Biography
Education
Institution | Degree | Dept or School | End Date |
---|---|---|---|
Memorial Sloan Kettering Cancer Center | Medical Oncology and cancer biology post-doctoral fellowship | 2011 | |
Brigham and Women's Hospital/Harvard | Internal Medicine | 2007 | |
New York University School of Medicine | M.D. | School of Medicine | 2005 |
New York University School of Medicine | Ph.D. | Cell and Molecular Biology | 2004 |
Board Certifications
American Board of Internal Medicine, Internal Medicine
American Board of Internal Medicine, Medical Oncology
Clinical Expertise
Bronchioloalveolar Carcinoma (BAC)
Chest Wall Tumors
Lung Carcinoid Tumors
Lung Metastases
Malignant Mesothelioma
Mediastinal Tumors
Non-Small Cell Lung Cancer
Small Cell Lung Cancer
Thymoma & Thymic Carcinoma
Target Therapies in Lung Cancer
Program Affiliations
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)
Grants and Funding
- UCSF Paul Calabresi K12 Career Development Program in Clinical Oncology | NIH | 2021-07-01 - 2026-06-30 | Role: Co-Principal Investigator
- (PQ7) Defining a new mode of RAS signaling in cancer from cytoplasmic protein granules | NIH | 2019-07-01 - 2024-06-30 | Role: Principal Investigator
- Rational Combined Inhibition of NF-kB and EGFR to Optimize Lung Cancer Treatment | NIH | 2013-02-01 - 2024-01-31 | Role: Principal Investigator
- Bay Area Team Against Resistance | NIH | 2017-09-30 - 2022-08-31 | Role: Principal Investigator
- The Cancer Target Discovery and Development Network at UCSF | NIH | 2017-08-10 - 2022-07-31 | Role: Co-Principal Investigator
- Characterization of YAP as a rational companion target in lung cancer | NIH | 2017-03-01 - 2022-02-28 | Role: Principal Investigator
- Optimizing biologically-based rational polytherapy in ALK+ lung cancer | NIH | 2017-01-11 - 2021-12-31 | Role: Principal Investigator
- Discovery of Rational Companion Therapeutic Targets to Optimize Cancer Treatment | NIH | 2012-09-15 - 2017-08-31 | Role: Principal Investigator
- Genetic Modifiers such as Fas Regulate Tumor-Cell Dependence on Mutant EGFR | NIH | 2011-09-21 - 2016-08-31 | Role: Principal Investigator
Research Narrative
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.
Research Interests
Lung cancer
Molecular pathogenesis of human cancers
Molecularly-targeted cancer therapies
Next-generation functional genomics
Novel, rational therapeutic strategies
Activating mutations in EGFR
Mechanisms of Secondary Resistance
Publications
- Author Correction: CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors.| | PubMed
- FET fusion oncoproteins disrupt physiologic DNA repair networks in cancer.| | PubMed
- Oncogenic EML4-ALK assemblies suppress growth factor perception and modulate drug tolerance.| | PubMed
- CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors.| | PubMed
- Macrophage-fibroblast crosstalk drives Arg1-dependent lung fibrosis via ornithine loading.| | PubMed
- Neoadjuvant Osimertinib for the Treatment of Stage I-IIIA Epidermal Growth Factor Receptor-Mutated Non-Small Cell Lung Cancer: A Phase II Multicenter Study.| | PubMed
- Current Trial Report: A Multicenter Phase I/Ib study of Capmatinib Plus Trametinib in Patients With Metastatic Nonsmall Cell Lung Center Harboring MET Exon 14 Skipping Mutations and Other MET-Alterations.| | PubMed
- Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling.| | PubMed
- Quantification of cerebrospinal fluid tumor DNA in lung cancer patients with suspected leptomeningeal carcinomatosis.| | PubMed
- Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in lung cancer.| | PubMed