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Anemia. 2012; 2012: 481583.
Published online May 24, 2012. doi:  10.1155/2012/481583
PMCID: PMC3368156
Targeting the Fanconi Anemia Pathway to Identify Tailored Anticancer Therapeutics
Chelsea Jenkins, Jenny Kan, and Maureen E. Hoatlin*
Department of Biochemistry and Molecular Biology, Oregon Health and Science University, 3181 SW Sam Jackson Parkway, Portland, OR 97239, USA
*Maureen E. Hoatlin: hoatlinm/at/gmail.com
Academic Editor: Henri J. Van De Vrugt
Received January 17, 2012; Accepted March 21, 2012.
Abstract
The Fanconi Anemia (FA) pathway consists of proteins involved in repairing DNA damage, including interstrand cross-links (ICLs). The pathway contains an upstream multiprotein core complex that mediates the monoubiquitylation of the FANCD2 and FANCI heterodimer, and a downstream pathway that converges with a larger network of proteins with roles in homologous recombination and other DNA repair pathways. Selective killing of cancer cells with an intact FA pathway but deficient in certain other DNA repair pathways is an emerging approach to tailored cancer therapy. Inhibiting the FA pathway becomes selectively lethal when certain repair genes are defective, such as the checkpoint kinase ATM. Inhibiting the FA pathway in ATM deficient cells can be achieved with small molecule inhibitors, suggesting that new cancer therapeutics could be developed by identifying FA pathway inhibitors to treat cancers that contain defects that are synthetic lethal with FA.
Articles from Anemia are provided here courtesy of
Hindawi Publishing Corporation