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Journal of Nucleic Acids
Volume 2010, Article ID 319754, 8 pages
Research Article

BLM Deficiency Is Not Associated with Sensitivity to Hydroxyurea-Induced Replication Stress

1Institut Curie, Centre de Recherche, Centre Universitaire, Bât. 110, 91405 Orsay, France
2CNRS, UMR 3348, 91405 Orsay, France

Received 11 May 2010; Accepted 19 July 2010

Academic Editor: Ashis Basu

Copyright © 2010 Kenza Lahkim Bennani-Belhaj et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Bloom's syndrome (BS) displays one of the strongest known correlations between chromosomal instability and a high risk of cancer at an early age. BS cells combine a reduced average fork velocity with constitutive endogenous replication stress. However, the response of BS cells to replication stress induced by hydroxyurea (HU), which strongly slows the progression of replication forks, remains unclear due to publication of conflicting results. Using two different cellular models of BS, we showed that BLM deficiency is not associated with sensitivity to HU, in terms of clonogenic survival, DSB generation, and SCE induction. We suggest that surviving BLM-deficient cells are selected on the basis of their ability to deal with an endogenous replication stress induced by replication fork slowing, resulting in insensitivity to HU-induced replication stress.