![]() ![]() In this review we will discuss the most recent results of new TKIs in order to describe a fast growing therapeutic landscape in this setting. Some of them were approved after the failure of crizotinib (ceritinib, alectinib, brigatinib and lorlatinib) and in first line setting (ceritinib, alectinib and brigatinib) while others are still under evaluation for TKI-naive patients such as lorlatinib, ensartinib and entrectinib. For instance, in order to overtake acquired resistance to crizotinib, prolong the control of the disease and manage CNS localizations, several II and III generation TKIs have been developed. This is primarily attributed to poor CNS penetration by crizotinib as many pre-clinical and clinical models suggest. Moreover, 60–90% of patients treated with crizotinib has a progression in the central nervous system (CNS) in absence of extracranial worsening of the disease. Despite its use improved significantly progression-free survival, overall response rate and duration of response of this illness, after a median period of 10.9 months all patients progress due to the development of acquired resistance mutations in the ALK tyrosine kinase domain in approximately one third of patients. The therapeutic strategy depends on anti-ALK tyrosine kinase inhibitors (TKIs) of which crizotinib was the first approved for clinical use. Policy of Dealing with Allegations of Research MisconductĪbstract: Anaplastic lymphoma kinase (ALK) gene translocations are pro-tumoral driver alterations that encompass 3–7% of non-squamous non-small cell lung cancer (NSCLC) with specific, clinic and histologic features.Policy of Screening for Plagiarism Process.
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