Seoul National University · Medicine
Professor Doo Hyun Chung's research lab focuses on the tumor microenvironment and immune evasion mechanisms in lung cancer, particularly exploring the interplay between oncogenic drivers like EML4-ALK and immune checkpoint molecules such as PD-L1. The lab investigates how tumor-intrinsic signaling pathways regulate immune cell infiltration and function, with a special emphasis on innate lymphoid cells (ILCs) and their plasticity in promoting tumor progression. Key research directions include the role of IL-23 in reprogramming ILC1 to ILC3-like cells to drive IL-17-mediated inflammation and immunosuppression in squamous cell carcinoma. The lab integrates molecular oncology, immunology, and translational research to identify novel therapeutic targets for improving immunotherapy outcomes in lung cancer.
Figures are computed from collected data and may differ slightly.
Programmed cell death (PD)-1/PD-1 ligand-1 (PD-L1)-targeted therapy has emerged as a promising therapeutic strategy for lung cancer. However, whether EML4-ALK regulates PD-L1 expression in lung cancer remains unknown. A total of 532 pulmonary adenocarcinomas (pADCs), including 58 <i>ALK</i>-translocated tumors, were immunohistochemically evaluated for PD-L1 and PD-1. H23 (<i>EGFR</i><sup>Wild-type</sup><i>EML4-ALK</i><sup>-</sup>PD-L1<sup>Low</sup>) and H2228 (<i>EGFR</i><sup>Wild-type</sup><i>E
Conversion from ILC1 into ILC3 by IL23-producing SqCCs promotes IL17-mediated tumor progression, resulting in a poor prognosis.
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