Simultaneous kinase inhibition with ibrutinib and BCL2 inhibition with venetoclax offers a therapeutic strategy for acute myeloid leukemia
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B. Druker | M. Mori | A. Agarwal | C. Tognon | J. Tyner | B. Chang | S. Kurtz | A. Kaempf | C. Eide | A. Danilov | Nicola Long
[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.