Fanconi anemia is characterized by hypersensitivity to DNA interstrand crosslinks (ICLs) and susceptibility to tumor formation. Despite the identification of numerous Fanconi anemia (FANC) genes, the mechanism by which proteins encoded by these genes protect a cell from DNA interstrand crosslinks remains unclear. The recent discovery of two DNA helicases that, when defective, cause Fanconi anemia tips the balance in favor of the direct involvement of the FANC proteins in DNA repair and the bypass of DNA lesions.
Bibliographical noteFunding Information:
We apologize for the limited number of references due to space limitations. A.S.L. and J.H.J.H. are supported by the Dutch Cancer Society, the EC, the NIH, and the Netherlands Organization for Scientific Research (NWO). L.J.N. is supported by the University of Pittsburgh Cancer Institute and the NCI (K22-CA111525).