Research interests

My work focuses on:

• How do small chemical changes in chromatin control cell-type-specific gene regulation?
• How do diseases exploit or disrupt epigenetic mechanisms?

I study these questions using chemical biology approaches, pooled genetic screens, and integrated analysis of multi-omics data, connecting molecular features to regulatory outcomes and potential therapeutic vulnerabilities.

Current research

I study how cancer-associated mutations in histone proteins disrupt nucleosome function. In healthy tissue, histone proteins form protein–DNA complexes, the nucleosomes, that govern access to the underlying genetic information. Although there are roughly 16 million nucleosomes for every copy of the human genome, there are only a few dozen per gene which can be enzymatically modified to signal different gene activity states. Defective nucleosomes can cause aberrant gene expression or silencing, promoting hallmark cancer phenotypes such as unrestrained proliferation, migration, and invasion.

A key challenge is distinguishing innocuous from detrimental histone mutations. To address this, I create and screen libraries of cancer-associated histones in cells, use chemical synthesis to reconstitute defined nucleosome substrates, and integrate screening data with structural and clinical information to identify functionally meaningful patterns.

Past projects

Engineered proteins to detect rare combinatorial DNA modifications in mammalian genomes