To the rescue: the Fanconi anemia genome stability pathway salvages replication forks.

Cancer cell ·Vol. 22 ·No. 1 ·2012-07-10 ·Pages 5-6

Moldovan GL, D'Andrea AD

Abstract

DNA damage can arrest replication forks during S phase. Failure to stabilize and restart arrested forks results in fork collapse and genomic instability. In this issue of Cancer Cell, Schlacher et al. show that the Fanconi anemia and BRCA2 tumor suppressor pathways cooperate to protect stalled replication forks from degradation.

Authors & Affiliations

2 authors, click to expand affiliations / ORCID

Moldovan George-Lucian

Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA.

D'Andrea Alan D

References (10)

10 references, click to expand

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Article Info

Journal

Cancer cell

Abbr.

Cancer Cell

ISSN

1878-3686

DOI

10.1016/j.ccr.2012.06.006

Published

2012-07-10

Pages

5-6

Language

English

Region

United States

NLM ID

101130617

PMCID

PMC3406730

Grants

NHLBI NIH HHS · P01 HL048546 · United States

NIDDK NIH HHS · R01 DK043889 · United States

NHLBI NIH HHS · R37 HL052725 · United States

Corrections

CommentOn

PMID: 22789542

External Links

PubMed source DOI: 10.1016/j.ccr.2012.06.006 PMC Full Text View journal details

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To the rescue: the Fanconi anemia genome stability pathway salvages replication forks.

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