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David Oh, MD

TitleAssistant Professor
InstitutionUniversity of California San Francisco
DepartmentMedicine
Address513 Parnassus Ave
San Francisco CA 94143
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    Collapse Biography 
    Collapse Education and Training
    Harvard CollegeAB2000Biochemical Sciences
    Stanford University School of MedicineMD/PhD2011Medicine, Physiology
    University of California, San FranciscoResidency2014Internal Medicine
    University of California, San FranciscoFellowship2017Hematology/Oncology
    Collapse Awards and Honors
    University of California, San Francisco2015Clinical Fellow Award
    Conquer Cancer Foundation of American Society of Clinical Oncology 2016Merit Award
    University of California, San Francisco2016Molecular Pathology of Cancer T32
    Conquer Cancer Foundation of American Society of Clinical Oncology2017Young Investigator Award
    Bladder Cancer Advocacy Network2018Young Investigator Award
    Prostate Cancer Foundation2018Young Investigator Award

    Collapse Overview 
    Collapse Overview
    I am a physician-scientist experienced in clinical and translational laboratory efforts to understand and improve upon cancer immunotherapies.

    Clinically, I see patients in the Cancer Immunotherapy Program where I am an attending physician and investigator on early-phase/first-in-human trials testing novel immunotherapies in advanced solid tumors, with a particular focus on genitourinary malignancies. This includes high-risk modalities such as bispecific T cell engaging therapies, immune agonist antibodies, and adoptive cell therapies.

    In the laboratory, I study samples from prostate and bladder cancer patients treated with immunotherapy using unbiased platforms such as single-cell RNA sequencing and T cell receptor sequencing. The goal of this work is to discover and validate novel T cell populations and antigenic specificities that are responsible for anti-tumor efficacy as well as immune-related adverse events (IRAEs) resulting from treatment.


    Collapse Bibliographic 
    Collapse Publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help.
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    1. Hagihara K, Chan S, Zhang L, Oh DY, Wei XX, Simko J, Fong L. Neoadjuvant sipuleucel-T induces both Th1 activation and immune regulation in localized prostate cancer. Oncoimmunology. 2019; 8(1):e1486953. PMID: 30546940.
      View in: PubMed
    2. Oh DY,* Cham J,* Zhang L, Fong G, Kwek SS, Klinger M, Faham M, Fong L. *co-first author.Immune Toxicities Elicted by CTLA-4 Blockade in Cancer Patients Are Associated with Early Diversification of the T-cell Repertoire. Cancer Res. 2017; 77(6):1322-1330.
    3. Oh DY, Venook AP, Fong L. On the Verge: Immunotherapy for Colorectal Carcinoma. J Natl Compr Canc Netw. 2015 Aug; 13(8):970-8. PMID: 26285242.
      View in: PubMed
    4. Ehrlich LI,* Oh DY,* Weissman IL, Lewis RS. *co-first author.Differential contribution of chemotaxis and substrate restriction to segregation of immature and mature thymocytes. Immunity. 2009; 31(6):986-98.
    5. Bhakta NR, Oh DY, Lewis RS. Calcium oscillations regulate thymocyte motility during positive selection in the three-dimensional thymic environment. Nat Immunol. 2005 Feb; 6(2):143-51. PMID: 15654342.
      View in: PubMed
    6. Fan Z, Beresford PJ, Oh DY, Zhang D, Lieberman J. Tumor suppressor NM23-H1 is a granzyme A-activated DNase during CTL-mediated apoptosis, and the nucleosome assembly protein SET is its inhibitor. Cell. 2003 Mar 07; 112(5):659-72. PMID: 12628186.
      View in: PubMed
    7. Beresford PJ, Zhang D, Oh DY, Fan Z, Greer EL, Russo ML, Jaju M, Lieberman J. Granzyme A activates an endoplasmic reticulum-associated caspase-independent nuclease to induce single-stranded DNA nicks. J Biol Chem. 2001 Nov 16; 276(46):43285-93. PMID: 11555662.
      View in: PubMed
    8. Gommerman JL,* Oh DY,* Zhou X, Tedder TF, Maurer M, Galli SJ, Carroll MC. *co-first author.A role for CD21/CD35 and CD19 in responses to acute septic peritonitis: a potential mechanism for mast cell activation. J Immunol. 2000; 165(12):6915-21.
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