Pei‐Chi Wei

The paper identifies replication environments associated with DNA breakage in cancer cell lines by integrating genomic and transcriptomic data.

This study identifies recurrent DNA break clusters (RDCs) as causal factors for CNV formation under replication stress and shows DNA polymerase theta's role in preventing these events.

The paper investigates NSPC proliferation dynamics in a mouse model, finding that adaptive clonal expansion by a small fraction of NSPCs can regenerate the entire neuronal population.

The paper investigates how strand-asymmetric processes like replication and transcription influence DNA damage, repair, and mutagenesis, revealing mechanisms that shape cancer genome evolution.

The paper investigates DNA break dynamics at recurrent DNA break clusters (RDCs) in mouse neural progenitor cells, revealing how replication-transcription collisions influence DSB formation and orientation.

The paper investigates RDC-gene breakage in neural progenitor cells derived from embryonic stem cells, finding that many RDCs in primary NSPCs are developmentally influenced and appear in cultured NPCs.