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Phenotypic transformation as a cause of secondary drug resistance to osimetinib clinical observation

https://doi.org/10.21518/2079-701X-2018-19-130-135

Abstract

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.

About the Authors

L. A. Nelyubina
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


E. V. Reutova
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


K. K. Laktionov
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


D. I. Yudin
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


D. T. Marinov
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


E. N. Kozak
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


V. V. Mochalnikova
Blokhin Russian Cancer Research Center of the Ministry of Health of Russia, Moscow
Russian Federation


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Review

For citations:


Nelyubina LA, Reutova EV, Laktionov KK, Yudin DI, Marinov DT, Kozak EN, Mochalnikova VV. Phenotypic transformation as a cause of secondary drug resistance to osimetinib clinical observation. Meditsinskiy sovet = Medical Council. 2018;(19):130-135. (In Russ.) https://doi.org/10.21518/2079-701X-2018-19-130-135

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ISSN 2079-701X (Print)
ISSN 2658-5790 (Online)