Основные закономерности ангиогенеза при онкогематологических заболеваниях

ОБЗОРЫ , , ,

А.А. Вартанян

ФГБУ «Российский онкологический центр им Н.Н. Блохина» РАМН, Москва, Российская Федерация

РЕФЕРАТ

Концепция о том, что VEGF-индуцируемый ангиогенез — фактор, лимитирующий рост солидных опухолей, сегодня считается общепринятой. Исследования последних лет показывают, что ангиогенез также необходимое условие прогрессии онкогематологических заболеваний. Процесс ветвления близлежащих сосудов в костном мозге начинается с выброса опухолевыми клетками растворимых активаторов ангиогенеза. Основным медиатором, стимулирующим формирование микрососудов в костном мозге, считается VEGF. С другой стороны, повышенная секреция VEGF приводит к высвобождению клетками микроокружения GM-CSF, G-CSF, IL-6, PlGF, HGF, IGF, цитокинов, способствующих выживанию и пролиферации злокачественных миелоидных и лимфоидных клеток. Увеличение уровня VEGF в плазме онкогематологических больных считается неблагоприятным прогностическим фактором течения болезни.

В настоящем обзоре обсуждаются основные закономерности формирования аутокринного и паракринного пула VЕGF, ангиогенез-зависимая и -независимая функции VEGF, а также результаты клинического изучения антиангиогенных препаратов в онкогематологии.

Ключевые слова: онкогематология, костный мозг, ангиогенез, антиангиогенная терапия.

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