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• W2740697669 abstract "Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance mechanism that occurs in a subset of cancers. By analyzing telomerase-positive cells and their human TERC knockout-derived ALT human cell lines, we show that ALT cells harbor more fragile telomeres representing telomere replication problems. ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner. Telomeric MiDAS is a conservative DNA synthesis process, potentially mediated by break-induced replication, similar to type II ALT survivors in Saccharomyces cerevisiae. Replication stresses induced by ectopic oncogenic expression of cyclin E, G-quadruplexes, or R-loop formation facilitate the ALT pathway and lead to telomere clustering, a hallmark of ALT cancers. The TIMELESS/TIPIN complex suppresses telomere clustering and telomeric MiDAS, whereas the SMC5/6 complex promotes them. In summary, ALT cells exhibit more telomere replication defects that result in persistent DNA damage responses at telomeres, leading to the engagement of telomeric MiDAS (spontaneous mitotic telomere synthesis) that is triggered by DNA replication stress, a potential driver of genomic duplications in cancer." @default.
• W2740697669 created "2017-08-08" @default.
• W2740697669 creator A5018167935 @default.
• W2740697669 creator A5029412437 @default.
• W2740697669 creator A5081012778 @default.
• W2740697669 date "2017-10-01" @default.
• W2740697669 modified "2023-10-16" @default.
• W2740697669 title "Alternative Lengthening of Telomeres Mediated by Mitotic DNA Synthesis Engages Break-Induced Replication Processes" @default.
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• W2740697669 doi "https://doi.org/10.1128/mcb.00226-17" @default.
• W2740697669 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5615184" @default.
• W2740697669 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28760773" @default.
• W2740697669 hasPublicationYear "2017" @default.
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