Novel method identifies new oncogene that contributes to development of cancer

A team of researchers at Case Western Reserve University School of Medicine, led by Dr. Mark W. Jackson, have developed a novel method to identify genes that, when overexpressed, make normal cells behave like cancer cells. Using this method, the Jackson laboratory has identified a new oncogene, which is a gene that contributes to the development of cancer, named FAM83B.

"We made our discovery in a model of breast cancer," said Mark W. Jackson, Ph.D., Assistant Professor, Department of Pathology, Case Western Reserve University School of Medicine, Case Comprehensive Cancer Center. "Using an unbiased screening approach, we let the biology of cancer formation tell us what genes are important and FAM83B was one of the genes that came out of our screen. When FAM83B was overproduced in normal breast cells, it transformed the normal cells, causing them to behave like breast cancer," stated Jackson.

There are relatively few oncogenes that are critical to breast cancer growth, and only one other breast cancer oncogene has been identified in the last 6 years. Breast cancers are classified clinically into subgroups based on the presence of specific proteins, including estrogen receptor (ER), progesterone receptor (PR), and HER2.

"Analysis of breast cancer revealed that elevated FAM83B expression is associated with the more aggressive, triple negative subgroup which lacks ER, PR and HER2," said Jackson. "In short, patients with triple-negative breast cancer would benefit most from the development of new therapeutics."

Novel oncogenes provide opportunities for drug development that may expand the number of therapies available for eradicating cancer and extending the life of patients. "Our discovery provides the foundation for developing new therapies that can inhibit FAM83B in these aggressive cancers, which have traditionally been difficult to treat." We are currently trying to identify drugs that that can inhibit the function of FAM83B." stated Jackson.