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Основным механизмом возникновения гастроинтестинальных стромальных опухолей (ГИСО) являются мутации генов KIT и PDGFRA. Иматиниб обладает крайне высокой эффективностью, однако вследствие вторичных мутаций развивается резистентность к терапии. Тирозинкиназные ингибиторы (ТКИ), применяемые после прогрессирования на фоне терапии иматинибом, обладают низкой эффективностью, в связи с чем в настоящее время изучаются новые молекулы, обладающие высокой противоопухолевой активностью при вторичных мутациях. Наша статья посвящена новым препаратам, которые активно изучаются при ГИСО.
Библиографические ссылки
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