About Us
Meet the Team
Conditions & Procedures
Patient Center
Education & Training
Research
Thoracic Oncology Clinical Trials
Program Labs
- Thoracic Oncology Lab
- Kratz Lab
- Thoracic ERAS Program
- Clincial Trials
News & Events
Vanderbilt University, B.S., 1998, Molecular Biology
New York University, School of Medicine, Ph.D., 2004, Cell and Mol. Biology
New York University, School of Medicine, M.D., 2005, Medicine
Trever G. Bivona, M.D., Ph.D. is a thoracic medical oncologist. His overarching goal is to develop paradigm-shifting treatment strategies that target the aberrant signal transduction pathways fueling tumor growth. He is Director of the Bivona Lab, a bench-to-bedside research enterprise investigating the molecular pathogenesis of human cancers, primarily lung cancer. In pursuit of that goal, the Bivona Lab uses interdisciplinary approaches and next-generation functional genomics methodologies, highly relevant cell line and tumor model systems, and human tumor specimens and clinical outcomes data. These help to define and elucidate the molecular events driving human lung cancer growth.
Dr. Bivona received his M.D. and Ph.D. from the joint Medical Scientist Training Program at NYU School of Medicine. He completed his residency in internal medicine at Brigham and Women's Hospital followed by advanced training at Memorial Sloan-Kettering Cancer Center as a medical oncology fellow, and research fellow in the Laboratory of Charles Sawyers, Human Oncology and Pathogenesis Program.
I am a laboratory-based physician-scientist and an academic medical oncologist with a Ph.D. in cell and molecular biology. Clinical experiences inspire my laboratory investigations and provide opportunities to translate scientific discoveries aimed at improving the personalized treatment of cancer patients. The goal of my research program is to define the molecular pathogenesis of human cancers through both basic and translational studies with a particular focus on lung cancer, the leading cause of cancer mortality in the United States.
Our aim is to discover tumor-cell specific vulnerabilities that can be therapeutically exploited as novel treatment strategies to improve the survival of patients with lung, and potentially, other cancers. To accomplish our goals, we have a developed an integrated approach to define the molecular mechanisms by which oncogenes drive the growth of human lung cancers and by which tumors evade oncogene-targeted treatments.
Our approach leverages state-of-the-art functional genomics RNA interference screening methodologies, highly relevant preclinical models of lung cancer that accurately represent human lung cancer, and prospectively acquired human lung cancer specimens and clinical data. Using this approach we recently identified several novel mechanisms of resistance to EGFR (epidermal growth factor receptor) inhibitors in lung cancers with activating (oncogenic) mutations in EGFR. Our work has defined new rational companion therapeutic targets that when inhibited may enhance responses to EGFR inhibitors in lung cancer patients
The studies proposed in this project build upon our prior research because they will allow us to further define molecular determinants of oncogene dependence in human lung cancers. Moreover, we are uniquely positioned to translate our findings into lung cancer patients through validation of our findings in human lung cancer specimens and, subsequently, hypothesis-driven clinical trials in lung cancer patients.