Chronic psychological stress exacerbates the growth and spread of ovarian cancer in a mouse model, an effect that commonly prescribed heart medications can cancel out. If the same holds true for humans, behavioral or pharmacological interventions may someday be used to slow the progression of this often-deadly disease.

Ovarian cancer is the eighth most common type of cancer among American women. Its vague and nonspecific symptoms make it notoriously tricky to diagnose; indeed, in more than half of cases diagnosis is delayed until the disease has already spread beyond the ovary, making it difficult, if not impossible, to treat. A better understanding of the mechanisms underlying disease progression would go a long way to solving this problem.

Several years ago, Anil K. Sood of the University of Texas M.D. Anderson Cancer Center (Houston, TX) and Susan Lutgendorf of the University of Iowa (Iowa City, IA) found that ovarian cancer patients who reported higher distress levels had elevated circulating levels of vascular endothelial growth factor (VEGF) compared to women under less stress. This signaling protein is involved in the formation of new blood vessels and plays an important role in the angiogenesis necessary for tumor growth and spread. To determine if stress levels were somehow affecting cancer progression, Sood's team turned to a mouse model for answers.

In a new study published in the August issue of Nature Medicine, Sood and his fellow researchers first sought to mimic chronic high stress conditions by immobilizing mice in a small enclosure for 2 or 6 hours daily. This caused significant increases in levels of the 'fight-or-flight' hormones norepinephrine and corticosterone. The researchers then inoculated chronically 'stressed' and 'unstressed' nude mice with human ovarian cancer cells. Three weeks later, not only did stressed mice show 2–3 fold elevations in VEGF, but they had more than twice the number of tumor nodules than controls. In addition, in more than half of the stressed mice the cancer had spread to the liver or spleen, while it remained confined to the peritoneal cavity in all of the unstressed animals.

After determining that 17 of the 19 ovarian cancer cell lines tested expressed stress hormone receptors (which, when activated tell the cell to produce VEGF), Sood's team examined the consequences of blocking these β-adrenergic receptors. In mice treated with the 'β-blocker' propranolol, the drug seemed to nullify the effects of the stress on cancer progression.

Building on these promising results, Sood tells Lab Animal that his team now “intends to investigate other biological pathways in the context of cancer that could be affected by chronic stress” and to look at “how frequently these receptors are expressed by human ovarian cancers.”