Francine Garrett-Bakelman, MD PhD

Photo of Dr. Francine Garrett-BakelmanPRIMARY APPOINTMENT:

Assistant Professor
Biochemistry and Molecular Genetics


LAB :PO Box 800733, 1340 JPA Pinn Hall Rm 6054A
UVA Cancer Center Clinic: PO Box 800334
Charlottesville, Virginia 22908

Telephone Office:
434-924-9220 (no patient-related calls accepted)
Clinical practice: 434-924-9333
Fax Office: 434-924-5069 (no patient-related information accepted)
Fax Clinical Practice: 434-244-7526
(for patients needing assistance, please call clinical practice)



  • Primary: Albert Einstein College of Medicine of Yeshiva University
  • Residency: New York Presbyterian – Weill Cornell
  • Fellowships: New York Presbyterian Hospital – Weill Cornell


Bioinformatics and Genomics, Cancer Biology, Epigenetics, Molecular Biology, Translational Science


Acute Myeloid Leukemia: molecular and cellular biology events that mediate aberrant epigenetic and transcriptional mechanisms during disease establishment and progression.


Acute Myeloid Leukemia (AML) is adults’ most common acute leukemia. AML prognosis and overall survival decline in patients older than 60 and in patients who develop disease relapse after initial treatments. Our main research goal is to understand molecular and epigenetic mechanisms responsible for AML disease phenotypes. Through this aim, in the long-term, findings will help identify novel therapeutic targets in AML.

We investigate these questions by studying samples from AML patients and functional validations in vitro and in vivo models. Epigenetic (DNA methylation, gene expression, and chromatin assays) and molecular and cellular biology techniques are implemented to study how aberrant expression of specific genes contribute to abnormal cellular phenotypes and leukemogenesis. Previous studies have determined that AML progression (from disease diagnosis to relapse) is characterized by significant epigenetic plasticity and differentially expressed genes. Studies are being pursued to identify genes affected by the epigenetic changes observed and how their function contributes to the malignant phenotype.