Home > Research > Publications & Outputs > Cancer Therapy and Replication Stress

Research

Links

Text available via DOI:

View graph of relations

Cancer Therapy and Replication Stress: Forks on the Road to Perdition

Research output: Contribution in Book/Report/Proceedings - With ISBN/ISSN › Chapter

Published

Standard

Cancer Therapy and Replication Stress: Forks on the Road to Perdition. / Kotsantis, P.; Jones, R.M.; Higgs, M.R. et al.
Advances in Clinical Chemistry. ed. / Gregory S. Makowski. Elsevier, 2015. p. 91-138 (Advances in Clinical Chemsitry; Vol. 69).

Research output: Contribution in Book/Report/Proceedings - With ISBN/ISSN › Chapter

Harvard

Kotsantis, P, Jones, RM, Higgs, MR & Petermann, E 2015, Cancer Therapy and Replication Stress: Forks on the Road to Perdition. in GS Makowski (ed.), Advances in Clinical Chemistry. Advances in Clinical Chemsitry, vol. 69, Elsevier, pp. 91-138. https://doi.org/10.1016/bs.acc.2014.12.003

APA

Kotsantis, P., Jones, R. M., Higgs, M. R., & Petermann, E. (2015). Cancer Therapy and Replication Stress: Forks on the Road to Perdition. In G. S. Makowski (Ed.), Advances in Clinical Chemistry (pp. 91-138). (Advances in Clinical Chemsitry; Vol. 69). Elsevier. https://doi.org/10.1016/bs.acc.2014.12.003

Vancouver

Kotsantis P, Jones RM, Higgs MR, Petermann E. Cancer Therapy and Replication Stress: Forks on the Road to Perdition. In Makowski GS, editor, Advances in Clinical Chemistry. Elsevier. 2015. p. 91-138. (Advances in Clinical Chemsitry). doi: 10.1016/bs.acc.2014.12.003

Author

Kotsantis, P. ; Jones, R.M. ; Higgs, M.R. et al. / Cancer Therapy and Replication Stress : Forks on the Road to Perdition. Advances in Clinical Chemistry. editor / Gregory S. Makowski. Elsevier, 2015. pp. 91-138 (Advances in Clinical Chemsitry).

Bibtex

@inbook{9ab113904b664691a8068e3aa39b02b2,
title = "Cancer Therapy and Replication Stress: Forks on the Road to Perdition",
abstract = "Deregulated DNA replication occurs in cancer where it contributes to genomic instability. This process is a target of cytotoxic therapies. Chemotherapies exploit high DNA replication in cancer cells by modifying the DNA template or by inhibiting vital enzymatic activities that lead to slowing or stalling replication fork progression. Stalled replication forks can be converted into toxic DNA double-strand breaks resulting in cell death, i.e., replication stress. While likely crucial for many cancer treatments, replication stress is poorly understood due to its complexity. While we still know relatively little about the role of replication stress in cancer therapy, technical advances in recent years have shed new light on the effect that cancer therapeutics have on replication forks and the molecular mechanisms that lead from obstructed fork progression to cell death. This chapter will give an overview of our current understanding of replication stress in the context of cancer therapy.",
author = "P. Kotsantis and R.M. Jones and M.R. Higgs and E. Petermann",
year = "2015",
doi = "10.1016/bs.acc.2014.12.003",
language = "English",
isbn = "9780128022658",
series = "Advances in Clinical Chemsitry",
publisher = "Elsevier",
pages = "91--138",
editor = "Makowski, {Gregory S.}",
booktitle = "Advances in Clinical Chemistry",

}

RIS

TY - CHAP

T1 - Cancer Therapy and Replication Stress

T2 - Forks on the Road to Perdition

AU - Kotsantis, P.

AU - Jones, R.M.

AU - Higgs, M.R.

AU - Petermann, E.

PY - 2015

Y1 - 2015

N2 - Deregulated DNA replication occurs in cancer where it contributes to genomic instability. This process is a target of cytotoxic therapies. Chemotherapies exploit high DNA replication in cancer cells by modifying the DNA template or by inhibiting vital enzymatic activities that lead to slowing or stalling replication fork progression. Stalled replication forks can be converted into toxic DNA double-strand breaks resulting in cell death, i.e., replication stress. While likely crucial for many cancer treatments, replication stress is poorly understood due to its complexity. While we still know relatively little about the role of replication stress in cancer therapy, technical advances in recent years have shed new light on the effect that cancer therapeutics have on replication forks and the molecular mechanisms that lead from obstructed fork progression to cell death. This chapter will give an overview of our current understanding of replication stress in the context of cancer therapy.

AB - Deregulated DNA replication occurs in cancer where it contributes to genomic instability. This process is a target of cytotoxic therapies. Chemotherapies exploit high DNA replication in cancer cells by modifying the DNA template or by inhibiting vital enzymatic activities that lead to slowing or stalling replication fork progression. Stalled replication forks can be converted into toxic DNA double-strand breaks resulting in cell death, i.e., replication stress. While likely crucial for many cancer treatments, replication stress is poorly understood due to its complexity. While we still know relatively little about the role of replication stress in cancer therapy, technical advances in recent years have shed new light on the effect that cancer therapeutics have on replication forks and the molecular mechanisms that lead from obstructed fork progression to cell death. This chapter will give an overview of our current understanding of replication stress in the context of cancer therapy.

U2 - 10.1016/bs.acc.2014.12.003

DO - 10.1016/bs.acc.2014.12.003

M3 - Chapter

SN - 9780128022658

T3 - Advances in Clinical Chemsitry

SP - 91

EP - 138

BT - Advances in Clinical Chemistry

A2 - Makowski, Gregory S.

PB - Elsevier

ER -