Bobae Park, PhD

The Challenge of Prostate Cancer Evolution

Prostate cancer remains a leading cause of cancer-related mortality, primarily due to its inevitable progression into lethal Castration-Resistant Prostate Cancer (CRPC). The defining clinical challenge in treating advanced CRPC is the tumor's extraordinary heterogeneity and biological adaptability. Under intense therapeutic pressure from androgen receptor (AR)-targeted therapies, these cancer cells exploit lineage plasticity—undergoing epithelial-mesenchymal transition (EMT) and shifting into aggressive, treatment-evasive subtypes such as Neuroendocrine Prostate Cancer (NEPC). This dynamic evolution not only renders standard therapies ineffective but also creates profound spatial and temporal heterogeneity, complicating diagnosis and patient monitoring.

Research Focus

Dr. Bobae Park is dedicated to uncovering novel metabolic and hormonal mechanisms to suppress CRPC. A major focus of work established the oxysterol sulfotransferase (aka SULT2B) as a pivotal negative regulator of prostate cancer, demonstrating that its restoration significantly arrests aggressive tumor growth and reshapes the innate and adaptive immune cells dynamics at tumor microenvironment. Additionally, she discovered a synergistic interplay between physiologic doses of androgen and vitamin D that effectively inhibits CRPC progression by inducing ferritinophagy-mediated ferroptosis, providing a new mechanistic rationale for combination endocrine therapies.

Future Directions

Dr. Park’s future research vision centers on combating the therapy-induced evolution of prostate cancer within the skeletal microenvironment. Currently, she is focusing on investigating the phenomenon of spontaneous cell-cell fusion driven by Androgen Receptor Signaling Inhibitors (ARSIs) such as clinically active enzalutamide. By elucidating how tumor-macrophage hybrid (TMH) cells, generated by therapeutic pressure, remodel the bone niche and amplify osteolytic progression, Dr. Park hopes to establish TMHs as therapeutic targets for ARSI-resistant prostate cancer and to uncover new therapeutic vulnerabilities that can overcome treatment resistance by blocking lineage plasticity.