Convergent mutations and kinase fusions lead to oncogenic STAT3 activation in anaplastic large cell lymphoma.

[1]  S. Swerdlow WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues , 2017 .

[2]  S. Pileri,et al.  A novel patient-derived tumorgraft model with TRAF1-ALK anaplastic large-cell lymphoma translocation , 2014, Leukemia.

[3]  K. Elenitoba-Johnson,et al.  A novel recurrent NPM1-TYK2 gene fusion in cutaneous CD30-positive lymphoproliferative disorders. , 2014, Blood.

[4]  Chris Wiggins,et al.  Pegasus: a comprehensive annotation and prediction tool for detection of driver gene fusions in cancer , 2014, BMC Systems Biology.

[5]  W. Wilson,et al.  ALK-negative anaplastic large cell lymphoma is a genetically heterogeneous disease with widely disparate clinical outcomes. , 2014, Blood.

[6]  K. Elenitoba-Johnson,et al.  Integrated genomic sequencing reveals mutational landscape of T-cell prolymphocytic leukemia. , 2014, Blood.

[7]  Adam R. Johnson,et al.  Structure of the pseudokinase–kinase domains from protein kinase TYK2 reveals a mechanism for Janus kinase (JAK) autoinhibition , 2014, Proceedings of the National Academy of Sciences.

[8]  M. Stern,et al.  Recurrent JAK1 and JAK3 somatic mutations in T-cell prolymphocytic leukemia , 2014, Leukemia.

[9]  G. Getz,et al.  Comprehensive genomic analysis of rhabdomyosarcoma reveals a landscape of alterations affecting a common genetic axis in fusion-positive and fusion-negative tumors. , 2014, Cancer discovery.

[10]  I. Lossos,et al.  Recurrent mutations in epigenetic regulators, RHOA and FYN kinase in peripheral T cell lymphomas , 2014, Nature Genetics.

[11]  N. Harris,et al.  A targeted mutational landscape of angioimmunoblastic T-cell lymphoma. , 2012, Blood.

[12]  J. Merker,et al.  STAT3 mutations are frequent in CD30+ T-cell lymphomas and T-cell large granular lymphocytic leukemia , 2013, Leukemia.

[13]  Jeffrey A. Engelman,et al.  Tyrosine kinase gene rearrangements in epithelial malignancies , 2013, Nature Reviews Cancer.

[14]  Raul Rabadan,et al.  SAVI: a statistical algorithm for variant frequency identification , 2013, BMC Systems Biology.

[15]  A. Rosenwald,et al.  PRDM1/BLIMP1 is commonly inactivated in anaplastic large T-cell lymphoma. , 2013, Blood.

[16]  S. Mustjoki,et al.  STAT3 mutations indicate the presence of subclinical T-cell clones in a subset of aplastic anemia and myelodysplastic syndrome patients. , 2013, Blood.

[17]  W. Curran,et al.  Inhibition of STAT3 by Niclosamide Synergizes with Erlotinib against Head and Neck Cancer , 2013, PloS one.

[18]  Angela G. Fleischman,et al.  TYK2-STAT1-BCL2 pathway dependence in T-cell acute lymphoblastic leukemia. , 2013, Cancer discovery.

[19]  G. Inghirami,et al.  The EGFR family members sustain the neoplastic phenotype of ALK+ lung adenocarcinoma via EGR1 , 2013, Oncogenesis.

[20]  A. Quintás-Cardama,et al.  Molecular Pathways: JAK/STAT Pathway: Mutations, Inhibitors, and Resistance , 2013, Clinical Cancer Research.

[21]  B. Firwana,et al.  Comprehensive review of JAK inhibitors in myeloproliferative neoplasms , 2013, Therapeutic advances in hematology.

[22]  Raul Rabadan,et al.  MutComFocal: an integrative approach to identifying recurrent and focal genomic alterations in tumor samples , 2013, BMC Systems Biology.

[23]  S. Mustjoki,et al.  Somatic STAT3 mutations in large granular lymphocytic leukemia. , 2012, The New England journal of medicine.

[24]  Michael L. Wang,et al.  Role of the microenvironment in mantle cell lymphoma: IL-6 is an important survival factor for the tumor cells. , 2010, Blood.

[25]  S. Salzberg,et al.  TopHat-Fusion: an algorithm for discovery of novel fusion transcripts , 2011, Genome Biology.

[26]  J. Zucman‐Rossi,et al.  Somatic mutations activating STAT3 in human inflammatory hepatocellular adenomas , 2011, The Journal of experimental medicine.

[27]  Joseph M. Connors,et al.  Oncogenically active MYD88 mutations in human lymphoma , 2011, Nature.

[28]  J. Grandis,et al.  STAT3 signaling: anticancer strategies and challenges. , 2011, Molecular interventions.

[29]  James R Kiefer,et al.  Structural and thermodynamic characterization of the TYK2 and JAK3 kinase domains in complex with CP-690550 and CMP-6. , 2010, Journal of molecular biology.

[30]  Enzo Medico,et al.  Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[31]  S. Imbeaud,et al.  Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours , 2009, Nature.

[32]  M. Djokic ALK− anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project , 2009 .

[33]  D. Weisenburger,et al.  International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[34]  Tsonwin Hai,et al.  A potential dichotomous role of ATF3, an adaptive-response gene, in cancer development , 2007, Oncogene.

[35]  Kenneth C Anderson,et al.  Targeted therapy of multiple myeloma based upon tumor-microenvironmental interactions. , 2007, Experimental hematology.

[36]  Lauren B. Smith,et al.  Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature , 2007, Annals of Hematology.

[37]  Roberto Piva,et al.  Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes. , 2006, The Journal of clinical investigation.

[38]  D. Levy,et al.  Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target , 2005, Nature Medicine.

[39]  M. Privalsky,et al.  The role of corepressors in transcriptional regulation by nuclear hormone receptors. , 2004, Annual review of physiology.

[40]  R. Chaganti,et al.  B cell lymphoma-associated chromosomal translocation involves candidate oncogene lyt-10, homologous to NF-κB p50 , 1991, Cell.

[41]  R. Chaganti,et al.  B cell lymphoma-associated chromosomal translocation involves candidate oncogene lyt-10, homologous to NF-kappa B p50. , 1991, Cell.