Research

We study genomic instability in cancer: how tumors manage the immune consequences of their own broken chromosomes, and what that instability writes into the cancer genome. Three lines of work, one origin.

01

Extrachromosomal DNA

Oncogenes amplified on circular DNA that has no centromere, and how those circles survive cell division anyway.

02

APOBEC3A mutagenesis and cell state

An enzyme responsible for a large share of the point mutations in human cancer, and the rare cell state that switches it on.

03

Genomic instability and innate immunity

How cells detect their own DNA when it escapes into the cytoplasm, and how tumors keep that from happening.