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.

journal_name

Adv Clin Chem

authors

Kotsantis P,Jones RM,Higgs MR,Petermann E

doi

10.1016/bs.acc.2014.12.003

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

91-138

eissn

0065-2423

issn

2162-9471

pii

S0065-2423(14)00042-0

journal_volume

69

pub_type

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