Targeting nuclear β-catenin as therapy for post-myeloproliferative neoplasm secondary AML

[1]  K. Bhalla,et al.  Targeting cistrome and dysregulated transcriptome of post-MPN sAML , 2017, Oncotarget.

[2]  M. Minden,et al.  Impact of genomic alterations on outcomes in myelofibrosis patients undergoing JAK1/2 inhibitor therapy. , 2017, Blood advances.

[3]  You-yang Zhao,et al.  β-Catenin Is a Candidate Therapeutic Target for Myeloid Neoplasms with del(5q). , 2017, Cancer research.

[4]  M. Kahn,et al.  CBP/Catenin antagonists: Targeting LSCs' Achilles heel. , 2017, Experimental hematology.

[5]  S. Verstovsek,et al.  JAK2 inhibitors for myeloproliferative neoplasms: what is next? , 2017, Blood.

[6]  R. Nusse,et al.  Wnt/β-Catenin Signaling, Disease, and Emerging Therapeutic Modalities , 2017, Cell.

[7]  A. Cuddihy,et al.  β-Catenin Inhibitor BC2059 Is Efficacious as Monotherapy or in Combination with Proteasome Inhibitor Bortezomib in Multiple Myeloma , 2017, Molecular Cancer Therapeutics.

[8]  S. Armstrong,et al.  ENL links histone acetylation to oncogenic gene expression in AML , 2017, Nature.

[9]  R. Young,et al.  Transcriptional Addiction in Cancer , 2017, Cell.

[10]  W. Vainchenker,et al.  Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms. , 2017, Blood.

[11]  S. Constantinescu,et al.  Rethinking JAK2 inhibition: towards novel strategies of more specific and versatile janus kinase inhibition , 2017, Leukemia.

[12]  P. Qiu,et al.  Novel BET protein Proteolysis Targeting Chimera (BET-PROTAC) exerts superior lethal activity than Bromodomain Inhibitor (BETi) against post-myeloproliferative Neoplasm (MPN) Secondary (s) AML Cells , 2016, Leukemia.

[13]  Claude Preudhomme,et al.  A 17-gene stemness score for rapid determination of risk in acute leukaemia , 2016, Nature.

[14]  G. Nolan,et al.  Mass Cytometry Analysis Reveals Hyperactive NF Kappa B Signaling in Myelofibrosis and Secondary Acute Myeloid Leukemia , 2016, Leukemia.

[15]  P. Qiu,et al.  BET protein bromodomain inhibitor-based combinations are highly active against post-myeloproliferative neoplasm secondary AML cells , 2016, Leukemia.

[16]  M. Alcalay,et al.  Nucleophosmin leukemogenic mutant activates Wnt signaling during zebrafish development , 2016, Oncotarget.

[17]  C. Crews,et al.  Small-Molecule PROTACS: New Approaches to Protein Degradation. , 2016, Angewandte Chemie.

[18]  Mark A. Dawson,et al.  BET inhibitor resistance emerges from leukaemia stem cells , 2015, Nature.

[19]  Łukasz M. Boryń,et al.  Transcriptional plasticity promotes primary and acquired resistance to BET inhibition , 2015, Nature.

[20]  Francisco Cervantes,et al.  A pooled analysis of overall survival in COMFORT-I and COMFORT-II, 2 randomized phase III trials of ruxolitinib for the treatment of myelofibrosis , 2015, Haematologica.

[21]  A. Look,et al.  HSP90 inhibition leads to degradation of the TYK2 kinase and apoptotic cell death in T-cell acute lymphoblastic leukemia , 2015, Leukemia.

[22]  K. Bhalla,et al.  Design, Synthesis, and Biological Evaluation of a Series of Anthracene-9,10-dione Dioxime β-Catenin Pathway Inhibitors. , 2015, Journal of medicinal chemistry.

[23]  W. Sellers,et al.  CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms. , 2015, Cancer cell.

[24]  Jian Yi Li,et al.  TBL1XR1 in physiological and pathological states. , 2015, American journal of clinical and experimental urology.

[25]  Jonathan J. Chen,et al.  JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response. , 2015, Cancer discovery.

[26]  S. Armstrong,et al.  Genomic and functional analysis of leukemic transformation of myeloproliferative neoplasms , 2014, Proceedings of the National Academy of Sciences.

[27]  Jianlong Wang,et al.  GPR84 sustains aberrant β-catenin signaling in leukemic stem cells for maintenance of MLL leukemogenesis. , 2014, Blood.

[28]  K. Bhalla,et al.  Pre-clinical efficacy of combined therapy with novel β-catenin antagonist BC2059 and histone deacetylase inhibitor against AML cells , 2014, Leukemia.

