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Jones, Martin R; Williamson, Laura M; Topham, James T; Lee, Michael K C; Goytain, Angela; Ho, Julie; Denroche, Robert E; Jang, GunHo; Pleasance, Erin; Shen, Yaoquing; Karasinska, Joanna M; McGhie, John P; Gill, Sharlene; Lim, Howard J; Moore, Malcolm J; Wong, Hui-Li; Ng, Tony; Yip, Stephen; Zhang, Wei; Sadeghi, Sara; Reisle, Carolyn; Mungall, Andrew J; Mungall, Karen L; Moore, Richard A; Ma, Yussanne; Knox, Jennifer J; Gallinger, Steven; Laskin, Janessa; Marra, Marco A; Schaeffer, David F; Jones, Steven J M; Renouf, Daniel J
Clinical cancer research, 2019-Aug-01, Volume: 25, Issue: 15Journal Article
Gene fusions involving neuregulin 1 ( ) have been noted in multiple cancer types and have potential therapeutic implications. Although varying results have been reported in other cancer types, the efficacy of the HER-family kinase inhibitor afatinib in the treatment of fusion-positive pancreatic ductal adenocarcinoma is not fully understood. Forty-seven patients with pancreatic ductal adenocarcinoma received comprehensive whole-genome and transcriptome sequencing and analysis. Two patients with gene fusions involving received afatinib treatment, with response measured by pretreatment and posttreatment PET/CT imaging. Three of 47 (6%) patients with advanced pancreatic ductal adenocarcinoma were identified as wild type by whole-genome sequencing. All wild-type tumors were positive for gene fusions involving the ERBB3 ligand . Two of 3 patients with fusion-positive tumors were treated with afatinib and demonstrated a significant and rapid response while on therapy. This work adds to a growing body of evidence that gene fusions are recurrent, therapeutically actionable genomic events in pancreatic cancers. Based on the clinical outcomes described here, patients with wild-type tumors harboring gene fusions may benefit from treatment with afatinib. .
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