Ping Mu

The paper identifies RUNX1T1 as a marker of lineage plasticity across cancers and shows that targeting the RUNX1T1-HDAC complex can suppress plastic cell growth.

ATHENA predicts functional genomic mutations and synergistic vulnerabilities in prostate cancer using deep learning, identifying driver events and therapeutic targets through integration with variant discovery pipelines.

This study identifies Notch signaling as a graded rheostat regulating lineage plasticity and therapy resistance in prostate cancer, showing that intermediate Notch activity maintains stem-like progenitor states and that modulating Notch levels can restore drug sensitivity.

This study identifies Notch signaling as a driver of lineage plasticity and therapeutic resistance in enzalutamide-resistant prostate cancer and shows its inhibition reverses resistance in vitro.

The paper identifies ectopic RUNX1T1 expression as a pan-cancer marker associated with lineage plasticity across multiple cancer types.

This study identifies TET2 activation in slow-cycling cells as a driver of prostate cancer progression through epigenetic changes and shows targeting TET2 suppresses tumor growth.

The paper introduces a Bayesian framework to map cell-cell interactions from spatial transcriptomics data, revealing new biological insights in cancer and immune responses.

This study shows ZNF397 loss leads to TET2-driven epigenetic changes, lineage plasticity, and resistance to AR-targeted therapies in AR-dependent cancers, with TET2 inhibitors reversing resistance.