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Unchecked DNA replication drives earliest steps toward cancer

an normal through this mechanism."

Fortunately, cells have an effective on-board damage control system, managed by the p53 gene. A protein called 53BP1, the critical role of which was reported by the same Wistar group in Nature last year, senses the DNA breaks caused by replication stress and activates the p53 pathway. That pathway shuts down the replication process, thus limiting further DNA damage. In some circumstances, p53 may even force the cell into apoptosis, or programmed death, as a way to protect against the cell developing into a tumor.

If the mutations occur in p53 itself, however, or the p53 pathway is unable to completely halt the process, further mutations will occur, leading the cell to become cancerous, with the number of mutations constantly growing. So, when p53 remains intact, it is often able to prevent cancers from developing. When it suffers damage itself, cancers commonly result, explaining why p53 mutations are so frequently seen in so many different cancers.

Halazonetis notes that the same techniques used in his experiments to monitor replications stress and DNA breaks could also be used as an effective diagnostic tool to identify precancerous cells.

"The presence of DNA breaks in precancerous and cancer cells may turn out to be the Achilles heel of cancer," Halazonetis says. "It might be possible to inhibit repair of these DNA breaks, in which case the cancer cells would die."

The lead authors on the Nature study are Vassilis G. Gorgoulis and Leandros-Vassilios F. Vassiliou at the University of Athens. In addition to senior author Halazonetis, the Wistar-based coauthors on the study are Monica Venere, Richard A. DiTullio, Jr., both also affiliated with the University of Pennsylvania, Akihiro Yoneta, and Meenhard Herlyn, D.V.M., professor and leader of the molecular and cellular oncogenesis program at Wistar. The remaining coauthors are Panagiotis Karakaidos, Panayotis Zacharatos, Athanassios Kotsinas
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Source:The Wistar Institute


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