Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Crescenzo, R; Abate, F; Lasorsa, E; Tabbo', F; Gaudiano, M; Chiesa, N; Di Giacomo, F; Spaccarotella, E; Barbarossa, L; Ercole, E; Todaro, M; Boi, M; Acquaviva, A; Ficarra, E; Novero, D; Rinaldi, A; Tousseyn, T; Rosenwald, A; Kenner, L; Cerroni, L; Tzankov, A; Ponzoni, M; Paulli, M; Weisenburger, D; Chan, WC; Iqbal, J; Piris, MA; Zamo', A; Ciardullo, C; Rossi, D; Gaidano, G; Pileri, S; Tiacci, E; Falini, B; Shultz, LD; Mevellec, L; Vialard, JE; Piva, R; Bertoni, F; Rabadan, R; Inghirami, G; European T-Cell Lymphoma Study Group, T-Cell Project: Prospective Collection of Data in Patients with Peripheral T-Cell Lymphoma and the AIRC 5xMille Consortium “Genetics-Driven Targeted Management of Lymphoid Malignancies”.
Convergent mutations and kinase fusions lead to oncogenic STAT3 activation in anaplastic large cell lymphoma.
Cancer Cell. 2015; 27(4):516-532
Doi: 10.1016/j.ccell.2015.03.006
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- Co-Autor*innen der Med Uni Graz
- Cerroni Lorenzo
- Kenner Lukas
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- Abstract:
- A systematic characterization of the genetic alterations driving ALCLs has not been performed. By integrating massive sequencing strategies, we provide a comprehensive characterization of driver genetic alterations (somatic point mutations, copy number alterations, and gene fusions) in ALK(-) ALCLs. We identified activating mutations of JAK1 and/or STAT3 genes in ∼20% of 88 [corrected] ALK(-) ALCLs and demonstrated that 38% of systemic ALK(-) ALCLs displayed double lesions. Recurrent chimeras combining a transcription factor (NFkB2 or NCOR2) with a tyrosine kinase (ROS1 or TYK2) were also discovered in WT JAK1/STAT3 ALK(-) ALCL. All these aberrations lead to the constitutive activation of the JAK/STAT3 pathway, which was proved oncogenic. Consistently, JAK/STAT3 pathway inhibition impaired cell growth in vitro and in vivo. Copyright © 2015 Elsevier Inc. All rights reserved.
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