Chronic stress triggers a chain of molecular events that protects breakaway ovarian cancer cells from destruction.
In preclinical research, scientists found that heightened levels of the fight-or-flight stress hormones epinephrine and norepinephrine permit more malignant cells to safely leave the primary tumor, a necessary step in metastasis and cancer progression.
They also found that ovarian cancer patients face earlier mortality when a crucial protein activated by the hormones is present at high levels in their tumors and that patients with depression have higher levels of this activated protein.
Two promising approaches — directly silencing a crucial protein or using beta blockers to preempt its activation — worked in cell culture and mouse models, making them candidates for human use.
“Restoring cancer cells’ vulnerability to anoikis (a form of programmed cell death) would open a new avenue for suppressing tumor growth and metastasis,” says Anil Sood, M.D., professor in MD Anderson’s departments of Gynecologic Oncology and Cancer Biology and first author.
Reported in the May 3 issue of the Journal of Clinical Investigation.