Simultaneous kinase inhibition with ibrutinib and BCL2 inhibition with venetoclax offers a therapeutic strategy for acute myeloid leukemia

[1]  G. Boucher,et al.  Genetic characterization of ABT-199 sensitivity in human AML , 2018, Leukemia.

[2]  A. Letai,et al.  Venetoclax combined with decitabine or azacitidine in treatment-naive, elderly patients with acute myeloid leukemia. , 2019, Blood.

[3]  D. Bottomly,et al.  Biomarkers Predicting Venetoclax Sensitivity and Strategies for Venetoclax Combination Treatment , 2018, Blood.

[4]  J. Gribben,et al.  Ibrutinib Plus Venetoclax in Relapsed/Refractory CLL: Results of the Bloodwise TAP Clarity Study , 2018, Blood.

[5]  M. Konopleva,et al.  Combined Ibrutinib and Venetoclax in Patients with Treatment-Naïve High-Risk Chronic Lymphocytic Leukemia (CLL) , 2018, Blood.

[6]  Austin E. Gillen,et al.  Venetoclax with azacitidine disrupts energy metabolism and targets leukemia stem cells in patients with acute myeloid leukemia , 2018, Nature Medicine.

[7]  Jeffrey A Jones,et al.  Phase 1b study of obinutuzumab, ibrutinib, and venetoclax in relapsed and refractory chronic lymphocytic leukemia. , 2018, Blood.

[8]  Beth Wilmot,et al.  Functional Genomic Landscape of Acute Myeloid Leukemia , 2018, Nature.

[9]  S. Lade,et al.  Ibrutinib plus Venetoclax for the Treatment of Mantle‐Cell Lymphoma , 2018, The New England journal of medicine.

[10]  A. Kentsis,et al.  Acute myeloid/T‐lymphoblastic leukaemia (AMTL): a distinct category of acute leukaemias with common pathogenesis in need of improved therapy , 2018, British journal of haematology.

[11]  Henning Hermjakob,et al.  The Reactome pathway knowledgebase , 2013, Nucleic Acids Res..

[12]  Krister Wennerberg,et al.  Methods for High-Throughput Drug Combination Screening and Synergy Scoring , 2016, bioRxiv.

[13]  E. Petricoin,et al.  Microenvironmental agonists generate de novo phenotypic resistance to combined ibrutinib plus venetoclax in CLL and MCL. , 2017, Blood advances.

[14]  S. Lonial,et al.  Bone marrow microenvironment-derived signals induce Mcl-1 dependence in multiple myeloma. , 2017, Blood.

[15]  A. Letai,et al.  Bruton’s tyrosine kinase inhibition increases BCL-2 dependence and enhances sensitivity to venetoclax in chronic lymphocytic leukemia , 2017, Leukemia.

[16]  A. Letai,et al.  Efficacy and Biological Correlates of Response in a Phase II Study of Venetoclax Monotherapy in Patients with Acute Myelogenous Leukemia. , 2016, Cancer discovery.

[17]  T. Kipps,et al.  Targeting BCL2 with Venetoclax in Relapsed Chronic Lymphocytic Leukemia. , 2016, The New England journal of medicine.

[18]  Henning Hermjakob,et al.  The Reactome pathway Knowledgebase , 2015, Nucleic acids research.

[19]  David E. Fisher,et al.  Precision medicine for cancer with next-generation functional diagnostics , 2015, Nature Reviews Cancer.

[20]  E. Budinská,et al.  ToPASeq: an R package for topology-based pathway analysis of microarray and RNA-Seq data , 2015, BMC Bioinformatics.

[21]  Krister Wennerberg,et al.  Corrigendum to “Searching for drug synergy in complex dose–response landscapes using an interaction potency model” [Comput. Struct. Biotechnol. J. 13 (2015) 504–513] , 2017, Computational and structural biotechnology journal.

[22]  E. Kimby,et al.  Targets for Ibrutinib Beyond B Cell Malignancies , 2015, Scandinavian journal of immunology.

[23]  M. Keating,et al.  Pharmacological and Protein Profiling Suggests Venetoclax (ABT-199) as Optimal Partner with Ibrutinib in Chronic Lymphocytic Leukemia , 2015, Clinical Cancer Research.

[24]  C. Reyes,et al.  Big data analysis of treatment patterns and outcomes among elderly acute myeloid leukemia patients in the United States , 2015, Annals of Hematology.

