Research

Research in the Wang Lab focuses on defining how RNA splicing and modifications dysregulation contribute to the pathogenesis, evolution, and therapeutic vulnerabilities of B cell malignancies, with particular emphasis on chronic lymphocytic leukemia (CLL). A central theme of our work is to understand how aberrant post-transcriptional regulation reshapes gene expression programs in malignant B cells and their interactions with the tumor microenvironment.

We leverage integrative multi-omics approaches—including RNA sequencing, long-read and single-cell transcriptomics, proteomics, and epitranscriptomic profiling—to systematically map alterations in splicing factor activity and RNA modification machinery across disease states. Our studies aim to uncover how these alterations arise, how they are regulated at transcriptional and post-transcriptional levels, and how they drive oncogenic signaling, immune evasion, and therapy resistance. By combining computational discovery with functional validation in patient-derived samples and experimental models, we seek to establish causal links between RNA regulatory defects and malignant phenotypes.

The Wang Lab aims to translate mechanistic insights into clinically actionable strategies. Ongoing efforts focus on identifying RNA splicing events and RNA modification–dependent vulnerabilities that can serve as biomarkers or therapeutic targets, enabling more precise stratification and treatment of patients with CLL and related B cell malignancies.