University of California San Francisco

Koh, James - 144
James Koh, PhD

Associate Professor of Surgery
Division of Surgical Oncology
Director, Endocrine Neoplasia Research Lab


513 Parnassus Ave, HSE, #563
San Francisco, CA 94143
United States

Email: [email protected]
Phone: 415-514-9648
Fax: 415-476-8694


    James Koh, Ph.D., is an Associate Professor of Surgery at UCSF and Director of the newly established Endocrine Neoplasia Research Lab. He earned his doctorate under the direction of Dr. Francis S. Collins at the University of Michigan, Ann Arbor, and then completed a post-doctoral fellowship in Dr. Ed Harlow's laboratory at Harvard University. Dr. Koh joined the UCSF faculty in December 2018.

    Building upon his background in cellular signaling, cell cycle regulation, and tumor suppressor function, Dr. Koh's laboratory has developed a combination of molecular, murine modeling, and live-cell imaging approaches to examine the underlying mechanisms of disrupted biochemical signaling behavior in human endocrine tumors.

    Recently, Dr. Koh and his research team utilized live tumor tissue functional analysis of calcium responsiveness to reveal two discrete classes of human parathyroid adenomas associated with differing patterns of clinical presentation and outcome. Towards the goal of establishing a novel dynamic functional axis of diagnostic criteria to supplement conventional tumor classification metrics, Dr. Koh will focus on the development of live-cell imaging methods for direct ex vivo provocative testing of endocrine tumor reactivity to physiological agonist engagement at single cell resolution.



    Institution Degree Dept or School End Date
    University of California Diversity, Equity, and Inclusion Champion Training 2019

    Grants and Funding

    • Regulation of parathyroid function by the amyloid precursor protein | NIH | 2021-05-01 - 2023-01-31 | Role: Principal Investigator
    • Single cell analysis of intratumoral heterogeneity in parathyroid neoplasia | NIH | 2015-01-16 - 2017-02-28 | Role: Principal Investigator
    • Molecular Mechanisms of Altered Calcium Sensing in Human Parathyroid Disease | NIH | 2010-06-01 - 2016-05-31 | Role: Co-Principal Investigator

    Research Narrative

    The Endocrine Neoplasia Research Lab employs a combination of molecular, murine modeling, and live-cell imaging approaches to examine the underlying mechanisms of disrupted biochemical sensing behaviors in human endocrine tumors. Recently, in contrast to the prevailing clonal origin model, our group has shown that parathyroid adenomas driving primary hyperparathyroidism are comprised of functionally discrete and separable cellular subpopulations that respond differentially to extracellular calcium stimulation and which arise in many cases following polyclonal expansion of multiple independent progenitor cells within the parathyroid gland.

    We are employing dynamic calcium response imaging at both the single cell and intact tissue level, in combination with transgenic mouse modeling to study how these newly identified cellular subpopulations drive the failure of appropriate calcium sensing in parathyroid disease. To examine cell-signaling behaviors in the native context of viable tumor tissue, we have developed a novel ex vivo imaging system that enables direct provocative testing of tumor reactivity to physiological agonist engagement at single-cell resolution. These methods form the foundation for our laboratory’s ongoing efforts to understand how perturbed biochemical signaling can contribute to the development of preneoplastic lesions in human endocrine neoplasia.

    Research Interests

    Parathyroid tumors

    Neoplastic transformation

    Live-cell imaging

    Primary hyperparathyroidism

    Endocrine cell signaling, differentiation, and development

    Single cell functional and genomic analysis




    1. Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency.
      Tu CL, Chang W, Sosa JA, Koh J| | View in PubMed
    2. Effects of Multi-stage Procurement on the Viability and Function of Human Donor Parathyroid Glands.
      Kelly YM, Ward C, Zhang R, Syed S, Stock PG, Duh QY, Sosa JA, Koh J| | View in PubMed
    3. Ex Vivo Intact Tissue Analysis Reveals Alternative Calcium-sensing Behaviors in Parathyroid Adenomas.
      Koh J, Zhang R, Roman S, Duh QY, Gosnell J, Shen W, Suh I, Sosa JA| | View in PubMed
    4. Parathyroid-Targeted Overexpression of Regulator of G-Protein Signaling 5 (RGS5) Causes Hyperparathyroidism in Transgenic Mice.
      Balenga N, Koh J, Azimzadeh P, Hogue J, Gabr M, Stains JP, Olson JA| | View in PubMed
    5. Transcriptional profiling reveals distinct classes of parathyroid tumors in PHPT.
      Koh J, Hogue JA, Roman SA, Scheri RP, Fradin H, Corcoran DL, Sosa JA| | View in PubMed
    6. Polyclonal origin of parathyroid tumors is common and is associated with multiple gland disease in primary hyperparathyroidism.
      Shi Y, Azimzadeh P, Jamingal S, Wentworth S, Ferlitch J, Koh J, Balenga N, Olson JA| | View in PubMed
    7. Live-Cell Visualization of Calcium Flux in Vibratome-Cut Thick Sections of Viable Tumor Tissue.
      Koh J, Hogue JA, Sosa JA| | View in PubMed
    8. Impaired calcium sensing distinguishes primary hyperparathyroidism (PHPT) patients with low bone mineral density.
      Weber TJ, Koh J, Thomas SM, Hogue JA, Scheri RP, Roman SA, Sosa JA| | View in PubMed
    9. Orphan Adhesion GPCR GPR64/ADGRG2 Is Overexpressed in Parathyroid Tumors and Attenuates Calcium-Sensing Receptor-Mediated Signaling.
      Balenga N, Azimzadeh P, Hogue JA, Staats PN, Shi Y, Koh J, Dressman H, Olson JA| | View in PubMed
    10. A Novel Ex Vivo Method for Visualizing Live-Cell Calcium Response Behavior in Intact Human Tumors.
      Koh J, Hogue JA, Sosa JA| | View in PubMed
    11. Single-cell approaches for molecular classification of endocrine tumors.
      Koh J, Allbritton NL, Sosa JA| | View in PubMed
    12. Single-cell functional analysis of parathyroid adenomas reveals distinct classes of calcium sensing behaviour in primary hyperparathyroidism.
      Koh J, Hogue JA, Wang Y, DiSalvo M, Allbritton NL, Shi Y, Olson JA, Sosa JA| | View in PubMed
    13. Functional and genetic studies of isolated cells from parathyroid tumors reveal the complex pathogenesis of parathyroid neoplasia.
      Shi Y, Hogue J, Dixit D, Koh J, Olson JA| | View in PubMed
    14. Regulator of G protein signaling 5 is highly expressed in parathyroid tumors and inhibits signaling by the calcium-sensing receptor.
      Koh J, Dar M, Untch BR, Dixit D, Shi Y, Yang Z, Adam MA, Dressman H, Wang X, Gesty-Palmer D, Marks JR, Spurney R, Druey KM, Olson JA| | View in PubMed
    15. Severe obesity is associated with symptomatic presentation, higher parathyroid hormone levels, and increased gland weight in primary hyperparathyroidism.
      Adam MA, Untch BR, Danko ME, Stinnett S, Dixit D, Koh J, Marks JR, Olson JA| | View in PubMed