Sergei Doulatov, PhD
- Associate Professor of Physiology and Cellular Biophysics
Overview
Sergei Doulatov, PhD, is an associate professor of physiology and cellular biophysics at Columbia University. His research focuses on the biology of hematopoietic stem cells and hematological malignancies, including myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML). Leveraging induced pluripotent stem cells and gene editing, his research seeks to understand how the acquisition of oncogenic mutations drives malignant transformation, with the long-term goal of identifying fundamental mechanisms of disease and developing targeted therapies to eradicate malignant stem cells.
Academic Appointments
- Associate Professor of Physiology and Cellular Biophysics
Credentials & Experience
Education & Training
- BS, Microbiology, University of California Los Angeles
- PhD, Hematopoiesis, University of Toronto, Canada
- Postdoctoral, Stem Cell Biology, Harvard Medical School, Boston
Committees, Societies, Councils
- Standing Member NIH Peer Review Committee: Basic Biology of Blood, Heart and Vasculature (BBHV) study section, 2023-Present
Honors & Awards
American Society of Hematology (ASH) Scholar Award, 2018
NIH Director's New Innovator Award (DP2), 2018
Fialkow Scholar Award, University of Washington School of Medicine, 2018
Gilead Sciences Research Scholar Award, 2017
Early Career Award, UW/Fred Hutch Cancer Consortium, 2017
Research
The Doulatov Lab at Columbia University Irving Medical Center investigates the fundamental mechanisms of human hematopoietic stem cell (HSC) function and the malignant transformation from clonal hematopoiesis (CH) to myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). The lab develops models of malignant transformation using patient-derived MDS and AML induced pluripotent stem cells (iPSCs) and applies precise gene editing techniques to primary human HSCs. The Doulatov Lab was the first to demonstrate that iPSC reprogramming can reveal the sequence and contribution of somatic mutations driving clonal evolution in MDS. Ongoing work explores how aberrant gene splicing due to SF3B1 spliceosome mutations dysregulates hematopoiesis leading to MDS. Through this work, the team identified mis-splicing of mitochondrial genes TMEM14C and ABCB7 as the cause of ring sideroblast formation in MDS, and uncovered CHK1 inhibition as a selective therapeutic vulnerability of SF3B1 mutated HSCs. In parallel, the lab recently identified lamin B1 (LMNB1) as the critical regulator of HSC function and nuclear morphology via higher-order genome organization, recurrently deleted in 5q- myeloid malignancies.