MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1080/08977194.2026.2671736

Медицинская библиотека · Growth factors (Chur, Switzerland) · 2026

The role of ERK signaling pathway in pituitary adenomas: from molecular mechanisms to targeted therapy.

Ye Jingwei, Wen Yuan, Zhan Jingyang, Hla Khaing Wut Yi, Li Tong, Xiao Zhiyu, Shu Xianghan

СтатьяОбзорПеревод в очереди

Аннотация

ERK, a core member of the MAPK family, operates through the classical Ras/Raf/MEK/ERK signaling cascade. Abnormal activation of this pathway is closely associated with malignant tumor progression and represents a critical target in anticancer drug development. In this article, we systematically describe the regulatory network of the ERK pathway, including negative feedback mechanisms, cross-pathway interactions, non-coding RNAs, and epigenetic regulation, with a particular focus on ERK's dual role-promoting both cell proliferation and apoptosis-in pituitary adenomas compared to other tumors. Additionally, we explore emerging ERK-targeted therapies and their associated resistance mechanisms. Despite substantial research on ERK, further investigation into its underlying mechanisms is warranted. We propose the construction of computational modeling approaches to analyze these complex regulatory relationships and to develop precise combination therapies aimed at overcoming resistance. Such strategies could enable personalized treatment and offer more effective solutions for managing pituitary tumors and other malignancies.

Для цитирования: Ye Jingwei, Wen Yuan, Zhan Jingyang, Hla Khaing Wut Yi, Li Tong, Xiao Zhiyu, Shu Xianghan. The role of ERK signaling pathway in pituitary adenomas: from molecular mechanisms to targeted therapy.. Growth factors (Chur, Switzerland). 2026. DOI: 10.1080/08977194.2026.2671736.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.