Jaemoon Koh

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

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

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

Invariant natural-killer T (<i>i</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>i</i>NKT cells is very limited. It is also not clear whether such metabolic regulation of <i>i</i>NKT cells could participate in their pathogenic activities in asthma. Here, we showed that acetyl-coA-carboxylase 1

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

NTM-PD exhibits distinct immunologic signatures characterized by the activation of macrophages without T cell activation.

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

&lt;div&gt;AbstractPurpose:&lt;p&gt;The plasticity of innate lymphoid cells (ILCs) has been reported &lt;i&gt;in vitro&lt;/i&gt; 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.&lt;/p&gt;Experimental Design:&lt;p&gt;We analyzed immune subsets and cytokine expression in lung cancers freshly obtained from 80 patients and explored

&lt;div&gt;AbstractPurpose:&lt;p&gt;The plasticity of innate lymphoid cells (ILCs) has been reported &lt;i&gt;in vitro&lt;/i&gt; 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.&lt;/p&gt;Experimental Design:&lt;p&gt;We analyzed immune subsets and cytokine expression in lung cancers freshly obtained from 80 patients and explored

&lt;p&gt;The most up- or downregulated gene sets in immune cells between IF_PDL1H and ID_PDL1H&lt;/p&gt;

Abstract 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)-

Invariant natural-killer T (iNKT) 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 iNKT cells is very limited. It is also not clear whether such metabolic regulation of iNKT cells could participate in their pathogenic activities in asthma. Here, we showed that acetyl-coA-carboxylase 1 (ACC1)-mediated de n

Invariant natural-killer T (iNKT) 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 iNKT cells is very limited. It is also not clear whether such metabolic regulation of iNKT cells could participate in their pathogenic activities in asthma. Here, we showed that acetyl-coA-carboxylase 1 (ACC1)-mediated de n

&lt;p&gt;The most up- or downregulated gene sets in immune cells between IF_PDL1H and IF_PDL1L&lt;/p&gt;