AI Insight
New research from UT Southwestern Medical Center shows that the glucocorticoid receptor (GR), which responds to the body's primary stress hormone cortisol, plays a previously unrecognized role in ovarian cancer. When GR is activated in ovarian cancer cells, it modifies the tumor microenvironment in ways that suppress immune responses, potentially allowing the tumor to evade detection and destruction by the immune system. These findings were published in the journal Endocrinology.
Why it matters
Understanding how stress hormone signaling helps ovarian cancer cells escape immune surveillance could open new therapeutic avenues, such as targeting GR activity to restore anti-tumor immune function in patients with this often late-diagnosed and difficult-to-treat cancer.
When activated in ovarian cancer cells, the receptor for the body’s primary stress hormone alters the tumor environment in ways that blunt immune response, according to new research led by UT Southwestern Medical Center. The findings, published in Endocrinology, identify a previously unrecognized role for the glucocorticoid receptor (GR) in shaping the ovarian cancer tumor microenvironment.
Source: Ovarian cancer cells use stress hormone signaling to shut down immune system, research reveals