• Co-targeting MCL1 + BCLXL induces strong apoptotic responses in patient-derived and mouse prostate cancer models

This opens new therapeutic possibilities for advanced disease.

Why this matters:
• MCL1 is highly expressed and linked to poor outcomes in lethal PCa
• Careful methodological validation is essential when studying MCL1 (siRNA screens!)
• Targeting MCL1 drives apoptosis in a subset of models

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Thanks for the support throughout this project and beyond! @prostateukprofs.bsky.social

Thank you, Craig!

These results highlight the power of predictive biomarkers to guide precision medicine and pave the way for biomarker-driven clinical trials in advanced prostate cancer.
Huge thanks to everyone involved!
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🔵 MCL1 + AKT inhibition synergistically induces apoptosis in PTEN-loss/PI3K-activated models → patients with these aberrations may benefit most.
🔵 CDK9 inhibition (fadraciclib) + AKT blockade mirrors MCL1i+AKTi combination effects, offering another therapeutic strategy.
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We investigated the role of MCL1, a key anti-apoptotic protein, in lethal prostate cancer.

Key findings:
🔵 MCL1 copy number gain occurs in a subset of patients → more aggressive disease & poorer outcomes.
🔵 MCL1-targeted monotherapy may benefit these patients.
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Thank you, Ana! Enjoy London!