Prostate Cancer Breakthrough — Epigenetics Driving New Treatments
The dailysciencedigest’s Podcast
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Show Notes
Prostate cancer breakthrough: how epigenetics is reshaping prostate cancer treatment and precision oncology New cancer research podcast episode uncovering how the KMT2D enzyme controls prostate cancer subtypes and hormone therapy resistance Understand how targeting KMT2D and epigenetic regulation could improve androgen deprivation therapy response and unlock new prostate cancer breakthroughs
What You'll Learn:
- How KMT2D functions as a central epigenetic regulator in prostate cancer and why it matters for tumor growth and survival
- The connection between KMT2D mutations or over-activity and their prevalence in primary (~7–10%) versus metastatic (~15%) prostate cancer cases (TCGA & SU2C datasets)
- Why KMT2D activity influences prostate cancer subtypes and contributes to hormone therapy resistance and treatment failure
- What organoid and CRISPR models reveal about restoring sensitivity to drugs like enzalutamide and how this could reshape prostate cancer treatment strategies
- How the H3K4-methyl transfer activity of KMT2D depends on its 4,500-aa SET domain and how a single Y5370C point mutation can abolish this enzymatic function
- Practical implications of this research for improving androgen deprivation therapy, overcoming resistance, and designing more precise, epigenetics-informed treatment plans
- Where KMT2D fits into the broader landscape of epigenetics and cancer, and what it tells us about future directions in precision oncology and prostate cancer breakthroughs
About the Guest:
About the Guest: Wouter Karthaus is head of the Endocrine Therapy Resistance and Molecular Genetics Lab at EPFL, where he leads cutting-edge research into how prostate tumors adapt and resist standard treatments. Along with co-lead investigator Eneda Toska of Johns Hopkins University, he focuses on the epigenetic and molecular mechanisms that drive hormone therapy resistance and metastatic progression in prostate cancer.