initially respond eventually relapse because their cancer has
become resistant to crizotinib ( 95).
NSCLC resistance to crizotinib occurs through a variety
of molecular mechanisms, including the emergence of
new mutations in ALK ( 96) (see sidebar on The Challenge
of Treatment Resistance). Recent research has shown that
ceritinib is able to block many of the unique forms of
ALK that result from these new mutations ( 97). In this
way, ceritinib benefits many patients, like James (Rocky)
Lagno (see p. 62), with crizotinib-resistant NSCLC driven
by ALK ( 98).