颅内动脉瘤的治疗目前仅限于侵入性手术和血管内治疗方式，并且一些动脉瘤无法用这些方法治疗。识别和靶向参与动脉瘤发病机制的特定分子途径可能会改善预后。癌症相关基因中发现的低频体细胞变异与颅内动脉瘤的发展有关。特别是，PDGFRB 基因的突变导致 ERK 和核因子 κB 信号通路持续激活，可以用酪氨酸激酶抑制剂来靶向。在这篇综述中，我们描述了致癌基因和其他基因中的低频体细胞变异如何影响动脉瘤发展的发病机制，重点关注基因治疗应用，例如化疗药物的血管内原位输送。©作者（或其雇主（ s)) 2024。禁止商业重复使用。请参阅权利和权限。英国医学杂志出版。

Treatment of intracranial aneurysms is currently limited to invasive surgical and endovascular modalities, and some aneurysms are not treatable with these methods. Identification and targeting of specific molecular pathways involved in the pathogenesis of aneurysms may improve outcomes. Low frequency somatic variants found in cancer related genes have been linked to intracranial aneurysm development. In particular, mutations in the PDGFRB gene lead to constitutively activated ERK and nuclear factor κB signaling pathways, which can be targeted with tyrosine kinase inhibitors. In this review, we describe how low frequency somatic variants in oncogenic and other genes affect the pathogenesis of aneurysm development, with a focus on gene therapy applications, such as endovascular in situ delivery of chemotherapeutics.© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.