ПРИОБРЕТЕННАЯ РЕЗИСТЕНТНОСТЬ К ИНГИБИТОРАМ ТИРОЗИНКИНАЗЫ EGFR: ПУТИ ПРЕОДОЛЕНИЯ

СтатьяМЕД СОВЕТ. 2017; № 14: 24–28. DOI:undefined

Реутова Е.В.^[1]

Лактионов К.К.^[1]

Ардзинба М.С.^[1]

Нелюбина Л.А.^[1]

Арзуманян А.Л.^[1]

^[1]Национальный медицинский исследовательский центр онкологии им. Н.Н. Блохина Минздрава России

Успехи в лечении диссеминированных больных с немелкоклеточным раком легкого напрямую связаны с таргетной терапией. Пациенты с активирующими мутациями в гене рецептора эпидермального фактора роста (EGFR) при назначении им в первую линию ингибиторов тирозинкиназы EGFR (ТКИ EGFR) первого и второго поколений имеют достоверное преимущество по непосредственной эффективности и времени до прогрессирования. Кроме того, у больных с делецией в 19 экзоне EGFR, получающих афатиниб, общая выживаемость достигает 30 мес., что статистически выше по сравнению со стандартной химиотерапией. Однако в течение 10–12 мес. развивается приобретенная резистентность к таргетным препаратам, основной причиной которой в 60[%] случаев является мутация Т790М. Осимертиниб – ТКИ третьего поколения, оказался высокоэффективен именно у этих больных. Для уточнения механизма резистентности требуется повторное молекулярно-генетическое тестирование. Таким образом, необходима повторная биопсия опухоли, оптимально из очага прогрессирования. К сожалению, это не всегда выполнимо, и альтернативой может быть жидкостная биопсия. Только такой индивидуальный подход может обеспечить выбор оптимальной лечебной тактики и добиться улучшения выживаемости пациентов.

немелкоклеточный рак легкого

EGFR

ингибиторы тирозинкиназы EGFR

резистентность

осимертиниб

Erbb рецепторы

Афатиниб

Биопсия

Болезнь

Больные

Выживаемость

Гефитиниб

Достижение

Жидкостная биопсия

Ингибиторы тирозинкиназы

Карповые

Легкие

Лекарственная терапия

Мутация

Новообразования

Причинная связь

Рост

Экзоны

Эпидермальный фактор роста

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Язык текста: Русский

ISSN: 2079-701X