We develop single-cell multi-omics technologies and computational methods to decipher cancer development. Contact us to learn more!
We identified that the effects of somatic mutations vary as a function of cell identity in myeloid neoplasms (Nam, Kim, Chaligne, et al, Nature, 2019). We seek to understand the cell identity-defining mechanisms that cause the variabilities in the impact of somatic mutations and interactions with the microenvironment.
The same driver mutations in the hematopoietic system may result in distinct disease states or may not even progress to a disease, a state termed clonal hematopoiesis (CH). We seek to understand the underlying molecular principles that determine the distinct phenotypic outcomes of the same driver mutations. Examples of specific contexts we are currently investigating include the diverging phenotypes of JAK2 or CALR mutations into distinct myeloproliferative neoplasms or CH, and molecular drivers that cooperate with recurring lymphoma driver mutations to develop into classic Hodgkin lymphoma versus non-Hodgkin lymphomas.