Clonal heterogeneity of acute myeloid leukemia treated with the IDH2 inhibitor enasidenib
暂无分享,去创建一个
P. Vyas | K. Yen | R. Levine | V. Penard-Lacronique | G. Vassiliou | M. Vijayabaskar | A. Shih | M. David | S. de Botton | S. Alsafadi | L. Quek | S. Agresta | C. Quivoron | B. Stoilova | V. Saada | C. Willekens | E. Stein | K. Macbeth | A. Thakurta | M. Heiblig | A. Peniket | M. Amatangelo | M. Metzner | A. Kennedy | O. A. Bernard
[1] S. Fröhling,et al. BCAT1 restricts αKG levels in AML stem cells leading to IDHmut-like DNA hypermethylation , 2017, Nature.
[2] F. Hamey,et al. Heterogeneity of human lympho-myeloid progenitors at the single cell level , 2018 .
[3] P. Vyas,et al. Enasidenib induces acute myeloid leukemia cell differentiation to promote clinical response. , 2017, Blood.
[4] P. Vyas,et al. Outcome of Azacitidine Therapy in Acute Myeloid Leukemia Is not Improved by Concurrent Vorinostat Therapy but Is Predicted by a Diagnostic Molecular Signature , 2017, Clinical Cancer Research.
[5] M. Teleanu. RUNX1 mutations in acute myeloid leukemia , 2017 .
[6] K. Nakano,et al. The crystal structure of human DEAH-box RNA helicase 15 reveals a domain organization of the mammalian DEAH/RHA family. , 2017, Acta crystallographica. Section F, Structural biology communications.
[7] I. Flinn,et al. Enasidenib in mutant IDH2 relapsed or refractory acute myeloid leukemia. , 2017, Blood.
[8] Sydney M. Shaffer,et al. Rare cell variability and drug-induced reprogramming as a mode of cancer drug resistance , 2017, Nature.
[9] Hua Yang,et al. AG-221, a First-in-Class Therapy Targeting Acute Myeloid Leukemia Harboring Oncogenic IDH2 Mutations. , 2017, Cancer discovery.
[10] Francine E. Garrett-Bakelman,et al. Combination Targeted Therapy to Disrupt Aberrant Oncogenic Signaling and Reverse Epigenetic Dysfunction in IDH2- and TET2-Mutant Acute Myeloid Leukemia. , 2017, Cancer discovery.
[11] Nicolai J. Birkbak,et al. Tracking the Evolution of Non‐Small‐Cell Lung Cancer , 2017, The New England journal of medicine.
[12] Ashwini Naik,et al. Phylogenetic ctDNA analysis depicts early stage lung cancer evolution , 2017, Nature.
[13] R. Lührmann,et al. Structural insights into the mechanism of the DEAH-box RNA helicase Prp43 , 2017, eLife.
[14] Heather L. Mulder,et al. The genomic landscape of core-binding factor acute myeloid leukemias , 2016, Nature Genetics.
[15] P. Vyas,et al. Genetically distinct leukemic stem cells in human CD34− acute myeloid leukemia are arrested at a hemopoietic precursor-like stage , 2016, The Journal of experimental medicine.
[16] Alex M. Fichtenholtz,et al. Integrated genomic DNA/RNA profiling of hematologic malignancies in the clinical setting. , 2016, Blood.
[17] Francine E. Garrett-Bakelman,et al. Distinct evolution and dynamics of epigenetic and genetic heterogeneity in acute myeloid leukemia , 2016, Nature Medicine.
[18] Nicola D. Roberts,et al. Genomic Classification and Prognosis in Acute Myeloid Leukemia. , 2016, The New England journal of medicine.
[19] D. Muzny,et al. Genomic Profiling of Pediatric Acute Myeloid Leukemia Reveals a Changing Mutational Landscape from Disease Diagnosis to Relapse. , 2016, Cancer research.
[20] Zev N. Kronenberg,et al. Age-related mutations and chronic myelomonocytic leukemia , 2016, Leukemia.
[21] Gary D. Bader,et al. Divergent clonal selection dominates medulloblastoma at recurrence , 2016, Nature.
[22] R. Levine,et al. Clonal evolution of preleukemic hematopoietic stem cells in acute myeloid leukemia. , 2015, Experimental hematology.
[23] Łukasz M. Boryń,et al. Transcriptional plasticity promotes primary and acquired resistance to BET inhibition , 2015, Nature.
[24] J. Byrd,et al. Resistance mechanisms for the Bruton's tyrosine kinase inhibitor ibrutinib. , 2014, The New England journal of medicine.
[25] P. Pandolfi,et al. Proto-oncogenic role of mutant IDH2 in leukemia initiation and maintenance. , 2014, Cell stem cell.
[26] Lincoln D. Stein,et al. Identification of pre-leukemic hematopoietic stem cells in acute leukemia , 2014, Nature.
[27] I. Weissman,et al. Preleukemic mutations in human acute myeloid leukemia affect epigenetic regulators and persist in remission , 2014, Proceedings of the National Academy of Sciences.
[28] P. Campbell,et al. Single-cell mutational profiling and clonal phylogeny in cancer , 2013, Genome research.