[29]  Michael Kahn,et al.  Can we safely target the WNT pathway? , 2014, Nature Reviews Drug Discovery.

[30]  Junwei Shi,et al.  The mechanisms behind the therapeutic activity of BET bromodomain inhibition. , 2014, Molecular cell.

[31]  T. Golub,et al.  Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis. , 2014, Blood.

[32]  J. Qi,et al.  Improved targeting of JAK2 leads to increased therapeutic efficacy in myeloproliferative neoplasms. , 2014, Blood.

[33]  J. Mascarenhas,et al.  Pathogenesis and management of acute myeloid leukemia that has evolved from a myeloproliferative neoplasm , 2014, Current opinion in hematology.

[34]  R. Levine,et al.  Molecular Pathways Molecular Pathways : Molecular Basis for Sensitivity and Resistance to JAK Kinase Inhibitors , 2014 .

[35]  Lincoln D. Stein,et al.  Identification of pre-leukemic hematopoietic stem cells in acute leukemia , 2014, Nature.

[36]  R. Rabadán,et al.  Leukemogenesis Induced by an Activating β-catenin mutation in Osteoblasts , 2014, Nature.

[37]  K. Bhalla,et al.  Dual PI3K/AKT/mTOR Inhibitor BEZ235 Synergistically Enhances the Activity of JAK2 Inhibitor against Cultured and Primary Human Myeloproliferative Neoplasm Cells , 2013, Molecular Cancer Therapeutics.

[38]  Hans Clevers,et al.  Wnt/β-Catenin Signaling and Disease , 2012, Cell.

[39]  G. Mufti,et al.  Fluorescence‐based experimental model to evaluate the concomitant effect of drugs on the tumour microenvironment and cancer cells , 2012, British journal of haematology.

[40]  M. Gönen,et al.  Genetic analysis of patients with leukemic transformation of myeloproliferative neoplasms shows recurrent SRSF2 mutations that are associated with adverse outcome. , 2012, Blood.

[41]  T. Naoe,et al.  Y654 of β‐catenin is essential for FLT3/ITD‐related tyrosine phosphorylation and nuclear localization of β‐catenin , 2012, European journal of haematology.

[42]  R. Mesa,et al.  Transformation of a Chronic Myeloproliferative Neoplasm to Acute Myelogenous Leukemia: Does Anything Work? , 2012, Current Hematologic Malignancy Reports.

[43]  B. Bernstein,et al.  Heterodimeric JAK-STAT Activation as a Mechanism of Persistence to JAK2 Inhibitor Therapy , 2011, Nature.

[44]  K. Bhalla,et al.  Heat Shock Protein 90 Inhibitor Is Synergistic with JAK2 Inhibitor and Overcomes Resistance to JAK2-TKI in Human Myeloproliferative Neoplasm Cells , 2011, Clinical Cancer Research.

[45]  J. Schwabe,et al.  Structural basis for the assembly of the SMRT/NCoR core transcriptional repression machinery , 2011, Nature Structural &Molecular Biology.

[46]  C. So,et al.  β-Catenin mediates the establishment and drug resistance of MLL leukemic stem cells. , 2010, Cancer cell.

[47]  C. Lieu,et al.  Blockade of JAK2 activity suppressed accumulation of β‐catenin in leukemic cells , 2010, Journal of cellular biochemistry.

[48]  Wolfram Goessling,et al.  The Wnt/β-Catenin Pathway Is Required for the Development of Leukemia Stem Cells in AML , 2010, Science.

[49]  W. Weis,et al.  Agonist-selective Dynamic Compartmentalization of Human Mu Opioid Receptor as Revealed by Resolutive FRAP Analysis* , 2009, The Journal of Biological Chemistry.

[50]  K. Basler,et al.  β-Catenin hits chromatin: regulation of Wnt target gene activation , 2009, Nature Reviews Molecular Cell Biology.

[51]  Christian Buske,et al.  A novel role for Lef-1, a central transcription mediator of Wnt signaling, in leukemogenesis , 2008, The Journal of experimental medicine.

[52]  Cun-Yu Wang,et al.  TBL1–TBLR1 and β-catenin recruit each other to Wnt target-gene promoter for transcription activation and oncogenesis , 2008, Nature Cell Biology.

[53]  T. Naoe,et al.  FLT3 regulates β-catenin tyrosine phosphorylation, nuclear localization, and transcriptional activity in acute myeloid leukemia cells , 2007, Leukemia.

[54]  M. Duñach,et al.  Bcr‐Abl stabilizes β‐catenin in chronic myeloid leukemia through its tyrosine phosphorylation , 2007, The EMBO journal.

[55]  Andrew J. Bannister,et al.  BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms , 2014, Leukemia.