
Phenotypic transformation as a cause of secondary drug resistance to osimetinib clinical observation
Author(s) -
Lidiia A Neliubina,
Е. В. Реутова,
К. К. Лактионов,
Д. И. Юдин,
D Marinov,
Eszter Kozák,
V. V. Mochalnikova
Publication year - 2018
Publication title -
medicinskij sovet
Language(s) - English
Resource type - Journals
eISSN - 2658-5790
pISSN - 2079-701X
DOI - 10.21518/2079-701x-2018-19-130-135
Subject(s) - osimertinib , t790m , medicine , drug resistance , disease , somatic evolution in cancer , drug , tyrosine kinase inhibitor , tyrosine kinase , mutation , phenotype , oncology , resistance mutation , cancer research , pharmacology , cancer , gene , biology , epidermal growth factor receptor , genetics , receptor , polymerase chain reaction , gefitinib , erlotinib , reverse transcriptase
Targeted therapy is the optimal treatment of patients with advanced EGFR-positive NSCLC. The first- and second-generation EGFR tyrosine kinase inhibitors provide a durable antitumor response in most patients during the year. Due to appearance of T790M secondary mutation of resistance at progression of the disease, the administration of osimertinib leads to full control of the tumour for another 10 months. However, this is not the only mechanism of acquired drug resistance. A repeated biopsy of the tumour followed by histological and molecular genetic research makes it possible to clarify the cause of resistance and personalize the further disease management.