ABOUT US
We are a close-knit group of hard working scientists at the University of Michigan Medical School who are dedicated to studying the genes and pathways that drive hematopoietic regeneration and malignancy.
OUR VISION
There is an urgent need to develop the first targeted agents to treat children with T-cell acute lymphoblastic leukemia (T-ALL). There are no viable agents to treat T-ALL beyond initial chemotherapy. Recent multi-omic studies have identified high-risk T-ALL subtypes with diverse genetic alterations, but finding shared transcriptional networks that drive these cancers has been challenging. This is a key knowledge gap as shutting down these networks might be an efficient way to treat these cancers that complements targeting of specific genetic lesions. Our work shows that T-ALL cancers hijack native transcriptional networks that are normally important for T-cell development and regeneration. Thus, our vision is that elucidating these networks in normal and malignant lymphoid cells will establish the basic science foundation for strategies that target the unifying stem cell and developmental states of these aggressive cancer cells.
OUR RESEARCH INTERESTS
· Early T-cell Precursor and T-cell leukemogenesis
​
· Transcriptional network analysis of oncogenes and oncogenic enhancers
​
· Protein-protein interactions of oncogenic transcriptional complexes
​
· Phase separation of ordered transcriptional regulatory structures
​
· Transcriptional regulation of early T-cell development
​
· T-cell regeneration after cytoreductive therapies like chemotherapy and bone marrow transplantation
​
· Genetically engineered mouse and human models of thymopoiesis and leukemogenesis
​
· Transcriptional genomics and enhancer profiling
​
· Gene editing of oncogenes and enhancers
​
· Preclinical anti-leukemic drug testing
NEWS
February 19, 2025 -- Out today! Qing (Alice) Wang leads our collaborative effort with the Iannis Aifantis, David Teachey, Kai Tan, and Charles Mullighan groups in identifying a shared stem cell network that drives the newly appreciated high-risk ETP leukemia subsets.

OUR SUPPORT











