Surgery Websites
General Surgery »  Faculty »  Endocrine Surgery »  James Koh, Ph.D.
James Koh, Ph.D.

James Koh, Ph.D.

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

Contact Information

513 Parnassus Ave, HSE, #563
San Francisco, CA 94143
Phone: 415-514-9648
Fax: 415-476-8694
[email protected]
Open Popup

Education

University of North Carolina at Chapel Hill, B.A., Zoology/Classics, 1983

University of Michigan at Ann Arbor, M.S., Human Genetics, 1988

University of Michigan at Ann Arbor, Ph.D., Human Genetics, 1994

Postdoctoral Training

  • Postdoctoral Fellow, Harvard University, 1994-1997

Research Interests

  • Endocrine cell signaling, differentiation, and development
  • Live-cell imaging
  • Neoplastic transformation
  • Parathyroid tumors
  • Primary hyperparathyroidism
  • Single cell functional and genomic analysis

Biography

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.

Research Overview

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 & Funding

Data provided by UCSF Profiles, powered by CTSI
  • Regulation of parathyroid function by the amyloid precursor protein
    Sponsor:
    Sponsor ID:
    Funding Period:
    May 2021
    -
    Jan 2023
    Principal Investigator
  • Single cell analysis of intratumoral heterogeneity in parathyroid neoplasia
    Sponsor:
    Sponsor ID:
    Funding Period:
    Jan 2015
    -
    Feb 2017
    Principal Investigator
  • Molecular Mechanisms of Altered Calcium Sensing in Human Parathyroid Disease
    Sponsor:
    Sponsor ID:
    Funding Period:
    Jun 2010
    -
    May 2016
    Co-Principal Investigator

Publications

MOST RECENT PUBLICATIONS FROM A TOTAL OF 17
Data provided by UCSF Profiles, powered by CTSI
  1. Tu CL, Chang W, Sosa JA, Koh J. Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency. PNAS Nexus. 2023 Mar; 2(3):pgad073. View in PubMed
  2. Kelly YM, Ward C, Zhang R, Syed S, Stock PG, Duh QY, Sosa JA, Koh J. Effects of Multi-stage Procurement on the Viability and Function of Human Donor Parathyroid Glands. J Surg Res. 2022 08; 276:404-415. View in PubMed
  3. Koh J, Zhang R, Roman S, Duh QY, Gosnell J, Shen W, Suh I, Sosa JA. Ex Vivo Intact Tissue Analysis Reveals Alternative Calcium-sensing Behaviors in Parathyroid Adenomas. J Clin Endocrinol Metab. 2021 10 21; 106(11):3168-3183. View in PubMed
  4. Balenga N, Koh J, Azimzadeh P, Hogue J, Gabr M, Stains JP, Olson JA. Parathyroid-Targeted Overexpression of Regulator of G-Protein Signaling 5 (RGS5) Causes Hyperparathyroidism in Transgenic Mice. J Bone Miner Res. 2019 05; 34(5):955-963. View in PubMed
  5. Koh J, Hogue JA, Roman SA, Scheri RP, Fradin H, Corcoran DL, Sosa JA. Transcriptional profiling reveals distinct classes of parathyroid tumors in PHPT. Endocr Relat Cancer. 2018 04; 25(4):407-420. View in PubMed
  6. View All Publications

 

 
Site Directory
    X