Michigan State University researchers have identified how the hormones progesterone and estrogen interact to increase cell growth in normal mammary cells and mammary cancers. Their study, led by Sandra Haslam, director of MSU’s Breast Cancer and the Environment Research Center, explains why postmenopausal women receiving hormone replacement therapy with estrogen plus progestin are at increased risk of breast cancer.
The discovery that both estrogen and progesterone or its synthetic compound, progestin, must be present for the increased production of the protein, amphiregulin, which binds to mammary cells and promotes cell growth, could lead to new treatment methods for breast cancer.
The study was published in Hormones and Cancer and was funded by the Department of Defense’s Breast Cancer Research Program.
Haslam states, “. . . breast cancers that develop in women receiving estrogen plus progestin are more invasive and deadlier.” Haslam and co-investigator, Anastasia Kariagina, a colleague in the College of Human Medicine and Department of Physiology, set out to determine why.
Haslam and Kariagina identified the protein, amphiregulin and its receptor as one potential reason. They found amphiregulin – acting through its receptor, epidermal growth factor receptor – along with progesterone leads to the activation of intracellular pathways that regulate cell growth. When activated, this promotes normal cell growth . . . and the growth of tumors.
The researchers performed the study on rats because breast cancers in rats contain receptors for estrogen and progesterone similar to the human breast and tumor growth is hormone-dependent, as are the majority of human breast cancers.
The research team found that a cancer drug called Iressa blocks the epidermal growth factor receptor effectively stopping the proliferation caused by amphiregulin. Although those studies were conducted only in cell cultures and not on tumors growing in animals, Haslam found the results promising.
Summing up, Haslam said, “The results indicate that the interactions between estrogen, progesterone and epidermal growth factor receptor pathways may be considered relevant targets for the treatment of hormone-dependent breast cancers. This may be especially important in premenopausal breast cancer because women produce their own estrogen and progesterone. A combined approach of inhibiting both the hormones and the epidermal growth factor receptor may be beneficial for some women in treating hormone-dependent breast cancer.”
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