Thierry Vilboux.

Thierry Vilboux, Ph.D., Atar Lev, M .Sc., Might Christine V. Malicdan, M.D., Ph.D., Amos J. Simon, B.Sc.D., Tomas Racek, Ph.D., Jacek Puchalka, Ph.D., Raman Sood, Ph.D., Blake Carrington, B.Sc., Kevin Bishop, B.Sc., James Mullikin, Ph.D., Marjan Huizing, Ph.D., Ben Zion Garty, M.D., Eran Eyal, Ph.D., Baruch Wolach, M.D., Ronit Gavrieli, M.Sc., Amos Toren, M.D., Ph.D., Michalle Soudack, M.D., Osama M. Atawneh, M.D., Tatiana Babushkin, Ph.D., Ginette Schiby, M.D., Andrew Cullinane, Ph.D., Camila Avivi, Ph.D., Sylvie Polak-Charcon, Ph.D., Iris Barshack, M.D., Ninette Amariglio, Ph.D., Gideon Rechavi, M.D., Ph.D., Jutte van der Werff ten Bosch, M.D., Ph.D., Yair Anikster, M.D., Ph.D., Christoph Klein, M.D., Ph.D., William A.

Engelman, M.D., Ph.D., and Alice T. Shaw, M.D., Ph.D. The identification of activating mutations within the kinase domain of the epidermal growth factor receptor 2,3 has led to the widespread use of kinase inhibitors in this genetically defined subset of lung cancers.4 More recently, chromosomal translocations that induce fusion proteins involving the tyrosine kinase domains of ALK5 or ROS16 have been the subject of intense investigation in lung adenocarcinoma due to the option of clinically active inhibitors of these kinases. Although kinase inhibitors can be highly effective, most cancers acquire resistance to these targeted therapies invariably, an impact that represents a major limitation with their long-term clinical advantage.