Alireza Heravi-Moussavi.

Kimberly C. Wiegand, B .Sc., Sohrab P. Shah, Ph.D., Osama M. Al-Agha, M.D., Yongjun Zhao, D.V.M., Kane Tse, B.Sc., Thomas Zeng, M.Sc., Janine Senz, B.Sc., Melissa K. McConechy, B.Sc., Michael S. Anglesio, Ph.D., Steve E. Kalloger, B.Sc., Winnie Yang, B.Sc., Alireza Heravi-Moussavi, Ph.D., Ryan Giuliany, B.Sc., Christine Chow, B.M.L.Sc., John Charge, B.Sc., Abdalnasser Zayed, B.Sc., Leah Prentice, Ph.D., Nataliya Melnyk, B.Sc., Gulisa Turashvili, M.D., Ph.D., Allen D. Delaney, Ph.D., Jason Madore, M.Sc., Stephen Yip, M.D., Ph.D., Andrew W. McPherson, B.A.Sc., Gavin Ha, B.Sc., Lynda Bell, R.T., Sian Fereday, B.Sc., Angela Tam, B.Sc., Laura Galletta, B.Sc., Patricia N.

Because we were not in a position to examine pleural-effusion specimens from the individual before he received crizotinib treatment, we do not know whether the resistant clones were initially or created secondarily present, during the treatment. Amino acid substitutions at the gatekeeper position of several tyrosine kinases have already been detected in tumors treated with tyrosine kinase inhibitors .19 The findings were in keeping with the results of our analysis of tumor cells in vivo: the introduction of methionine at this position rendered NPM-ALK resistant to ALK inhibitors.g., C1156 in ALK) have not been confirmed for additional tyrosine kinases in tumor specimens.20 A transformation at C1156 of ALK might therefore interfere allosterically with the binding of tyrosine kinase inhibitors.