医学
动静脉畸形
相伴的
克拉斯
颅内动静脉畸形
对偶(语法数字)
病理
突变
癌症研究
MAPK/ERK通路
神经科学
脑瘤
双重角色
生物信息学
胶质瘤
血管张力
信号转导
作者
Ryan M. Naylor,Yasuhito Ueki,Fatmah R. Alsereidi,Devrim Bektaş,Anna Haugen,Ram Kadirvel
标识
DOI:10.3171/2025.7.jns25708
摘要
Our findings suggest that, in addition to promoting bAVM formation, KRAS mutations in cerebral endothelial cells might be causally implicated in bAVM rupture. Additionally, concomitant inhibition of the MAPK and VEGF pathways could be a promising novel therapeutic strategy for KRAS-mutated bAVMs.
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