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Timing of treatment may predict cancer cell response

DNA damage to cells caused by normal processes, smoking or sun exposure happens regularly during the process of making new DNA.

By Amy Wallace

Oct. 25 (UPI) -- A study at the University of North Carolina Lineberger Comprehensive Cancer Center found that the timing of DNA damage impacts the fate of cells, and could lead to new cancer treatments.

DNA damage to cells caused by normal processes, smoking or sun exposure happens regularly during the process of making new DNA.

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The study, published today in Cell Systems, showed that checkpoints within cells preventing them from dividing before damaged DNA can be repaired are ignored and, in the case of cancer cells, go on to divide with damaged DNA -- essentially spreading cancer.

Using time-lapse microscopy to study cells as they transition through cycle phases, UNC Chapel Hill researchers found cellular response to DNA damage during certain phases could be strong and halt the cycle, while in other phases cells were less sensitive or showed delayed progression.

The researchers found "commitment points" in cell phases that allow them to move forward to the next cycle regardless of unrepaired damage to DNA.

"It's very important to look at the timing of cell damage because depending on when it occurs within a certain cell cycle, there can be a totally different outcome," Sherry Chao, a graduate research assistant in the UNC School of Medicine Department of Genetics, said in a press release. "Some stages of the cell cycle are very vulnerable to DNA damage."

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Researchers used the information to create a mathematical model of how timing affects checkpoint behavior to show that exact timing of DNA damage determines checkpoint behaviors and can also change the outcome for damaged cells.

These new findings could create new treatment strategies for treating cancer.

"Conceptually, it makes sense that if you could get all of the cells in the same cycle at the same time, you could damage them all with one shot," Jeremy Purvis, UNC Lineberger member and assistant professor in the UNC School of Medicine Department of Genetics, said. "The key will be finding ways to separate cancerous and healthy cells based on the timing and synchronization of their cell cycles."

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