[25]  H. Urlaub,et al.  FLT3-ITD and TLR9 use Bruton tyrosine kinase to activate distinct transcriptional programs mediating AML cell survival and proliferation. , 2015, Blood.

[26]  S. Maïga,et al.  Biological rational for sequential targeting of Bruton tyrosine kinase and Bcl-2 to overcome CD40-induced ABT-199 resistance in mantle cell lymphoma , 2015, Oncotarget.

[27]  E. Hsi,et al.  Combination of ibrutinib with ABT‐199: synergistic effects on proliferation inhibition and apoptosis in mantle cell lymphoma cells through perturbation of BTK, AKT and BCL2 pathways , 2015, British journal of haematology.

[28]  L. Leclercq,et al.  Absorption, Metabolism, and Excretion of Oral 14C Radiolabeled Ibrutinib: An Open-Label, Phase I, Single-Dose Study in Healthy Men , 2015, Drug Metabolism and Disposition.

[29]  Daniel J Weisdorf,et al.  Acute Myeloid Leukemia. , 2015, The New England journal of medicine.

[30]  W. Huber,et al.  Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 , 2014, Genome Biology.

[31]  D. MacEwan,et al.  Identification of Bruton's tyrosine kinase as a therapeutic target in acute myeloid leukemia. , 2014, Blood.

[32]  M. Wang,et al.  Combinatorial drug screening identifies synergistic co-targeting of Bruton's tyrosine kinase and the proteasome in mantle cell lymphoma , 2013, Leukemia.

[33]  F. Lo‐Coco,et al.  Treatment of acute promyelocytic leukemia. , 2013, The New England journal of medicine.

[34]  Paola Fazi,et al.  Retinoic acid and arsenic trioxide for acute promyelocytic leukemia. , 2013, The New England journal of medicine.

[35]  Juthamas Sukbuntherng,et al.  Targeting BTK with ibrutinib in relapsed chronic lymphocytic leukemia. , 2013, The New England journal of medicine.

[36]  Armand Bankhead,et al.  Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening. , 2013, Cancer research.

[37]  Sabah Jassim,et al.  A Topology-Based Score for Pathway Enrichment , 2012, J. Comput. Biol..

[38]  K. Hansen,et al.  Removing technical variability in RNA-seq data using conditional quantile normalization , 2012, Biostatistics.

[39]  M. Vogler,et al.  BCL2A1: the underdog in the BCL2 family , 2011, Cell Death and Differentiation.

[40]  Gabriele Sales,et al.  graphite - a Bioconductor package to convert pathway topology to gene network , 2012, BMC Bioinformatics.

[41]  Douglas H. Thamm,et al.  The Bruton tyrosine kinase inhibitor PCI-32765 blocks B-cell activation and is efficacious in models of autoimmune disease and B-cell malignancy , 2010, Proceedings of the National Academy of Sciences.

[42]  Derek W. Yecies,et al.  Acquired resistance to ABT-737 in lymphoma cells that up-regulate MCL-1 and BFL-1. , 2010, Blood.

[43]  M. Butterworth,et al.  Concurrent up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia. , 2009, Blood.

[44]  Lincoln Stein,et al.  Reactome knowledgebase of human biological pathways and processes , 2008, Nucleic Acids Res..

[45]  John D. Storey,et al.  Capturing Heterogeneity in Gene Expression Studies by Surrogate Variable Analysis , 2007, PLoS genetics.

[46]  L. Honigberg,et al.  Discovery of Selective Irreversible Inhibitors for Bruton’s Tyrosine Kinase , 2007, ChemMedChem.

[47]  N. Suzuki,et al.  Skewed Th1 responses caused by excessive expression of Txk, a member of the Tec family of tyrosine kinases, in patients with Behcet's disease. , 2006, Clinical medicine & research.

[48]  H. Kantarjian,et al.  Acute myeloid leukemia , 2018, Methods in Molecular Biology.

[49]  R. Bataille,et al.  Mcl‐1 and Bcl‐xL are co‐regulated by IL‐6 in human myeloma cells , 1999, British journal of haematology.

[50]  Y. Benjamini,et al.  Controlling the false discovery rate: a practical and powerful approach to multiple testing , 1995 .

[51]  A. Buja,et al.  Remarks on Parallel Analysis. , 1992, Multivariate behavioral research.

[52]  Y. Hochberg A sharper Bonferroni procedure for multiple tests of significance , 1988 .

[53]  B. Altshuler Modeling of dose-response relationships. , 1981, Environmental health perspectives.