Tyrosine kinase gene rearrangements in epithelial malignancies
Cet article passe en revue les travaux récents sur les caractéristiques étiologiques, pathogéniques et cliniques associées aux tumeurs épithéliales qui présentent des réarrangements chromosomiques induisant une activation de certaines kinases, notamment ALK, ROS1 et RET
Chromosomal rearrangements that lead to oncogenic kinase activation are observed in many epithelial cancers. These cancers express activated fusion kinases that drive the initiation and progression of malignancy, and often have a considerable response to small-molecule kinase inhibitors, which validates these fusion kinases as 'druggable' targets. In this Review, we examine the aetiologic, pathogenic and clinical features that are associated with cancers harbouring oncogenic fusion kinases, including anaplastic lymphoma kinase (ALK), ROS1 and RET. We discuss the clinical outcomes with targeted therapies and explore strategies to discover additional kinases that are activated by chromosomal rearrangements in solid tumours.