Smart Doctor: Triple-negative breast cancer (TNBC) is gaining research traction in Asia-Pacific. What’s fueling this surge, and how could it reshape global research dynamics?
Sarah Rose Anderson: The rise of TNBC research in the Asia-Pacific (APAC) region is both significant and strategic. A major driver is access to a vast and genetically diverse patient population. Countries like China and India have seen increasing breast cancer incidence, which naturally supports the growth of region-specific research. This diversity is crucial when investigating a disease as heterogeneous as TNBC.
But there’s more to it. Over the past decade, countries like Japan, South Korea, and Singapore have made major investments in biotech infrastructure and clinical trial capacity. These governments have introduced policies to support research while keeping operational costs comparatively low. That combination—population access and efficient infrastructure—makes APAC incredibly attractive for oncology trials.
Ultimately, this regional momentum signals a broader shift. Global oncology research is becoming more inclusive and balanced. APAC’s emergence is not just helping accelerate progress against TNBC but also contributing to the global cancer research ecosystem in a meaningful way.
SD: TNBC has long posed therapeutic challenges. How are emerging biomarkers—like BRCA1/2, PD-L1, and FGFR—reshaping treatment strategies and improving outcomes?
Sarah Rose Anderson: TNBC is notoriously aggressive and difficult to treat, primarily because it lacks estrogen, progesterone, and HER2 receptors—making conventional hormone and HER2-targeted therapies ineffective.
But biomarkers are changing the game. BRCA1/2 mutations, for instance, are among the best-known markers in TNBC. These mutations compromise the DNA repair mechanisms of cancer cells, rendering them vulnerable to PARP inhibitors. This class of targeted therapies has shown strong efficacy while sparing healthy cells—a big leap forward.
Then we have PD-L1 expression, which is opening doors to immunotherapy. Immune checkpoint inhibitors targeting the PD-L1 protein work by reactivating immune responses that cancer cells typically evade. For TNBC, where options have historically been scarce, this is an exciting frontier.
FGFR amplification is a newer, but equally promising, target. The FGFR signaling pathway is implicated in tumor growth and survival. Inhibitors targeting FGFR are being actively explored in clinical trials. While still in early stages compared to BRCA- or PD-L1–guided therapies, FGFR-directed treatments may prove invaluable— especially for patients with resistance to existing therapies.
SD: Do you have any final thoughts?
Sarah Rose Anderson: The convergence of molecular insights and regional clinical capacity is driving a new era in TNBC research. We’re not just expanding treatment options—we’re tailoring them. With APAC’s growing role and biomarker-driven innovations, we’re getting closer to delivering precision oncology to every corner of the world.
