Jaemoon Ko
Seoul National University · 医学
研究室紹介
Professor Jaemoon Ko's research lab focuses on the tumor microenvironment, immune cell crosstalk, and molecular pathogenesis in lung and gastrointestinal malignancies. Key research directions include the regulation of immune checkpoint molecules like PD-L1 by oncogenic drivers such as EML4-ALK, the plasticity of innate lymphoid cells in tumor progression, and the prognostic significance of tissue-resident immune cells like CD103+ T cells in non-small cell lung cancer. The lab also develops diagnostic algorithms for accurate subtyping of small biopsies and investigates the role of metabolic mutations in glioblastoma. These studies aim to improve precision oncology through integrated pathological and immunological insights.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Programmed 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 ALK-translocated tumors, were immunohistochemically evaluated for PD-L1 and PD-1. H23 (EGFRWild-typeEML4-ALK−PD-L1Low) and H2228 (EGFRWild-typeEML4-ALK+PD-L1High) cells were transfected with EML4-ALK or ALK short interf
Abstract Purpose: The plasticity of innate lymphoid cells (ILCs) has been reported in vitro and in the microenvironment of the intestine. However, whether ILC plasticity contributes to regulation of the tumor microenvironment remains unknown. In this study, we explored plasticity of ILCs in human lung cancer. Experimental Design: We analyzed immune subsets and cytokine expression in lung cancers freshly obtained from 80 patients and explored conversion of ILC1 into ILC3 in coculture with lung ca
CD103 is the αE subunit of αEβ7 integrin that is expressed in tissue-resident memory T cells, where it promotes cytotoxic T cell responses against tumors. However, little is known about its expression or clinicopathological implications in non-small cell lung cancer (NSCLC). This study investigated the prognostic implications of CD103+ tumor-infiltrating lymphocytes (TILs) in NSCLC. We established two cohorts: patients with resected NSCLC (n = 132) and patients with pulmonary squamous cell carci
AIMS: Need for accurate histologic subtyping of non-small cell lung carcinomas (NSCLCs) is growing. IHC patterns may be ambiguous in some cases, rendering it difficult to determine subtypes. METHODS AND RESULTS: Tissue microarrays composed of 184 resected NSCLCs were stained for TTF-1, Napsin A, CK7, p40, p63, CK5/6, and mucicarmine. TTF-1 and Napsin A were chosen as the most accurate adenocarcinoma (ADC) marker (ACM), and p40 as squamous cell carcinoma (SCC) marker (SCM). We then prospectively
Glioblastomas (GBMs) are the most aggressive type of primary brain tumors and provide a dismal prognosis. Thus far, several key genes have been identified in GBMs as prognostic and therapeutic targets. Mutations in two isocitrate dehydrogenase (IDH) genes, IDH1 and IDH2, commonly occur in low-grade gliomas and secondary high-grade gliomas, but are rare in primary GBMs. These mutations alter the catalytic activity of IDH proteins, promoting gliomagenesis. Gliomas with IDH1 or IDH2 mutation have b
The gastrointestinal (GI) tract is the most common site of primary extranodal lymphomas. Although B-cell non-Hodgkin lymphomas account for the majority of GI lymphoma, T- or natural killer (NK)-cell lymphomas, including peripheral T-cell lymphoma, enteropathy-associated T-cell lymphoma (EATL), extranodal NK/T-cell lymphoma, and anaplastic large cell lymphoma, also involves the GI tract.1,2 T- or lymphomas are an aggressive disease typically managed with systemic chemotherapy or radiotherapy; how
Acquired resistance to inhibitors of anaplastic lymphoma kinase (ALK) is a major clinical challenge for ALK fusion-positive non-small-cell lung cancer (NSCLC). In the absence of secondary ALK mutations, epigenetic reprogramming is one of the main mechanisms of drug resistance, as it leads to phenotype switching that occurs during the epithelial-to-mesenchymal transition (EMT). Although drug-induced epigenetic reprogramming is believed to alter the sensitivity of cancer cells to anticancer treatm
Invariant natural-killer T ( i NKT) cells play pathogenic roles in allergic asthma in murine models and possibly also humans. While many studies show that the development and functions of innate and adaptive immune cells depend on their metabolic state, the evidence for this in i NKT cells is very limited. It is also not clear whether such metabolic regulation of i NKT cells could participate in their pathogenic activities in asthma. Here, we showed that acetyl-coA-carboxylase 1 (ACC1)-mediated
CAGE, a cancer/testis antigen, was originally isolated from the sera of patients with gastric cancers. Previously, we have shown the role of CAGE in resistance to chemotherapy and target therapy. The aim of this study was to investigate the role of CAGE in osimertinib resistance and determine the prognostic value of CAGE in patients with pulmonary adenocarcinomas. The clinicopathological correlation with CAGE and autophagy flux in patients was examined using immunohistochemistry and in situ hybr
BACKGROUND: The immunologic features of nontuberculous mycobacterial pulmonary disease (NTM-PD) are largely unclear. This study investigated the immunologic features of NTM-PD using digital spatial profiling techniques. METHODS: Lung tissues obtained from six patients with NTM-PD between January 1, 2006, and December 31, 2020, at Seoul National University Hospital were subjected to RNA sequencing. Cores from the peribronchial areas were stained with CD3, CD68, and DNASyto13, and gene expression
The expression of PD-L1 on tumor cells (TC) is used as an immunotherapy biomarker in lung cancer, but heterogeneous intratumoral expression is often observed. To better understand heterogeneity in the lung cancer tumor microenvironment, we performed proteomic and whole-transcriptomic digital spatial profiling analyses of TCs and immune cells (IC) in spatially matched areas based on tumor PD-L1 expression and the status of the immune microenvironment. We validated our findings using IHC, data fro
<div>AbstractPurpose:<p>The plasticity of innate lymphoid cells (ILCs) has been reported <i>in vitro</i> and in the microenvironment of the intestine. However, whether ILC plasticity contributes to regulation of the tumor microenvironment remains unknown. In this study, we explored plasticity of ILCs in human lung cancer.</p>Experimental Design:<p>We analyzed immune subsets and cytokine expression in lung cancers freshly obtained from 80 patients and explored