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Replication stress results from obstacles to replication fork progression, including ongoing transcription, which can cause transcription–replication conflicts. Oncogenic signaling can promote global increases in transcription activity, also termed hypertranscription. 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. 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. 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.
Bibliographical noteFunding Information:
This work was supported by a Cancer Research UK Programme Foundation Award to E.P. ( C25526/A28275 ).
© 2021 The Authors
- genomic instability
- replication stress
ASJC Scopus subject areas
- Cancer Research
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1/09/19 → 31/08/25