[29] Benjamin J. Raphael,et al. Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia. , 2013, The New England journal of medicine.
[30] Gustavo F. Bayón,et al. DNA methylation signatures identify biologically distinct thyroid cancer subtypes. , 2013, The Journal of clinical endocrinology and metabolism.
[31] Angela G. Fleischman,et al. Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML. , 2013, The New England journal of medicine.
[32] Fang Wang,et al. Targeted Inhibition of Mutant IDH2 in Leukemia Cells Induces Cellular Differentiation , 2013, Science.
[33] Benjamin L. Ebert,et al. (R)-2-Hydroxyglutarate Is Sufficient to Promote Leukemogenesis and Its Effects Are Reversible , 2013, Science.
[34] H. Urlaub,et al. Dissection of the factor requirements for spliceosome disassembly and the elucidation of its dissociation products using a purified splicing system. , 2013, Genes & development.
[35] A. Kohlmann,et al. GATA2 mutations are frequent in intermediate-risk karyotype AML with biallelic CEBPA mutations and are associated with favorable prognosis , 2013, Leukemia.
[36] A. McKenna,et al. Evolution and Impact of Subclonal Mutations in Chronic Lymphocytic Leukemia , 2012, Cell.
[37] Alfonso Valencia,et al. Epigenomic analysis detects widespread gene-body DNA hypomethylation in chronic lymphocytic leukemia , 2012, Nature Genetics.
[38] I. Weissman,et al. Clonal Evolution of Preleukemic Hematopoietic Stem Cells Precedes Human Acute Myeloid Leukemia , 2012, Science Translational Medicine.
[39] S. Berger,et al. IDH mutation impairs histone demethylation and results in a block to cell differentiation , 2012, Nature.
[40] K. Kinzler,et al. Somatic mutations in the transcriptional corepressor gene BCORL1 in adult acute myelogenous leukemia. , 2011, Blood.
[41] R. Hills,et al. The prognostic significance of IDH2 mutations in AML depends on the location of the mutation. , 2011, Blood.
[42] Martin Goodson,et al. Stampy: a statistical algorithm for sensitive and fast mapping of Illumina sequence reads. , 2011, Genome research.
[43] Verena I Gaidzik,et al. RUNX1 mutations in acute myeloid leukemia: results from a comprehensive genetic and clinical analysis from the AML study group. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[44] P. Vyas,et al. Coexistence of LMPP-like and GMP-like leukemia stem cells in acute myeloid leukemia. , 2011, Cancer cell.
[45] Bin Wang,et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of α-ketoglutarate-dependent dioxygenases. , 2011, Cancer cell.
[46] J. Licht,et al. Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation. , 2010, Cancer cell.
[47] E. Wang,et al. Analysis and design of RNA sequencing experiments for identifying isoform regulation , 2010, Nature Methods.
[48] Young Lim Choi,et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. , 2010, The New England journal of medicine.
[49] Manuela Zucknick,et al. IDH1 and IDH2 mutations are frequent genetic alterations in acute myeloid leukemia and confer adverse prognosis in cytogenetically normal acute myeloid leukemia with NPM1 mutation without FLT3 internal tandem duplication. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[50] R. Hills,et al. Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials. , 2010, Blood.
[51] Ben S. Wittner,et al. A Chromatin-Mediated Reversible Drug-Tolerant State in Cancer Cell Subpopulations , 2010, Cell.
[52] Fabien Campagne,et al. DNA methylation signatures identify biologically distinct subtypes in acute myeloid leukemia. , 2010, Cancer cell.
[53] N. Tanner,et al. The DEAD-box protein family of RNA helicases. , 2006, Gene.
[54] M. Meyerson,et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. , 2005, The New England journal of medicine.
[55] Doriano Fabbro,et al. Prediction of Resistance to Small Molecule FLT3 Inhibitors , 2004, Cancer Research.
[56] J. Kuriyan,et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. , 2002, Cancer cell.
[57] J. Abelson,et al. Prp43: An RNA helicase-like factor involved in spliceosome disassembly. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[58] F. Hamey,et al. Heterogeneity of human lympho-myeloid progenitors at the single cell level , 2017, Nature Immunology.
[59] Thomas R. Gingeras,et al. STAR: ultrafast universal RNA-seq aligner , 2013, Bioinform..
[60] R. Hills,et al. Refinement of cytogenetic classification in acute myeloid leukaemia: Determination of prognostic significance of rarer recurring chromosomal abnormalities amongst 5,876 younger adult patients treated in the UK Medical Research Council trials , 2010 .
[61] R. Stone,et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. , 2006, Blood.
[62] John M. Walker,et al. Myeloid Leukemia , 2020, Methods In Molecular Medicine™.
[63] N. Hanna. EGFR Mutation and Resistance of Non-Small-Cell Lung Cancer to GefitinibKobayashi S, Boggon TJ, Dayaram T, et al (Harvard Med School, Boston; Univ Hosps of Cleveland, Ohio) N Engl J Med 352:786-792, 2005§ , 2006 .
[64] H. Kantarjian,et al. Acute myeloid leukemia , 2018, Methods in Molecular Biology.
[65] R. Fink,et al. [Blast crisis in chronic myeloid leukemia]. , 1983, Folia haematologica.