Activating the G protein-coupled estrogen receptor (GPER)—a receptor found on the surface of many normal and cancer tissues—has been shown to stop pancreatic cancer from growing, but may also make tumors more visible to the immune system and thus more susceptible to modern immunotherapy. Researchers at the Perelman School of Medicine and the Abramson Cancer Center observed the effects of GPER activation in human and mouse pancreatic cancer models and published their findings in Cellular and Molecular Gastroenterology and Hepatology.
For most cancer types, including pancreas, women generally have better outcomes than men. Although the reasons for this are only now emerging, researchers have known for decades that there is a link between the body’s sex hormones and some types of cancer, especially those arising in reproductive tissues such as breast and prostate. However, the idea that cancers in non-reproductive tissues might also be influenced by sex steroid hormones has only recently been considered.
Building on their research showing the anti-cancer activity of GPER in melanoma models, Todd W. Ridky, an assistant professor of dermatology at and the study’s senior author, and his lab, examined whether GPER activators may also inhibit other cancer types.
“We know that activating GPER in melanoma models stops the growth of cancer cells and make the tumors themselves more immunogenic, so we wanted to find out what would happen if we selectively activated GPER other tumor types. In this study we examined several pancreatic cancer models and found that synthetic small molecule GPER activators potently inhibited pancreatic cancer cells, and simultaneously rendered the tumor cells more sensitive to other anti-cancer therapies,” Ridky says.
Read more at Penn Medicine News.
