New research suggests that patients without a particular protein have a higher likelihood of surviving ovarian cancer.

Ovarian cancer is one of the five leading causes of cancer-related death in American women, according to the Ovarian Cancer Research Fund Alliance. Each year, over 14,000 women in the US die of ovarian cancer. While all women are at risk of ovarian cancer, those with a family history of ovarian, breast or colon cancer, post-menopausal women and women who have never been pregnant or given birth are more at risk.

In the UK, over 4000 women die of ovarian cancer each year, with more than 7000 women diagnosed each year, and the majority of those suffering from epithelial ovarian cancer. Slightly more than 50% are over the age of 65. Early diagnosis is crucial for increasing the likelihood of survival: chances of surviving for more than five years after diagnosis decrease from 90% with early detection to below 20% with late detection.

Researchers at the University of Northampton may have found an important chemical clue regarding survival rates for ovarian cancer patients. The scientists reviewed the cases of over 500 patients (194 cases of epithelial ovarian cancer treated at Nottingham University Hospitals and 360 cases that had been treated at Derby City Hospitals) and determined that those with no or very low levels of high-mobility group protein B1 (HMGB1) survived twice as long as those patients with tumors that produced high levels of this DNA binding protein. 

Specifically, in the ovarian cancer patients evaluated in this recent study, those whose tumors expressed HMGB1 had average survival times of about 4.5 years compared to nearly 9 years for those with tumors that did not express the protein or only expressed low levels. Nottingham patients with high levels of HMGB1 exhibited poor progression-free survival, while those from Derby had poor overall survival results.

The scientists have not yet determined how HMGB1 influences progression of the disease, but they have suggested that the protein may play a role in increasing the amount of energy produced by tumor cells. “This energy is then used by cancer cells to grow, multiply and ultimately spread throughout the body,” said Dr. Lee Machado, Associate Professor of Biochemistry at the University of Nottingham and lead author of the study.

In previously reported studies, HMGB1 was found to be involved in bowel, lung, liver and other types of cancers and appears to have the ability to protect cancer cells from stresses (e.g., chemotherapy) through a process known as autophagy, in which: “high levels of HMGB1 are also known to confer tumors with resistance to therapy and future studies should determine the exact mechanism of HMGB1 function in ovarian cancer. If this can be determined, then strategies designed to disrupt HMGB1 production may one day produce new therapies.”