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Targeted treatment

Targeted treatment

A photonic crystal fiber condenses incoming laser light into ultra-short pulses that make fluorescently tagged molecules glow brightly. Bioengineering Associate Professor George Alexandrakis uses the method to monitor how individual DNA proteins interact with the DNA of cells damaged by radiation treatment.

Chemotherapy and radiation therapy have long been the most aggressive treatments available in the fight against cancer. Research in the Bioengineering Department may soon help these treatments become more effective in killing cancer at its roots.

Associate Professor George Alexandrakis has received grants totaling $1.2 million from the National Institutes of Health and the Cancer Prevention and Research Institute of Texas to determine how cells repair their DNA and how to use that knowledge to destroy cancer cells while sparing healthy ones.

“When you irradiate or give chemotherapy to a tumor, you inadvertently expose the healthy cells in which the tumor is embedded to the radiation or chemicals as well, which damages or kills those cells,” Dr. Alexandrakis explains. “We are looking for ways to kill more of the tumor and less of those healthy cells. To do this, we have to understand how it works and how DNA damage is repaired.”

George Alexandrakis

George Alexandrakis, bioengineering associate professor

Alexandrakis is collaborating with David Chen, director of the Molecular Radiation Biology Division in the Department of Radiation Oncology at UT Southwestern Medical Center at Dallas.

Using sub-cellular imaging, Alexandrakis tracks how cancerous cells damaged by radiation therapy work to repair themselves and applies that system to research focused on better cancer care. To do so, he makes a specific protein uniquely fluorescent within a cell. He then tracks that protein to see how it works in repairing the cell.

In the long run this should enable cancer treatment specialists to see how different variations of radiation and chemotherapy are working at very early stages and to make adjustments.

Researchers have found that as cells repair DNA, there are sometimes specific areas where the repair breaks down. The cell essentially bypasses a section of DNA and links the section before and the section after the sticking point. This sometimes causes more damage to the cell.

“If this damage happens once, it’s not a big deal. But if it happens millions of times, it can be a problem,” Alexandrakis says. “If we can identify where cancer cells get stuck when repairing DNA, we can insert a sensitizer to kill those cells without harming healthy ones. My work helps find those stalling points so biologists know where to target the sensitizer.”