Article
Cancer-associated SMARCAL1 loss-of-function mutations promote alternative lengthening of telomeres and tumorigenesis in telomerase-negative glioblastoma cells.
Neuro-oncology - 5 Sept 2023
Liu Heng, Xu Cheng, Diplas Bill H, Brown Alexandrea, Strickland Laura M, Yao Haipei, Ling Jinjie, McLendon Roger E, Keir Stephen T, Ashley David M, He Yiping, Waitkus Matthew S
Abstract excerpt
BACKGROUND: Telomere maintenance mechanisms are required to enable the replicative immortality of malignant cells. While most cancers activate the enzyme telomerase, a subset of cancers uses telomerase-independent mechanisms termed alternative lengthening of telomeres (ALT). ALT occurs via homology-directed-repair mechanisms and is frequently associated with ATRX mutations. We previously showed that a subset of...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
