Synthesis a Publication of UC Davis Cancer Center

Wrench in the machinery
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Like healthy cells, cancer cells, too, have the capacity to repair themselves. The most malignant heal themselves even after assaults from the most potent weapons medicine can deploy. If Heyer can find a way to disable the DNA repair machinery in cancer cells, he will render malignant cells more vulnerable to medical treatment. “Radiation and chemotherapy kill cancer cells,” the molecular biologist says. “If we can stop repair, we can kill them quicker.”

Heyer’s large laboratory in the Life Sciences Addition on the Davis campus is a quiet, modern space. New-age piano music emanates from a portable stereo. An inflatable plastic tyrannosaurus, a shark and a cheetah, reminders of evolution and biodiversity, hang from the ceiling.

The laboratory, which employs 10 research scientists and three undergraduate students, is a hub of DNA repair research at a university known for its work in the field. When UC Davis Cancer Center and Lawrence Livermore National Laboratory three years ago formed a cancer research partnership — the first such partnership in the nation — DNA repair groups at the two institutions joined forces, becoming one of the strongest such groups in the country.

Almost from the initial discovery of the double helix structure of DNA by Watson and Crick in the 1950s, it was apparent that damage in one strand of the double helix could easily be repaired, with the other strand serving as a template. But the field of DNA repair didn’t take off until the late 1980s and early 1990s. “In the last 10 years we have seen a phenomenal increase in understanding of the molecular detail of the repair process,” Heyer says. “We now know probably most of the key players, what most of them do and how they interact. We know they all cooperate, they all work in concert, they all talk to each other.”

Edwin Hjaghnazari, a researcher in Heyer’s lab, uses a plasmid gap repair assay to investigate DNA repair.