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Protein Molecule Corrects Double-Strand DNA Breaks

Small Ubiquitin-like Modifier (SUMO) protein holds potential for blocking the genetic mechanisms underlying breast and ovarian cancers.

In that mutations in the BRCA1 gene are associated with a high risk of breast and ovarian cancer and that BRCA1 participates in the DNA damage response, Joanna R. Morris, from Kings College London (United Kingdom), and colleagues have studied the role of a protein molecule known as the Small Ubiquitin-like Modifier (SUMO) in modulating the cellular response to genotoxic stress. The researchers found that the SUMO mechanism is able to repair double-strand DNA breaks affecting the BRCA1 gene, attaching itself to the damaged gene and switching it back on, thereby helping to prevent the formation of breast cancer.  Writing that: ”These data demonstrate that the SUMOylation pathway plays a significant role in mammalian DNA damage response,” the findings suggest a potential for the development of innovative approaches to stop the growth of cancerous cells.

Joanna R. Morris, Chris Boutell, Melanie Keppler, Ruth Densham, Daniel Weekes, Amin Alamshah, Laura Butler, Yaron Galanty, Laurent Pangon, Tai Kiuchi, et al. “The SUMO modification pathway is involved in the BRCA1 response to genotoxic stress.”  Nature 462, 886-890 (17 December 2009) doi:10.1038/nature08593 Article.

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