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Significance Lung cancers are frequently driven by well-characterized mutations in proto-oncogenes, includingERBB2 . Evidence from other cancers demonstrates thatERBB2 is also activated by alternative splicing that causes skipping of exon 16. Here, we find evidence for increasedERBB2 alternative splicing in a subset of lung cancers and a range of other solid tumors, including deletions and previously undescribed mutations promoting exon 16 skipping. We show that the ERBB2 isoform lacking exon 16 transforms lung epithelial cells in vitro and in vivo, arguing that alternative splicing of ERBB2 is a mechanism promoting lung carcinogenesis. These findings extend our knowledge of lung cancer biology and may lead to improved patient stratification to facilitate future use of ERBB2-targeted therapies.

An ErbB2 splice variant lacking exon 16 drives lung carcinoma