Hypertranscription and replication stress in cancer

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Hypertranscription and replication stress in cancer. / Bowry, Akhil; Kelly, Richard; Petermann, Eva.

In: Trends in Cancer, 26.05.2021.

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@article{1ae4846d7410468bab6102f98cd208e9,
title = "Hypertranscription and replication stress in cancer",
abstract = "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.",
keywords = "R-loops, genomic instability, hypertranscription, oncogenes, replication stress",
author = "Akhil Bowry and Richard Kelly and Eva Petermann",
note = "Funding Information: This work was supported by a Cancer Research UK Programme Foundation Award to E.P. ( C25526/A28275 ). Publisher Copyright: {\textcopyright} 2021 The Authors",
year = "2021",
month = may,
day = "26",
doi = "10.1016/j.trecan.2021.04.006",
language = "English",
journal = "Trends in Cancer",
issn = "2405-8033",
publisher = "Cell Press",

}

RIS

TY - JOUR

T1 - Hypertranscription and replication stress in cancer

AU - Bowry, Akhil

AU - Kelly, Richard

AU - Petermann, Eva

N1 - Funding Information: This work was supported by a Cancer Research UK Programme Foundation Award to E.P. ( C25526/A28275 ). Publisher Copyright: © 2021 The Authors

PY - 2021/5/26

Y1 - 2021/5/26

N2 - 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.

AB - 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.

KW - R-loops

KW - genomic instability

KW - hypertranscription

KW - oncogenes

KW - replication stress

UR - http://www.scopus.com/inward/record.url?scp=85107630139&partnerID=8YFLogxK

U2 - 10.1016/j.trecan.2021.04.006

DO - 10.1016/j.trecan.2021.04.006

M3 - Review article

C2 - 34052137

JO - Trends in Cancer

JF - Trends in Cancer

SN - 2405-8033

ER -