Dangerous liaisons: Fanconi anemia and toxic nonhomologous end joining in DNA crosslink repair

Samuel F Bunting; André Nussenzweig

doi:10.1016/j.molcel.2010.07.016

Dangerous liaisons: Fanconi anemia and toxic nonhomologous end joining in DNA crosslink repair

Mol Cell. 2010 Jul 30;39(2):164-6. doi: 10.1016/j.molcel.2010.07.016.

Authors

Samuel F Bunting¹, André Nussenzweig

Affiliation

¹ Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.

Abstract

The proper choice of repair pathway is critical to tolerating various types of DNA damage. In a recent issue of Molecular Cell, Adamo et al. (2010), along with a second report (Pace et al., 2010), describe how the Fanconi anemia (FA) pathway is involved in preventing aberrant DNA repair. These studies suggest a potentially significant new opportunity for the treatment of FA.

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