Associate Professor of Pathology
Associate Director of Adult Transfusion Medicine
Brigham and Women's Hospital, Boston, MA
Brigham & Women's Hospital
NRB 6, Boston, MA 02115
M.D., 1993, Shandong Medical University, China.
Dr. Chai's research is focused on the homeotic gene family SALL in human development, tumorigenesis and hematopoiesis. SALL gene family is the mammalian homologue of Drosophila gene Spalt (sal). In Drosophila, sal mutation can lead to the incomplete separation of the head and trunk of the fly. In human, heterogenous mutation of SALL1 cause Townes-Brock Syndrome with renal, cardiac, digit, genital malformation. Heterogenous mutation of SALL4 in human is associated with Okihiro Syndrome with limitation of eye abduction, deafness and digit malformation. SALL2 is a potential tumor suppressor gene in ovary carcinogenesis, and may play a role in hematopoiesis and leukemogenesis.
Her research areas range from characterization of SALL family gene structure, transcriptional regulation, tissue distributions to its function study by generating knock out or transgene mouse model.
SALL2 is a unique sal gene that has two isoforms each with its own promotor. Like the rest SALL gene family member, the transcription of SALL2 is regulated by Wilms' tumor suppressor gene (WT1). Despite its relative normal phenotype, the SALL-null mouse has reduced mature myeloid population, the defect of its myeloid differentiation is further demonstrated by impaired myeloid differentiation in Colony formation unit (CFU) and transplantation studies These results indicate that the defect of myeloid maturation is transplantable and thus intrinsic to the hematopoietic stem cell. The mechanism(s) of SALL2 involved in hematopoiesis is under investigation currently.