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Many modern cancer drugs typically target a specific protein or signaling pathway to treat tumors. Now, researchers at the University of Michigan Health Rogel Cancer Center are taking a new approach by throwing a molecular wrench into the machinery driving prostate cancer. In preclinical studies, this new approach demonstrated greater antitumor activity while sparing normal cells.

The approach targets two proteins that work together to activate genes that fuel prostate cancer growth. Instead of blocking their interaction, researchers glued them together using a specially designed bifunctional small molecule, reprogramming the network of interactions between proteins. The result: greater antitumor activity than a combination of inhibitors targeting the two proteins separately, with less toxicity to normal cells.

"Our molecule acts like a molecular brace, connecting these two cancer-driving proteins in an abnormal configuration that traps them in an inactive state," said senior study author Arul M. Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology and S.P. Hicks professor of pathology at Michigan Medicine.

"This shuts down two oncogenic signaling pathways simultaneously, enabling highly effective killing of tumor cells while sparing normal cells. Our preclinical findings suggest that this approach could offer a more effective treatment strategy for prostate cancer," Chinnaiyan said.

The two proteins are the androgen receptor , or AR, and a helper protein called p300. The researchers call the new approach DALTAC, short for domain-alteration chimeras.

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