1. KIF5B-RET fusions in lung adenocarcinoma.
- Author
-
Kohno T, Ichikawa H, Totoki Y, Yasuda K, Hiramoto M, Nammo T, Sakamoto H, Tsuta K, Furuta K, Shimada Y, Iwakawa R, Ogiwara H, Oike T, Enari M, Schetter AJ, Okayama H, Haugen A, Skaug V, Chiku S, Yamanaka I, Arai Y, Watanabe S, Sekine I, Ogawa S, Harris CC, Tsuda H, Yoshida T, Yokota J, and Shibata T
- Subjects
- Adenocarcinoma pathology, Adenocarcinoma of Lung, Anaplastic Lymphoma Kinase, Animals, Cell Transformation, Neoplastic drug effects, ErbB Receptors genetics, Gene Expression Regulation, Neoplastic, High-Throughput Nucleotide Sequencing, Humans, Japan, Lung Neoplasms pathology, Mice, NIH 3T3 Cells, Norway, Piperidines pharmacology, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins c-ret antagonists & inhibitors, Proto-Oncogene Proteins p21(ras), Quinazolines pharmacology, Receptor Protein-Tyrosine Kinases genetics, Receptor, ErbB-2 genetics, United States, ras Proteins genetics, Adenocarcinoma genetics, Kinesins genetics, Lung Neoplasms genetics, Oncogene Proteins, Fusion genetics, Proto-Oncogene Proteins c-ret genetics
- Abstract
We identified in-frame fusion transcripts of KIF5B (the kinesin family 5B gene) and the RET oncogene, which are present in 1-2% of lung adenocarcinomas (LADCs) from people from Japan and the United States, using whole-transcriptome sequencing. The KIF5B-RET fusion leads to aberrant activation of RET kinase and is considered to be a new driver mutation of LADC because it segregates from mutations or fusions in EGFR, KRAS, HER2 and ALK, and a RET tyrosine kinase inhibitor, vandetanib, suppresses the fusion-induced anchorage-independent growth activity of NIH3T3 cells.
- Published
- 2012
- Full Text
- View/download PDF