Conclusion


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In the recent past, tyrosine kinases have become an important area of cancer research, both in the understanding of their role in malignant growth pathways and the mechanisms necessary to inhibit their oncogenic activities in cancer patients. The ALK is one such target, having been identified as an oncogenic driver in a small subset (3%–7%) of NSCLC. The advent of molecularly targeted therapies for NSCLCs has allowed for significantly improved clinical outcomes in ALK+ patients. After limitations concerning treatment with the first-generation TKI crizotinib surfaced, ceritinib received Food and Drug Administration approval in April 2014 for treating crizotinib-resistant ALK+-NSCLC patients. Ceritinib appears to be a potent successor to the first-generation TKI crizotinib in its ability to suppress untreated ALK+ tumors as well as tumors harboring resistance mutations that render crizotinib ineffective. Several trials are currently underway.

Disclosure

The authors indicated no conflicts of interest in this work.


Mark W. Burns, Eric S. Kim

Wilmot Cancer Center, University of Rochester, Rochester, NY, USA


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Source: Lung Cancer: Targets and Therapy.
Originally published on May 15, 2015.