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The researchers discovered that a protein called ETV4 plays a key role in how estrogen communicates with endometrial cancer cells. Estrogen sends pro-growth signals to the cells, and estrogen receptor carries out these signals. The study found that when ETV4 was removed from endometrial cancer cells, estrogen signaling was greatly reduced, subsequently leading to diminished tumor growth. “To our surprise, we found that ETV4 helped to promote estrogen signaling in two ways: first, it was telling estrogen receptor where to bind in the genome; and second, it was causing more estrogen receptor to be active,” said , a cancer researcher at HCI and assistant professor of oncological sciences at the U of U. Gertz’s lab led the study. “If we can find out what is causing ETV4 to be active, then we have a chance of reducing growth-promoting estrogen signaling in uterine tumors.”

Gertz’s lab used state-of-the-art genomics techniques and collaborated with several research teams with different expertise to expand the study. Using tissue from human tumors growing in mice, the team analyzed ETV4 and estrogen receptor in endometrial cancer. 

“Uterine cancer is the most common gynecologic cancer and the fourth most common cancer in Utah women,” says Gertz. “Unfortunately, this cancer is on the rise and there are limited treatments for the disease. We believe this study lays the groundwork for future research into ways of blocking estrogen signaling in endometrial cancer.”

The study was supported by the National Institutes of �����г���Ƶ/National Cancer Institute, including P30 CA042014; the National Institutes of �����г���Ƶ/National Human Genome Research Institute, including R00 HG006922 and R01 HG008974; and Huntsman Cancer Foundation. Other study contributors include the Barbara Graves, Bryan Welm, and Margit Janat-Amsbury labs.