Yu Chen

MYC drives endothelial transformation and dedifferentiation in angiosarcoma

This study shows MYC drives endothelial transformation and dedifferentiation in angiosarcoma by promoting lineage plasticity and cell growth.

Dependencies in heterogeneous, lineage plastic patient-derived prostate cancer organoids revealed through integrated single-cell multiomics and CRISPR screening

The paper integrates single-cell multiomics and CRISPR screening in prostate cancer organoids to reveal lineage-specific dependencies and heterogeneity effects on gene essentiality.

Cell-Autonomous AR Dependence in Luminal Prostatic Epithelium Governs Survival and Lineage Plasticity

This study shows that luminal prostatic epithelial cells depend on AR signaling for survival and differentiation, and their loss triggers compensatory pathways and lineage plasticity.

PRC2 Restricts Malignant Peripheral Nerve Sheath Tumorigenesis in a Genetically Engineered Mouse Model of MPNST

This study shows that PRC2 inactivation promotes MPNST by reprogramming Schwann-lineage cells and presents a mouse model that recapitulates human PRC2-loss MPNST.

Genomic alterations in the YAP/TAZ pathway are associated with stem cell-like castration-resistant prostate cancer

The paper identifies genomic alterations in the YAP/TAZ pathway associated with stem cell-like castration-resistant prostate cancer using transcriptomic and whole-genome sequencing data.

TAD hierarchy restricts poised LTR activation and loss of TAD hierarchy promotes LTR co-option in cancer

The paper shows that TAD hierarchy restricts LTR activation, and its loss in cancer allows LTRs to act as alternative promoters, driving oncogene activation and transcriptional diversity.

BET inhibitors as a therapeutic intervention in gastrointestinal gene signature-positive castration-resistant prostate cancer.

This study identifies BET inhibitors as effective against GI transcriptome-positive CRPC by targeting HNF1A and HNF4G, improving outcomes in preclinical models.

Loss of Kmt2c/d promotes gastric cancer initiation and confers vulnerability to mTORC1 inhibition and anti-PD1 immunotherapy

This study shows that loss of Kmt2c/d promotes gastric cancer initiation and makes tumors sensitive to mTORC1 inhibitors and anti-PD1 immunotherapy.