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James Koh, Ph.D.

James Koh, Ph.D.

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

Contact Information

Division of Vascular and Endovascular Surgery
513 Parnassus Ave, HSE
San Francisco, CA 94143
Phone: 415-514-9648
Fax: 415-476-8694
James.Koh@ucsf.edu
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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 Fellow, Harvard University, 1994-1997
  • Endocrine cell signaling, differentiation, and development
  • Live-cell imaging
  • Neoplastic transformation
  • Parathyroid tumors
  • Primary hyperparathyroidism
  • Single cell functional and genomic analysis

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.

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.

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  • Regulation of parathyroid function by the amyloid precursor protein
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    May 2021
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    Jan 2023
    Principal Investigator
  • Single cell analysis of intratumoral heterogeneity in parathyroid neoplasia
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    Jan 2015
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    Feb 2017
    Principal Investigator
  • Molecular Mechanisms of Altered Calcium Sensing in Human Parathyroid Disease
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    Jun 2010
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    May 2016
    Co-Principal Investigator
MOST RECENT PUBLICATIONS FROM A TOTAL OF 11
Data provided by UCSF Profiles, powered by CTSI
  1. 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 Jul 17. View in PubMed
  2. 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
  3. Koh J, Hogue JA, Sosa JA. Live-Cell Visualization of Calcium Flux in Vibratome-Cut Thick Sections of Viable Tumor Tissue. Curr Protoc Cell Biol. 2017 Dec 11; 77:4.34.1-4.34.16. View in PubMed
  4. Weber TJ, Koh J, Thomas SM, Hogue JA, Scheri RP, Roman SA, Sosa JA. Impaired calcium sensing distinguishes primary hyperparathyroidism (PHPT) patients with low bone mineral density. Metabolism. 2017 09; 74:22-31. View in PubMed
  5. Koh J, Hogue JA, Sosa JA. A Novel Ex Vivo Method for Visualizing Live-Cell Calcium Response Behavior in Intact Human Tumors. PLoS One. 2016; 11(8):e0161134. View in PubMed
  6. View All Publications

 

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