UCSF researchers have discovered why drugs designed to target about one out of every four cases of breast cancer often fail to save women's lives or to stop these tumors from growing.
Due to genetic abnormalities, the breast cancers targeted by these drugs make unusually large amounts of a protein called HER2. HER2 relays signals within the cancer cells that drive tumor growth. Drugs are designed to inhibit the functioning of HER2 and prevent it from relaying these signals.
But for most women with HER2-driven tumors, these treatments do not work, or they keep the disease in check for only a limited time. Until now, researchers and clinicians have been mystified as to why treatments aimed at this promising target often fail to stop breast cancer growth.
UCSF breast oncologist and lab scientist Mark Moasser, MD
, and his colleagues now say they have identified a compensatory biochemical response that enables HER2-driven tumor cells to survive all but complete inhibition of HER2. The researchers reported their findings in the January 25 issue of the scientific journal Nature.
"It is much more difficult to stop tumor growth signals from HER2 than was previously thought," Moasser says. "But the discovery of the explanation for why this is so also points the way to much more effective therapies for HER-driven breast cancers. The road to the complete cure of this disease is now clearer than ever before."
Read more at Jeffrey Norris, UCSF Today