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Thoracic Oncology Program »  Meet the Team »  Medical Oncologists »  Trever G. Bivona, M.D., Ph.D.
Trever G. Bivona, M.D., Ph.D.

Trever G. Bivona, M.D., Ph.D.

Assistant Professor in Residence
Division of Hematology/Oncology
Department of Medicine

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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

  • Brigham and Women's Hospital/Harvard, 2005-2007, Internal Medicine
  • Memorial Sloan-Kettering Cancer Center, 2007-2011, Medical Oncology
  • Research Fellow, Laboratory of Charles Sawyers, Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, 2008-2011
  • American Board of Internal Medicine, Internal Medicine
  • American Board of Internal Medicine, Medical Oncology
  • Department of Medicine, Division of Hematology/Oncology
  • Thoracic Oncology Program
  • Member, UCSF Helen Diller Family Comprehensive Cancer Center
  • Member, UCSF Biomedical Sciences Graduate Program (BMS)
  • Member, California Institute for Quantitative Biosciences (QB3)
  • Activating mutations in EGFR
  • Lung cancer
  • Mechanisms of Secondary Resistance
  • Molecular pathogenesis of human cancers
  • Molecularly-targeted cancer therapies
  • Next-generation functional genomics
  • Novel, rational therapeutic strategies

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.

Data provided by UCSF Profiles, powered by CTSI
  • (PQ7) Defining a new mode of RAS signaling in cancer from cytoplasmic protein granules
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    Jul 2019
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    Jun 2024
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  • Rational Combined Inhibition of NF-kB and EGFR to Optimize Lung Cancer Treatment
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    Feb 2013
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    Jan 2024
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  • Bay Area Team Against Resistance
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    Sep 2017
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    Aug 2022
    Principal Investigator
  • The Cancer Target Discovery and Development Network at UCSF
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    Aug 2017
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    Jul 2022
    Co-Principal Investigator
  • Characterization of YAP as a rational companion target in lung cancer
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    Mar 2017
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    Feb 2022
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  • Optimizing biologically-based rational polytherapy in ALK+ lung cancer
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    Jan 2017
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    Dec 2021
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  • Discovery of Rational Companion Therapeutic Targets to Optimize Cancer Treatment
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    Sep 2012
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    Aug 2017
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  • Genetic Modifiers such as Fas Regulate Tumor-Cell Dependence on Mutant EGFR
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    Sep 2011
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    Aug 2016
    Principal Investigator
MOST RECENT PUBLICATIONS FROM A TOTAL OF 101
Data provided by UCSF Profiles, powered by CTSI
  1. Cao W, Lee H, Wu W, Zaman A, McCorkle S, Yan M, Chen J, Xing Q, Sinnott-Armstrong N, Xu H, Sailani MR, Tang W, Cui Y, Liu J, Guan H, Lv P, Sun X, Sun L, Han P, Lou Y, Chang J, Wang J, Gao Y, Guo J, Schenk G, Shain AH, Biddle FG, Collisson E, Snyder M, Bivona TG. Multi-faceted epigenetic dysregulation of gene expression promotes esophageal squamous cell carcinoma. Nat Commun. 2020 Jul 22; 11(1):3675. View in PubMed
  2. Negrao MV, Raymond VM, Lanman RB, Robichaux JP, He J, Nilsson MB, Ng PKS, Amador BE, Roarty EB, Nagy RJ, Banks KC, Zhu VW, Ng C, Chae YK, Clarke JM, Crawford JA, Meric-Bernstam F, Ou SH, Gandara DR, Heymach JV, Bivona TG, McCoach CE. Molecular landscape of BRAF-mutant NSCLC reveals an association between clonality and driver mutations and identifies targetable non-V600 driver mutations. J Thorac Oncol. 2020 Jun 12. View in PubMed
  3. Bivona TG. EGFR targeted therapy resistance: current status, challenges, and future outlook. J Thorac Dis. 2020 May; 12(5):2849-2850. View in PubMed
  4. Lotsberg ML, Wnuk-Lipinska K, Terry S, Tan TZ, Lu N, Trachsel-Moncho L, Røsland GV, Siraji MI, Hellesøy M, Rayford A, Jacobsen K, Ditzel HJ, Vintermyr OK, Bivona TG, Minna J, Brekken RA, Baguley B, Micklem D, Akslen LA, Gausdal G, Simonsen A, Thiery JP, Chouaib S, Lorens JB, Engelsen AST. AXL Targeting Abrogates Autophagic Flux and Induces Immunogenic Cell Death in Drug-Resistant Cancer Cells. J Thorac Oncol. 2020 Jun; 15(6):973-999. View in PubMed
  5. Zargar A, Chang S, Kothari A, Snijders AM, Mao JH, Wang J, Hernández AC, Keasling JD, Bivona TG. Overcoming the challenges of cancer drug resistance through bacterial-mediated therapy. Chronic Dis Transl Med. 2019 Dec; 5(4):258-266. View in PubMed
  6. View All Publications

 

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