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Replication at DNA damage sites highlights Fanconi anemia and breast cancer proteins
Date:9/10/2009

scientists have been following for many years is that all 13 genes must work together to deal with DNA crosslinks, that there must be some kind of cascade or chain reaction," Li said. "We developed a new genetic technique to look specifically at what proteins are present at the crosslinks."

New method yields answers

Using this new tool, researchers found that all the FA genes are present in the site of a crosslink. This is the first time FA proteins have been linked directly with DNA crosslinking damage at the molecular level.

"The surprise is that the breast cancer proteins, although they are present at crosslinks, must have DNA replication at the crosslinks," Li said. "If there is a DNA lesion on the genome but no DNA replication, the canonical FA proteins are used to deal with the damage. The breast cancer-related FA proteins are taking care of the DNA lesion that stops DNA replication."

Li said this leads to a new paradigm that there must be two separate subgroups or subpathways within the 13 FA genes.

"The major implication of this study is that now we have a new working model," Li said. "This provides a new direction for future research of breast cancer proteins and DNA damage response in general.

"Our next step is to continue to look at how FA proteins and the subgroup of breast cancer-related proteins help protect cells from DNA crosslink damage. And, in a more general sense, how these cellular mechanisms eventually may help us minimize mutations that ultimately lead to cancer."


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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