Exploiting replicative stress to treat cancer

Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt

Standard

Exploiting replicative stress to treat cancer. / Dobbelstein, Matthias; Sørensen, Claus Storgaard.

I: Nature Reviews. Drug Discovery, Bind 14, Nr. 6, 06.2015, s. 405-23.

Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt

Harvard

Dobbelstein, M & Sørensen, CS 2015, 'Exploiting replicative stress to treat cancer', Nature Reviews. Drug Discovery, bind 14, nr. 6, s. 405-23. https://doi.org/10.1038/nrd4553

APA

Dobbelstein, M., & Sørensen, C. S. (2015). Exploiting replicative stress to treat cancer. Nature Reviews. Drug Discovery, 14(6), 405-23. https://doi.org/10.1038/nrd4553

Vancouver

Dobbelstein M, Sørensen CS. Exploiting replicative stress to treat cancer. Nature Reviews. Drug Discovery. 2015 jun.;14(6):405-23. https://doi.org/10.1038/nrd4553

Author

Dobbelstein, Matthias ; Sørensen, Claus Storgaard. / Exploiting replicative stress to treat cancer. I: Nature Reviews. Drug Discovery. 2015 ; Bind 14, Nr. 6. s. 405-23.

Bibtex

@article{0aed2c74ed89491e81f65edf82f7738b,
title = "Exploiting replicative stress to treat cancer",
abstract = "DNA replication in cancer cells is accompanied by stalling and collapse of the replication fork and signalling in response to DNA damage and/or premature mitosis; these processes are collectively known as 'replicative stress'. Progress is being made to increase our understanding of the mechanisms that govern replicative stress, thus providing ample opportunities to enhance replicative stress for therapeutic purposes. Rather than trying to halt cell cycle progression, cancer therapeutics could aim to increase replicative stress by further loosening the checkpoints that remain available to cancer cells and ultimately inducing the catastrophic failure of proliferative machineries. In this Review, we outline current and future approaches to achieve this, emphasizing the combination of conventional chemotherapy with targeted approaches.",
keywords = "Animals, Antineoplastic Agents, Cell Cycle Checkpoints, DNA Damage, DNA Replication, Drug Delivery Systems, Humans, Neoplasms, Treatment Outcome",
author = "Matthias Dobbelstein and S{\o}rensen, {Claus Storgaard}",
year = "2015",
month = jun,
doi = "10.1038/nrd4553",
language = "English",
volume = "14",
pages = "405--23",
journal = "Nature Reviews. Drug Discovery",
issn = "1474-1776",
publisher = "nature publishing group",
number = "6",

}

RIS

TY - JOUR

T1 - Exploiting replicative stress to treat cancer

AU - Dobbelstein, Matthias

AU - Sørensen, Claus Storgaard

PY - 2015/6

Y1 - 2015/6

N2 - DNA replication in cancer cells is accompanied by stalling and collapse of the replication fork and signalling in response to DNA damage and/or premature mitosis; these processes are collectively known as 'replicative stress'. Progress is being made to increase our understanding of the mechanisms that govern replicative stress, thus providing ample opportunities to enhance replicative stress for therapeutic purposes. Rather than trying to halt cell cycle progression, cancer therapeutics could aim to increase replicative stress by further loosening the checkpoints that remain available to cancer cells and ultimately inducing the catastrophic failure of proliferative machineries. In this Review, we outline current and future approaches to achieve this, emphasizing the combination of conventional chemotherapy with targeted approaches.

AB - DNA replication in cancer cells is accompanied by stalling and collapse of the replication fork and signalling in response to DNA damage and/or premature mitosis; these processes are collectively known as 'replicative stress'. Progress is being made to increase our understanding of the mechanisms that govern replicative stress, thus providing ample opportunities to enhance replicative stress for therapeutic purposes. Rather than trying to halt cell cycle progression, cancer therapeutics could aim to increase replicative stress by further loosening the checkpoints that remain available to cancer cells and ultimately inducing the catastrophic failure of proliferative machineries. In this Review, we outline current and future approaches to achieve this, emphasizing the combination of conventional chemotherapy with targeted approaches.

KW - Animals

KW - Antineoplastic Agents

KW - Cell Cycle Checkpoints

KW - DNA Damage

KW - DNA Replication

KW - Drug Delivery Systems

KW - Humans

KW - Neoplasms

KW - Treatment Outcome

U2 - 10.1038/nrd4553

DO - 10.1038/nrd4553

M3 - Review

C2 - 25953507

VL - 14

SP - 405

EP - 423

JO - Nature Reviews. Drug Discovery

JF - Nature Reviews. Drug Discovery

SN - 1474-1776

IS - 6

ER -

ID: 162985927