Scientists have identified a long-sought gene that is fatefully switched on in 30 to 40 percent of all breast cancer patients, spreading the disease, resisting traditional chemotherapies and eventually leading to death.
The gene, called 'Metadherin' or MTDH, is situated in a small region of human chromosome 8 and appears to be crucial to cancer's spread or metastasis because it helps tumour cells stick tightly to blood vessels in distant organs.
The gene also makes tumours more resistant to the powerful chemotherapeutic agents normally used to wipe out the deadly cells.
In identifying the genetic mechanism at play in the metastasis of breast cancer, researchers at Princeton University and The Cancer Institute of New Jersey may have answered one of the biggest mysteries in cancer research and paved the way for new drugs that could thwart the gene's diabolical actions.
"Inhibiting this gene in breast cancer patients will simultaneously achieve two important goals - reduce the chance of recurrence and, at the same time, decrease the risk of metastatic dissemination. Clinically, these are the two major reasons why breast cancer patients die from the disease," said Yibin Kang, an assistant professor of molecular biology at Princeton, who led the study.
According to co-author Michael Reiss, director of the Breast Cancer Research Program at The Cancer Institute of New Jersey, the discovery is important for several other reasons,
"Not only has a new metastasis gene been identified, but this also is one of a few such genes for which the exact mode of action has been elucidated. That gives us a real shot at developing a drug that will inhibit metastasis," said Reiss, also a professor of medicine, molecular genetics and microbiology at UMDNJ-Robert Wood Johnson Medical School.
The discovery is based on three years of work, using an approach that combines the emerging science of integrative genomics with the classical methods of clinical research and laboratory experiments.
The study appears in the Jan. 6 edition of Cancer Cell.