DNA replication stress and cancer chemotherapy

DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have e...

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Published inCancer science Vol. 109; no. 2; pp. 264 - 271
Main Authors Kitao, Hiroyuki, Iimori, Makoto, Kataoka, Yuki, Wakasa, Takeshi, Tokunaga, Eriko, Saeki, Hiroshi, Oki, Eiji, Maehara, Yoshihiko
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.02.2018
John Wiley and Sons Inc
Subjects
Cancer
Cancer therapies
chemotherapeutic drugs
Chemotherapy
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA Damage
DNA damage response
DNA Replication
DNA replication stress
Gene Regulatory Networks
Genetic diversity
genome instability
Genomes
Genomic Instability
Humans
Kinases
Mutation
Neoplasms - genetics
Pharmaceuticals
Replication
Review
Tumorigenesis
Yeast
Japan
tumorigenesis
genome instability
DNA damage response
chemotherapeutic drugs
DNA replication stress
Online AccessGet full text
ISSN1347-9032
1349-7006
1349-7006
DOI10.1111/cas.13455

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Abstract DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have experienced and overcome the stresses caused by the perturbation of DNA replication, which is also referred to as DNA replication stress (DRS). When we consider therapeutic approaches for tumors, it is important to exploit the differences in DRS between tumor and normal cells. In this review, we introduce the current understanding of DRS in tumors and discuss the underlying mechanism of cancer therapy from the aspect of DRS. This review summarizes how DNA replication stress is induced and determines the cell destiny in the process of tumor development. This review also explains how cancer therapeutic drugs exploit the stress in malignant tumors.
AbstractList DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have experienced and overcome the stresses caused by the perturbation of DNA replication, which is also referred to as DNA replication stress (DRS). When we consider therapeutic approaches for tumors, it is important to exploit the differences in DRS between tumor and normal cells. In this review, we introduce the current understanding of DRS in tumors and discuss the underlying mechanism of cancer therapy from the aspect of DRS.
DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have experienced and overcome the stresses caused by the perturbation of DNA replication, which is also referred to as DNA replication stress (DRS). When we consider therapeutic approaches for tumors, it is important to exploit the differences in DRS between tumor and normal cells. In this review, we introduce the current understanding of DRS in tumors and discuss the underlying mechanism of cancer therapy from the aspect of DRS.DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have experienced and overcome the stresses caused by the perturbation of DNA replication, which is also referred to as DNA replication stress (DRS). When we consider therapeutic approaches for tumors, it is important to exploit the differences in DRS between tumor and normal cells. In this review, we introduce the current understanding of DRS in tumors and discuss the underlying mechanism of cancer therapy from the aspect of DRS.
DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of cancer and confers genetic diversity during tumorigenesis. Numerous experimental and clinical studies have indicated that most tumors have experienced and overcome the stresses caused by the perturbation of DNA replication, which is also referred to as DNA replication stress (DRS). When we consider therapeutic approaches for tumors, it is important to exploit the differences in DRS between tumor and normal cells. In this review, we introduce the current understanding of DRS in tumors and discuss the underlying mechanism of cancer therapy from the aspect of DRS. This review summarizes how DNA replication stress is induced and determines the cell destiny in the process of tumor development. This review also explains how cancer therapeutic drugs exploit the stress in malignant tumors.
Author Kataoka, Yuki
Wakasa, Takeshi
Maehara, Yoshihiko
Kitao, Hiroyuki
Tokunaga, Eriko
Saeki, Hiroshi
Oki, Eiji
Iimori, Makoto
AuthorAffiliation 2 Taiho Pharmaceutical Co. Ltd. Tokushima Ibaraki Japan
4 Department of Breast Oncology National Hospital Organization Kyushu Cancer Center Fukuoka Japan
3 Department of Surgery and Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan
1 Department of Molecular Cancer Biology Graduate School of Pharmaceutical Sciences Kyushu University Fukuoka Japan
AuthorAffiliation_xml – name: 3 Department of Surgery and Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan
– name: 2 Taiho Pharmaceutical Co. Ltd. Tokushima Ibaraki Japan
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– name: 1 Department of Molecular Cancer Biology Graduate School of Pharmaceutical Sciences Kyushu University Fukuoka Japan
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  organization: Kyushu University
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  fullname: Oki, Eiji
  organization: Kyushu University
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  givenname: Yoshihiko
  surname: Maehara
  fullname: Maehara, Yoshihiko
  organization: Kyushu University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29168596$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2017 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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Issue 2
Keywords tumorigenesis
genome instability
DNA damage response
chemotherapeutic drugs
DNA replication stress
Language English
License Attribution-NonCommercial
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2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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Snippet DNA replication is one of the fundamental biological processes in which dysregulation can cause genome instability. This instability is one of the hallmarks of...
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proquest
pubmed
crossref
wiley
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StartPage 264
SubjectTerms Cancer
Cancer therapies
chemotherapeutic drugs
Chemotherapy
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA Damage
DNA damage response
DNA Replication
DNA replication stress
Gene Regulatory Networks
Genetic diversity
genome instability
Genomes
Genomic Instability
Humans
Kinases
Mutation
Neoplasms - genetics
Pharmaceuticals
Replication
Review
Tumorigenesis
Yeast
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Title DNA replication stress and cancer chemotherapy
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcas.13455
https://www.ncbi.nlm.nih.gov/pubmed/29168596
https://www.proquest.com/docview/2287882309
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https://pubmed.ncbi.nlm.nih.gov/PMC5797825
Volume 109
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