![]() Oncogenic signaling can promote global increases in transcription activity, also termed hypertranscription. Here we discuss our mechanistic understanding of hypertranscription-induced replication stress and the resulting cellular responses, in the context of oncogenes and targeted cancer therapies.ĪB - Replication stress results from obstacles to replication fork progression, including ongoing transcription, which can cause transcription–replication conflicts. A growing number of recent studies are reporting that oncogenes, such as RAS, and targeted cancer treatments, such as bromodomain and extraterminal motif (BET) bromodomain inhibitors, increase global transcription, leading to R-loop accumulation, transcription–replication conflicts, and the activation of replication stress responses. Despite the widely accepted importance of oncogene-induced hypertranscription, its study remains neglected compared with other causes of replication stress and genomic instability in cancer. N2 - Replication stress results from obstacles to replication fork progression, including ongoing transcription, which can cause transcription–replication conflicts. This work was supported by a Cancer Research UK Programme Foundation Award to E.P. T1 - Hypertranscription and replication stress in cancer Here we discuss our mechanistic understanding of hypertranscription-induced replication stress and the resulting cellular responses, in the context of oncogenes and targeted cancer therapies.", ![]() Abstract = "Replication stress results from obstacles to replication fork progression, including ongoing transcription, which can cause transcription–replication conflicts.
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