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Predictive biomarkers in the management of EGFR mutant lung cancer
Author(s) -
Rosell Rafael,
Moran Teresa,
Cardenal Felipe,
Porta Rut,
Viteri Santiago,
Molina Miguel Angel,
Benlloch Susana,
Taron Miquel
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05775.x
Subject(s) - gefitinib , erlotinib , t790m , missense mutation , epidermal growth factor receptor , medicine , lung cancer , tyrosine kinase , mutation , cancer research , osimertinib , oncology , tyrosine kinase inhibitor , protein kinase domain , mutant , biology , cancer , receptor , genetics , gene
Activating mutations in the form of deletions in exon 19 (del 19) or the missense mutation L858R in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) predict outcome to use of EGFR tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib. Pooled data from several phase II studies show that gefitinib and erlotinib induce responses in over 70% of NSCLC patients harboring EGFR mutations, with progression‐free survival (PFS) ranging from 9 to 13 months. Two studies in Caucasian and Asian patients have confirmed that these subgroups of patients attain PFS up to 14 months. These landmark outcomes have been accompanied by new challenges, primarily the additional role of chemotherapy and the management of tumors with the secondary T790M mutation that confers resistance to EGFR TKIs. Mechanisms of resistance to reversible EGFR TKIs should be further clarified and could be related to modifications in DNA repair.