in leukemogenesis. , 2010, Molecular cell.
[17] W. Alkema,et al. BioVenn – a web application for the comparison and visualization of biological lists using area-proportional Venn diagrams , 2008, BMC Genomics.
[18] Dinshaw J. Patel,et al. Multivalent engagement of chromatin modifications by linked binding modules , 2007, Nature Reviews Molecular Cell Biology.
[19] Jean-François Couture,et al. Molecular recognition of histone H3 by the WD40 protein WDR5 , 2006, Nature Structural &Molecular Biology.
[20] Matthew Meyerson,et al. The Menin Tumor Suppressor Protein Is an Essential Oncogenic Cofactor for MLL-Associated Leukemogenesis , 2005, Cell.
[21] G. Kay,et al. Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. , 2004, Molecular cell.
[22] Thomas A Milne,et al. MLL targets SET domain methyltransferase activity to Hox gene promoters. , 2002, Molecular cell.