Activating a specific estrogen receptor may stop pancreatic cancer cells from growing and make the tumors more visible to the immune system. (2020)
From the article:
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.
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Using new PCRC mouse pancreatic cancer models, the multidisciplinary team was able to show GPER’s [G protein-coupled estrogen receptor] impact on pancreatic cancer growth. In some models, GPER [G protein-coupled estrogen receptor] activation inhibited growth and made tumors more sensitive to anti-PD-1 immunotherapy, pointing to the translational potential of improving the efficacy of existing treatments in a cancer type where PD-1 inhibitors have not historically been very effective.
The use of GPER activators is a novel idea in cancer therapy, and has a key difference from most anti-cancer agents. Nearly all current cancer drugs act to block the activity of cellular proteins that are needed by not only the cancer cells, but also by normal cells. As a result, most cancer drugs are associated with major toxicity. In contrast, the estrogenic analog used in the Penn study activates GPER. This approach mirrors something that naturally occurs in the body, as GPER is already present and normally activated by estrogen, especially in females during pregnancy.
“Likely because this is something the human body is already accustomed to, evidence from preclinical animal studies suggested that side effects to this approach would likely be minimal when this moves into the clinic,”