John Oh

Research Advisor:

Juanita Merchant

Research Topic:

During Helicobacter-induced gastric spasmolytic-polypeptide expressing metaplasia (SPEM), a finding stone to gastric adenocarcinoma (GAC), Schlafen4⁺ myeloid-derived suppressor cells (Slfn4⁺ MDSCs) arise in the immune microenvironment. The appearance of Slfn4+ MDSCs prevents the maturation of T cells, consequently reducing the cytotoxicity in the metaplastic niche and promoting neoplastic transformation. Interestingly, the absence of Slfn4 reduced the immunosuppressive function of MDSCS – suggesting the interplay between Slfn4 and MDSC polarization. Current research under study is deciphering the role Slfn4 plays in myeloid differentiation to MDSCs.

Selected Publications:

El-Zaatari, M., Kao, J. Y., Tessier, A., Bai, L., Hayes, M. M., Fontaine, C., Eaton, K. A., & Merchant, J. L. (2013). Gli1 deletion prevents Helicobacter-induced gastric metaplasia and expansion of myeloid cell subsets. PloS one, 8(3), e58935. https://doi.org/10.1371/journal.pone.0058935

Ding, L., Hayes, M. M., Photenhauer, A., Eaton, K. A., Li, Q., Ocadiz-Ruiz, R., & Merchant, J. L. (2016). Schlafen 4-expressing myeloid-derived suppressor cells are induced during murine gastric metaplasia. The Journal of clinical investigation, 126(8), 2867–2880. https://doi.org/10.1172/JCI82529

Selected Presentations:

Jaiswal SK, Oh JJ, DePamphilis ML. Cell cycle arrest and apoptosis are not dependent on p53 prior to p53-dependent embryonic stem cell differentiation. Stem Cells. 2020 Sep;38(9):1091-1106. doi: https://doi.org/10.1002/stem.3199. Epub 2020 Jun 1. PMID: 32478947.