Felix Yi-Chung Feng

This study quantifies cancer stemness in prostate cancer across progression stages, showing its association with therapy resistance, poor survival, and lineage plasticity.

This paper expands structural surfaceomics to identify cancer-specific protein conformations across multiple tumor models, revealing potential immunotherapy targets through crosslinking mass spectrometry and structural modeling.

ProPer-seq is a cost-effective, barcode-free single-cell perturbation profiling method that enables scalable analysis of synthetic biology perturbations and reveals transcriptional control principles.

This study uses CRISPR screens to identify PTGES3 as a novel modulator of AR protein levels and function in prostate cancer, showing its role in therapy resistance.

The paper identifies a subgroup of mCRPC characterized by LINE1 repeat DNA elements flanking the AR gene, which drive AR overexpression and confer resistance to androgen signaling inhibitors.

This study identifies PCAHIT, a lncRNA linked to poor outcomes in prostate cancer, showing it promotes aggressive phenotypes by affecting steroid biosynthesis and immune response.

This study develops an in vivo platform called SETs to reconstruct tumor evolution without chromosomal instability, identifying therapeutic response determinants in prostate cancer.

This study identifies canonical AREs as tumor suppressive regulatory elements in prostate cancer, showing their reactivation can induce death in AR+ cancer cells and is linked to better prognosis.

This study shows CDK12 loss drives prostate cancer development and identifies CDK13 as a therapeutic target through paralog-based synthetic lethality in CDK12-mutant tumors.

MechRNA predicts lncRNA mechanisms by integrating RNA-RNA and RNA-protein interaction predictions to identify potential targets and mechanisms for cancer-related lncRNAs.