Thoracic Oncology Program »  Meet the Team »  Medical Oncologists »  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

Contact Information

University of California, San Francisco
Mission Bay/Genentech Hall
600 16th Street, Room: N212D
San Francisco, CA 94158-2140
UCSF intercampus mail, please use mail code: 2140 
TBivona@medicine.ucsf.edu
Phone: 415-476-9907 / Lab Fax: 415-514-0169 / Clinic Fax #: 415-514-6676

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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.

Most recent publications from a total of 55
  1. Kyung Rho J, Young Lee I, Jung Choi Y, Choi CM, Hur JY, Koh JS, Lee J, Suh BC, Song HJ, Salgaonkar P, Lee J, Lee J, Jung DS, Kim SY, Woo DC, Baek IJ, Lee JY, Ha CH, Sung YH, Kim JK, Kim WS, Song JS, Kim CH, Bivona TG, Lee JC. Superior efficacy and selectivity of novel small molecule kinase inhibitors of T790M mutant EGFR in preclinical models of lung cancer. Cancer Res. 2017 Jan 12. View in PubMed
  2. Okimoto RA, Bivona TG. Metastasis: From Head to Tail. Cell Cycle. 2017 Jan 05; 0. View in PubMed
  3. Okimoto RA, Breitenbuecher F, Olivas VR, Wu W, Gini B, Hofree M, Asthana S, Hrustanovic G, Flanagan J, Tulpule A, Blakely CM, Haringsma HJ, Simmons AD, Gowen K, Suh J, Miller VA, Ali S, Schuler M, Bivona TG. Inactivation of Capicua drives cancer metastasis. Nat Genet. 2016 Nov 21. View in PubMed
  4. Thiagarajan PS, Wu X, Zhang W, Shi I, Bagai R, Leahy P, Feng Y, Veigl M, Lindner D, Danielpour D, Yin L, Rosell R, Bivona TG, Zhang Z, Ma PC. Transcriptomic-metabolomic reprogramming in EGFR-mutant NSCLC early adaptive drug escape linking TGFß2-bioenergetics-mitochondrial priming. Oncotarget. 2016 Nov 11. View in PubMed
  5. Okimoto RA, Lin L, Olivas V, Chan E, Markegard E, Rymar A, Neel D, Chen X, Hemmati G, Bollag G, Bivona TG. Preclinical efficacy of a RAF inhibitor that evades paradoxical MAPK pathway activation in protein kinase BRAF-mutant lung cancer. Proc Natl Acad Sci U S A. 2016 Nov 9. View in PubMed
  6. Sabnis AJ, Bivona TG. HSP70 dependence in rhabdomyosarcoma: Seed or soil? Cell Cycle. 2016 Sep 29; 1-2. View in PubMed
  7. Sabnis AJ, Guerriero CJ, Olivas V, Sayana A, Shue J, Flanagan J, Asthana S, Paton AW, Paton JC, Gestwicki JE, Walter P, Weissman JS, Wipf P, Brodsky JL, Bivona TG. Combined chemical-genetic approach identifies cytosolic HSP70 dependence in rhabdomyosarcoma. Proc Natl Acad Sci U S A. 2016 Aug 9; 113(32):9015-20. View in PubMed
  8. Premasekharan G, Gilbert E, Okimoto RA, Hamirani A, Lindquist KJ, Ngo VT, Roy R, Hough J, Edwards M, Paz R, Foye A, Sood R, Copren KA, Gubens M, Small EJ, Bivona TG, Collisson EA, Friedlander TW, Paris PL. An improved CTC isolation scheme for pairing with downstream genomics: Demonstrating clinical utility in metastatic prostate, lung and pancreatic cancer. Cancer Lett. 2016 Sep 28; 380(1):144-52. View in PubMed
  9. McCoach CE, Bivona TG, Blakely CM, Doebele RC. Neoadjuvant Oncogene-Targeted Therapy in Early Stage Non-Small-Cell Lung Cancer as a Strategy to Improve Clinical Outcome and Identify Early Mechanisms of Resistance. Clin Lung Cancer. 2016 Sep; 17(5):466-469. View in PubMed
  10. Bivona TG, Doebele RC. A framework for understanding and targeting residual disease in oncogene-driven solid cancers. Nat Med. 2016 May 5; 22(5):472-8. View in PubMed
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