Scientists Discover Molecule That Stops Aggressive Breast Cancer in Its Tracks

For the roughly 15 percent of breast cancer patients diagnosed with the triple-negative subtype, the prognosis has long been grim. Triple-negative breast cancer (TNBC) is among the most aggressive forms of the disease, grows quickly, spreads easily, and responds to almost none of the targeted therapies that have transformed outcomes for other breast cancers.

Now, a team at Oregon Health & Science University (OHSU) has published findings that could change the story. In a study published in the journal Cell Reports Medicine, researchers describe a newly developed molecule called SU212 that targets and destroys a key enzyme driving cancer growth — and in preclinical testing, it stopped triple-negative tumors in their tracks.

Targeting the Fuel Supply

The molecule works by attaching to an enzyme called enolase 1, or ENO1. Under normal conditions, ENO1 helps cells convert glucose into energy — a fundamental metabolic process. But cancer cells, which have voracious energy demands to fuel their rapid growth, produce ENO1 in unusually high amounts.

Once SU212 binds to ENO1, it causes the enzyme to break down. Without this critical metabolic component, cancer cells lose access to the energy pathway they depend on to survive and spread. In experiments using a humanized mouse model designed to mimic human triple-negative breast cancer, the molecule reduced tumor growth and limited metastasis.

"It's an important step forward to treat triple-negative breast cancer," said senior author Sanjay V. Malhotra, Ph.D., co-director of the Center for Experimental Therapeutics in the OHSU Knight Cancer Institute. "Triple-negative breast cancer is an aggressive form of cancer and there are no effective drugs available right now."

Why Triple-Negative Is So Hard to Treat

Most breast cancers can be classified by the receptors found on their cell surfaces — estrogen receptors, progesterone receptors, or HER2 proteins. These receptors serve as targets for highly effective therapies like tamoxifen and trastuzumab (Herceptin). Triple-negative breast cancer, as the name suggests, lacks all three of these markers, leaving oncologists with far fewer treatment options.

Patients with TNBC typically rely on chemotherapy, which is effective for some but comes with severe side effects and doesn't work for everyone. The five-year survival rate for metastatic TNBC remains below 15 percent — a statistic that has barely budged in decades.

A Broader Potential

What makes SU212 particularly promising is that the mechanism it exploits — cancer cells' dependence on overproduced metabolic enzymes — isn't unique to breast cancer. Malhotra noted that the same strategy could potentially be applied to other cancer types that show elevated ENO1 levels, including certain lung, liver, and pancreatic cancers.

"We're not just looking at one disease," Malhotra said. "We're looking at a vulnerability that many cancers share."

The Road Ahead

SU212 is still in the preclinical stage, meaning it has not yet been tested in human patients. The next steps will involve moving the molecule toward clinical trials — a process that requires significant resources, FDA approval, and studies involving patients.

But for a disease that has long been considered one of oncology's most stubborn challenges, SU212 represents exactly the kind of breakthrough that patients and researchers have been waiting for: a new angle of attack against a cancer that has resisted nearly everything thrown at it.

For the thousands of women diagnosed with triple-negative breast cancer each year, the message from Oregon is one of cautious but genuine hope: science is closing in.