Distinct pathways affected by menin versus MLL1/MLL2 in MLL-rearranged acute myeloid leukemia.

[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.