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  • Taylor FO review 2016

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DNA replication stress and cancer: cause or cure?

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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DNA replication stress and cancer: cause or cure? / Taylor, Elaine Moira; Lindsay, Howard David.
In: Future Oncology, Vol. 12, No. 2, 01.2016, p. 221-237.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Taylor, EM & Lindsay, HD 2016, 'DNA replication stress and cancer: cause or cure?', Future Oncology, vol. 12, no. 2, pp. 221-237. https://doi.org/10.2217/fon.15.292

APA

Taylor, E. M., & Lindsay, H. D. (2016). DNA replication stress and cancer: cause or cure? Future Oncology, 12(2), 221-237. https://doi.org/10.2217/fon.15.292

Vancouver

Taylor EM, Lindsay HD. DNA replication stress and cancer: cause or cure? Future Oncology. 2016 Jan;12(2):221-237. doi: 10.2217/fon.15.292

Author

Taylor, Elaine Moira ; Lindsay, Howard David. / DNA replication stress and cancer : cause or cure?. In: Future Oncology. 2016 ; Vol. 12, No. 2. pp. 221-237.

Bibtex

@article{19b0d40f3fbd4814baeff82ac9319446,
title = "DNA replication stress and cancer: cause or cure?",
abstract = "There is an extensive and growing body of evidence that DNA replication stress is a major driver in the development and progression of many cancers, and that these cancers rely heavily on replication stress response pathways for their continued proliferation. This raises the possibility that the pathways that ordinarily protect cells from the accumulation of cancer-causing mutations may actually prove to be effective therapeutic targets for a wide range of malignancies. In this review, we explore the mechanisms by which sustained proliferation can lead to replication stress and genome instability, and discuss how the pattern of mutations observed in human cancers is supportive of this oncogene-induced replication stress model. Finally, we go on to consider the implications of replication stress both as a prognostic indicator and, more encouragingly, as a potential target in cancer treatment.",
author = "Taylor, {Elaine Moira} and Lindsay, {Howard David}",
year = "2016",
month = jan,
doi = "10.2217/fon.15.292",
language = "English",
volume = "12",
pages = "221--237",
journal = "Future Oncology",
issn = "1479-6694",
publisher = "Future Medicine Ltd.",
number = "2",

}

RIS

TY - JOUR

T1 - DNA replication stress and cancer

T2 - cause or cure?

AU - Taylor, Elaine Moira

AU - Lindsay, Howard David

PY - 2016/1

Y1 - 2016/1

N2 - There is an extensive and growing body of evidence that DNA replication stress is a major driver in the development and progression of many cancers, and that these cancers rely heavily on replication stress response pathways for their continued proliferation. This raises the possibility that the pathways that ordinarily protect cells from the accumulation of cancer-causing mutations may actually prove to be effective therapeutic targets for a wide range of malignancies. In this review, we explore the mechanisms by which sustained proliferation can lead to replication stress and genome instability, and discuss how the pattern of mutations observed in human cancers is supportive of this oncogene-induced replication stress model. Finally, we go on to consider the implications of replication stress both as a prognostic indicator and, more encouragingly, as a potential target in cancer treatment.

AB - There is an extensive and growing body of evidence that DNA replication stress is a major driver in the development and progression of many cancers, and that these cancers rely heavily on replication stress response pathways for their continued proliferation. This raises the possibility that the pathways that ordinarily protect cells from the accumulation of cancer-causing mutations may actually prove to be effective therapeutic targets for a wide range of malignancies. In this review, we explore the mechanisms by which sustained proliferation can lead to replication stress and genome instability, and discuss how the pattern of mutations observed in human cancers is supportive of this oncogene-induced replication stress model. Finally, we go on to consider the implications of replication stress both as a prognostic indicator and, more encouragingly, as a potential target in cancer treatment.

U2 - 10.2217/fon.15.292

DO - 10.2217/fon.15.292

M3 - Journal article

VL - 12

SP - 221

EP - 237

JO - Future Oncology

JF - Future Oncology

SN - 1479-6694

IS - 2

ER -