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dc.contributor.authorRomanidou, Ourania
dc.contributor.authorLandi, L
dc.contributor.authorCappuzzo, F
dc.contributor.authorCalifano, Raffaele
dc.date.accessioned2016-06-24T11:40:34Z
dc.date.available2016-06-24T11:40:34Z
dc.date.issued2016-05en
dc.identifier.citationOvercoming resistance to first/second generation epidermal growth factor receptor tyrosine kinase inhibitors and ALK inhibitors in oncogene-addicted advanced non-small cell lung cancer. 2016, 8 (3):176-87 Ther Adv Med Oncolen
dc.identifier.issn1758-8340en
dc.identifier.pmid27239236en
dc.identifier.doi10.1177/1758834016631531en
dc.identifier.urihttp://hdl.handle.net/10541/614531
dc.description.abstractEpidermal growth factor receptor (EGFR) activating mutations and anaplastic lymphoma kinase (ALK) gene rearrangement in advanced non-small cell lung cancer (NSCLC) represent the two oncogenic events with an impact on current clinical practice. EGFR tyrosine kinase inhibitors (TKIs) and crizotinib are the standard of care for the treatment of EGFR mutant and ALK gene rearranged advanced NSCLC patients. Unfortunately, despite initial clinical benefit, acquired resistance to EGFR-TKIs or crizotinib usually develops after an average of 10-12 months of treatment. The aim of this review is to describe the mechanisms of resistance to first/second generation EGFR-TKIs and crizotinib. In particular, we focus on strategies to overcome resistance due to secondary EGFR T790M mutation and mutations of the ALK domain.
dc.language.isoenen
dc.rightsArchived with thanks to Therapeutic advances in medical oncologyen
dc.titleOvercoming resistance to first/second generation epidermal growth factor receptor tyrosine kinase inhibitors and ALK inhibitors in oncogene-addicted advanced non-small cell lung cancer.en
dc.typeArticleen
dc.contributor.departmentCancer Research UK Department of Medical Oncology, The Christie NHS Foundation Trust, Manchester, UKen
dc.identifier.journalTherapeutic Advances in Medical Oncologyen
html.description.abstractEpidermal growth factor receptor (EGFR) activating mutations and anaplastic lymphoma kinase (ALK) gene rearrangement in advanced non-small cell lung cancer (NSCLC) represent the two oncogenic events with an impact on current clinical practice. EGFR tyrosine kinase inhibitors (TKIs) and crizotinib are the standard of care for the treatment of EGFR mutant and ALK gene rearranged advanced NSCLC patients. Unfortunately, despite initial clinical benefit, acquired resistance to EGFR-TKIs or crizotinib usually develops after an average of 10-12 months of treatment. The aim of this review is to describe the mechanisms of resistance to first/second generation EGFR-TKIs and crizotinib. In particular, we focus on strategies to overcome resistance due to secondary EGFR T790M mutation and mutations of the ALK domain.


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