A new study has reported a method for reducing the reduced immune system functioning and metastatic progression that can occur after breast cancer surgery. There is some evidence that surgical procedures can impair the immune system temporarily and promote postoperative infections and cancer metastasis. Catecholamines and prostaglandins were recently implicated in these processes and in directly promoting tumor angiogenesis and invasion. Catecholamines, including epinephrine, norepinephrine, and dopamine, are "flight or fight" hormones produced by the adrenal glands in response to various forms of stress. Prostaglandins are hormone-like substances that participate in a wide variety of functions, including inflammation.

The two treatments tested in the present study were (1) administration of the immunostimulant CpG-C; and (2) suppression of the tumor-promoting and immunosuppressing effects of catecholamines (with propranolol) and prostaglandins (etodolac). To conduct the study, rats were intravenously inoculated with mammary cancer cells and were treated before surgery with either (1) CpG-C; (2) propranolol plus etodolac; or (3) CpG-C, propranolol and etodolac. Blood was drawn from the rats, marginating-pulmonary leukocytes were harvested, and natural killer cell (NK) activity and lung metastases were measured. In a separate study, other mice were implanted with melanoma cells. When the melanoma tumor in a given mouse reached 100 mm3 in size, the mouse was treated with CpG-C. Twenty-four hours later, the tumor was surgically removed, and the mouse was treated with propranolol plus etodolac. The mice were monitored thereafter and recurrence-free survival was assessed.

When administered separately, both CpG-C and propranolol plus etodolac resulted in improvements in most of the measures examined, including long-term recurrence-free survival rates. Importantly, combining the CpG-C and propranolol plus etodolac treatments resulted in additive or synergistic effects. The combination was found to enhance tumor clearance from the lungs and increase natural killer cell numbers and cell death by means of different, but complimentary, mechanisms. The authors conclude that treatment around the time of surgery aimed at enhancing cell-mediated immune response and simultaneously inhibiting excessive catecholamine and prostaglandin responses, could be successful in limiting postoperative immunosuppression and metastatic progression.