Jennifer A Pietenpol, Ph.D.
Chief Scientific and Strategy Officer, Vanderbilt University Medical Center
Executive Vice President for Research, Vanderbilt University Medical Center
Professor, Biochemistry
Ingram Professor, Cancer Research
Brock Family Directorship, Career Development
- : j.pietenpol@vumc.org
- : (615) 936-1512
- :
652 PRB
- : More Information/Publications
- : Lab Website
Areas of Interest: Cancer Biology; Cell Signaling
Member: VICC; Center for Matrix Biology
The research program in the laboratory focuses on epithelial cancers, with a focus on triple-negative breast cancer and the p53 family-signaling network. The Pietenpol Lab pioneered techniques for analysis of p53-chromatin binding and identification of p53 target genes. They discovered that p63 signaling confers key epithelial differentiation properties to cells by regulating novel target genes and transcriptional programs. The group deciphered the functional p73 binding sites in the genome, was the first to link the mTOR signaling pathway to regulation of p73 activity and define a role for mTOR-p73 signaling in epithelial and mesenchymal differentiation. More recently, the laboratory has integrated expertise in molecular genetics with bioinformatics to molecularly subclassify difficult-to-treat, triple negative breast cancer into subtypes. The subtypes include basal-like (BL1, BL2), mesenchymal (M) and luminal androgen receptor (LAR). This work has been validated, and cited over 2,500 times since 2011. These results are being translated to clinical trials and alignment of patients to appropriate, molecularly targeted therapy.
Also, the Pietenpol laboratory made the seminal discovery that p73 is required for multiciliogenesis and regulates the FoxJ1-associated gene network; thus providing a unifying mechanism for many inflammation-mediated phenotypes observed in p73-knockout mice. The defects in multi-ciliated cell differentiation and immune signaling in the p73-deficient mice provide an animal model for the study of several human inflammatory diseases. Most recently, my team demonstrated that p73 is essential for ovarian folliculogenesis.