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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/2079-701X-2015-8-50-54</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-228</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОНКОЛОГИЯ И ОНКОГЕМАТОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ONCOLOGY AND ONCOHEMATOLOGY</subject></subj-group></article-categories><title-group><article-title>Афатиниб: новые возможности терапии рака легкого с наличием активирующих мутаций EGFR</article-title><trans-title-group xml:lang="en"><trans-title>Afatinib: new treatment options for lung cancer with activating EGFR mutations</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Степанченко</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Stepanchenko</surname><given-names>M. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зайцев</surname><given-names>В. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Zaitsev</surname><given-names>V. G.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гуторов</surname><given-names>С. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Gutorov</surname><given-names>S. L.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Российский онкологический научный центр им. Н.Н. Блохина, Москва</institution><country>Россия</country></aff><aff xml:lang="en"><institution>N. N. Blokhin Cancer Research Center, Moscow</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>30</day><month>12</month><year>2015</year></pub-date><volume>0</volume><issue>8</issue><fpage>50</fpage><lpage>54</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Степанченко М.В., Зайцев В.Г., Гуторов С.Л., 2015</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="ru">Степанченко М.В., Зайцев В.Г., Гуторов С.Л.</copyright-holder><copyright-holder xml:lang="en">Stepanchenko M.V., Zaitsev V.G., Gutorov S.L.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.med-sovet.pro/jour/article/view/228">https://www.med-sovet.pro/jour/article/view/228</self-uri><abstract><p>Применение ингибиторов EGFR первого поколения существенно улучшило результаты лекарственного лечения пациентов с метастатическим немелкоклеточным раком легкого, включая значимое увеличение частоты достижения объективного эффекта и времени до прогрессирования болезни. В настоящее время арсенал эффективных препаратов расширился за счет внедрения в клиническую практику ингибитора EGFR второго поколения - афатиниба. По данным клинических исследований, максимальная реализация его лечебного эффекта зависит не только от статуса активирующей мутации, но и от ее типа. При наличии мутации EGFr в 19 экзоне афатиниб значимо увеличивает и медиану общей выживаемости. Это представляется чрезвычайно важным обстоятельством, определяющим выбор рационального лечения. Афатиниб эффективен также при развитии резистентности к ингибиторам EGFR первого поколения и представляет собой альтернативный вариант второй линии терапии. Трудно переоценить данное преимущество препарата, позволяющее существенно отсрочить назначение химиотерапии таким больным.</p></abstract><trans-abstract xml:lang="en"><p>First generation EGFR inhibitors have significantly improved the outcomes of drug treatment of patients with metastatic NSCLC, as well as notably increased the frequency of achieving objective response and time to progression of the disease. Today, the arsenal of efficient drugs is enlarged by the introduction into clinical practice of the second-generation EGFR inhibitor - afatinib. According to clinical studies, its full therapeutic effect is determined not only by the status of activating mutation but also its type. Afatinib also significantly increases the overall survival median in case of exon 19 EGFR mutation. This is an extremely important factor in the choice of adequate treatment. Afatinib is also effective in developing resistance to first-generation EGFR inhibitors and is an alternative to second-line therapy. It is hard to overestimate the benefits of the drug which allows for a meaningful delay in chemotherapy for such patients.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>немелкоклеточный рак легкого</kwd><kwd>ингибиторы</kwd><kwd>EGFR</kwd><kwd>афатиниб</kwd><kwd>EGFR inhibitors</kwd><kwd>afatinib</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Suda K, Mizuuchi H, Maehara Y, et al. Acquired resistance mechanisms to tyrosine kinase inhibitors in lung cancer with activating epidermal growth factor receptor mutation -diversity, ductility, and destiny. Cancer Metastasis Rev., 2012, 31: 807-814.</mixed-citation><mixed-citation xml:lang="en">Suda K, Mizuuchi H, Maehara Y, et al. 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