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Duke Experiments Boost Radiation's Cancer-Killing Effects

or "hypoxic" do not respond as well to radiation and chemotherapy. Blocking HIF-1 production does not increase oxygen levels, but it does alter the behaviors that are caused by hypoxia.

Similarly, tumors with an intact tumor suppressor gene known as p53 respond more readily to radiation and to HIF-1 inhibition than tumors with a mutated P53 gene. Understanding such factors can aid scientists in determining the best conditions under which to inhibit HIF-1.
"We want to maximize the benefits of HIF-1 blockage while minimizing the drawbacks," said Moeller.

Moeller used a unique, targeted approach of blocking HIF-1 in cells to ensure that HIF-1, and not other proteins, was responsible for the effects they saw. He inserted a mutated form of HIF-1 into the cancer cell and turned it on and off by exposing it to the antibiotic tetracycline.

With this reversible switch, the team could observe the effects while HIF-1 was active and when it was blocked. Drugs to block HIF-1 have been used in previous studies conducted at Duke and elsewhere, but such drugs inhibit other proteins as well, making it impossible to distinguish which effects are related to HIF-1 and which are not.

The team's next step is to test the effects of blocking HIF-1 following chemotherapy. The research was funded by the National Cancer Institute, the Howard Hughes Medical Institute and the Aeolus Corporation.


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Source:DukeHealth


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