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Grantee: Paraic Kenny, PhD
Institution: University of Wisconsin School of Medicine and Public Health
Area of Focus: Biochemistry and Immunology of Cancer
Term: The research described here was supported by an ACS grant that has ended.
“Our goal is to better understand the biology that underlies hormone-resistant breast tumors so that we may identify and validate appropriate targets for therapy.”
—Paraic Kenny, PhD
Some types of breast cancer are affected by hormones, like estrogen and progesterone. Those breast cancer cells have receptors that attach to estrogen and progesterone, which help them grow. Treatments that stop their attachment are called hormone therapy.
For instance, some drugs, including letrozole (Femara), keep estrogen from being made. Others, like tamoxifen (Nolvadex, Soltamox), keep estrogen from attaching to the receptors on the cancer cells.
Studies have shown that these drugs work in large part because they also suppress the effect of a substance called amphiregulin, which is found in normal, healthy cells. Amphiregulin helps normal cells grow, but it also helps hormone-positive cancer cells grow. Unfortunately, tumors can develop resistance to these successful hormone therapies, rendering them ineffective.
ACS grantee Paraic Kenny, PhD, recently published results of a mouse study showing that amphiregulin is closely linked to the growth of estrogen-receptor positive breast tumors. Importantly, these findings may provide a strategy to treat certain types of breast cancers
Why does it matter? This could mean drugs that reduce the effect of amphiregulin in hormone positive cancers could also be used to treat hormone negative cancers. For example, drugs that target amphiregulin in the future may be used to treat triple-negative breast cancer, which has many fewer treatment options available today.