Lab studies find two drug targets in triple-negative breast cancer

In three-dimensional tumor models, researchers at the National University of Singapore found a molecular switch that helps aggressive breast cancer cells keep growing, spreading and resisting treatment. The switch, called DP103, was tied to triple-negative breast cancer, or TNBC—the subtype that lacks hormone receptors and HER2 proteins targeted by many existing therapies. An investigational drug, RX-5902, slowed that process in laboratory tests.

The NUS team, led by Research Assistant Professor Alan Prem Kumar, traced DP103 to the Wnt signaling pathway, a cancer-promoting chain of molecular signals. The researchers also tested human breast cancer cells, patient-derived data sets and human tumor organoids—three-dimensional models grown to better mimic tumors. Across 21 samples, RX-5902 reduced cancer stem cell viability by 40% to 60%, while growth in laboratory-grown tumor models fell by about 50%.

The second study, from Adelaide University and the Olivia Newton-John Cancer Research Institute, focused on metastasis: the spread of cancer to distant organs. The researchers found that low levels of the naturally occurring molecule miR-342 were associated with high E2F activity and a greater likelihood of metastatic disease. Restoring miR-342 reduced spread to the lungs and bones in preclinical models. The team also found that palbociclib, a CDK4/6 inhibitor already used for advanced hormone receptor-positive breast cancer, reduced metastatic tumor growth in models with low miR-342.

And so what, concretely? These results suggest that some patients with TNBC might eventually be selected for treatment using a tumor marker: high DP103 could identify people most likely to benefit from RX-5902, while low miR-342 could point to a subgroup that might respond to palbociclib. That could turn a biologically diverse disease into smaller groups matched to drugs, rather than treating every patient identically.

The distance to clinical care remains substantial. The Singapore study reported around 90% tumor-size reduction in laboratory models and longer survival in treated models, while the Australian researchers say their next step is validation in patient-derived preclinical models before clinical trials. The findings are promising laboratory evidence, not proof that either strategy improves survival in people; larger cohorts and human studies still have to establish who benefits and how durable the effect is.