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Cancer Res. 2019 Apr 1;79(7):1297-1298. doi: 10.1158/0008-5472.CAN-19-0216.

Remodeling Collapsed DNA Replication Forks for Cancer Development.

Author information

1
Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
2
Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
3
Department of Molecular Biology, University of Geneva, Geneva, Switzerland. thanos.halazonetis@unige.ch.

Abstract

DNA replication stress is prevalent in human cancers, but absent in normal cells, suggesting that proteins involved in the cellular response to DNA replication stress could be potential therapeutic targets. SMARCAL1 and ZRANB3 are annealing helicases that mediate the repair of collapsed DNA replication forks. In a study in this issue of Cancer Research, Puccetti and colleagues report that mice lacking either SMARCAL1 or ZRANB3 activity have delayed development of MYC-induced B-cell lymphomas. Thus, inhibiting the response to DNA replication stress could benefit patients with cancer.See related article by Puccetti et al., p. 1612.

PMID:
30936075
DOI:
10.1158/0008-5472.CAN-19-0216
[Indexed for MEDLINE]

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