Abstract
Progress in defining molecular targets of oncogenesis and drugs to inhibit cancer growth in specific populations has led to augmented outcomes for patients and new expectations in the development of treatments. The EML4–ALK fusion protein was identified in patients with non-small-cell lung cancer (NSCLC) in 2007.1 Rearrangements in the ALK gene lead to constitutive signalling, triggering transforming properties. Up to now, two drugs have been approved by the US Food and Drug Administration for ALK-rearranged NSCLC—crizotinib and ceritinib.
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