This article explores the cellular response to DNA double-strand breaks (DSBs) in highly aggressive cancer cells and how they manage genomic stability during chromosome duplication. It reveals the activation of a local genome maintenance mechanism that inhibits replication at sites of DSBs without disrupting DNA synthesis elsewhere. Key players in this process include the TIMELESS-TIPIN complex and WEE1 kinase, which work together to prevent replication initiation near DSBs. Dysregulation of this mechanism can lead to increased genomic instability, highlighting a vulnerability that could be targeted for therapeutic intervention in cancer treatment.
A local genome maintenance mechanism is induced by DNA double-strand breaks (DSBs), which inhibits replication initiation in DSB-containing topologically associating domains (TADs).
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