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Cell Press, Cancer Cell, 4(27), p. 516-532, 2015

DOI: 10.1016/j.ccell.2015.03.006

Cell Press, Cancer Cell, 5(27), p. 744, 2015

DOI: 10.1016/j.ccell.2015.04.014

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Convergent Mutations and Kinase Fusions Lead to Oncogenic STAT3 Activation in Anaplastic Large Cell Lymphoma

Journal article published in 2015 by Chan Wc, Ramona Crescenzo, Francesco Abate, Elena Lasorsa, Fabrizio Tabbo’, Marcello Gaudiano, Fabrizio Tabbo, Nicoletta Chiesa, Tabbo' F., Filomena Di Giacomo, Elisa Spaccarotella, Luigi Barbarossa, Elisabetta Ercole, Maria Todaro, Michela Boi and other authors.
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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 155 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.