Jeong Yung Hong
Sungkyunkwan University · Medicine
About the Lab
Professor Jeong Yung Hong's research lab specializes in translational oncology, focusing on the molecular characterization of cancer genomics, particularly in hepatocellular carcinoma, myelodysplastic syndromes, and rare sarcomas. The lab integrates multi-omics approaches—including whole-exome and single-cell RNA sequencing—to identify predictive biomarkers and therapeutic targets in immunotherapy and hypomethylating agent responses. A key research direction involves understanding the tumor microenvironment and inflammatory biomarkers, such as CXCL10 and systemic inflammatory markers, to improve prognostic prediction in lymphomas and other malignancies. The lab also investigates mechanisms of drug resistance in targeted therapies, especially in dermatofibrosarcoma protuberans treated with imatinib.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15BACKGROUND: A limited number of studies have characterized genomic properties of hepatocellular carcinoma (HCC) patients in response to anti-PD-1 immunotherapy. METHODS: Herein, we performed comprehensive molecular characterization of immediate (D-42 to D-1) pre-treatment tumor biopsy specimens from 60 patients with sorafenib-failed HCC in a single-arm prospective phase II trial of pembrolizumab. Objective response rate was the primary efficacy endpoint. We used whole-exome sequencing, RNA seque
Our results add to the emerging literature about claudin 18.2 expression in various cancer types and support the need for extended clinical exploration of zolbetuximab.
// Seyoung Seo 1, * , Jung Yong Hong 1, * , Shinkyo Yoon 1, 7 , Changhoon Yoo 1 , Ji Hyun Park 1 , Jung Bok Lee 2 , Chan-sik Park 3 , Jooryung Huh 4 , Yoonse Lee 4 , Kyung Won Kim 5 , Jin-Sook Ryu 6 , Seok Jin Kim 8 , Won Seog Kim 8 , Dok Hyun Yoon 1 , Cheolwon Suh 1 1 Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 2 Department of Medical Statistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 3 Department of Path
BACKGROUND: Hypomethylating agents, such as azacitidine and decitabine, now constitute one of the mainstays of myelodysplastic syndrome (MDS) treatment. In recent years, novel recurrent mutations in multiple genes encoding RNA spliceosomal machinery (SRSF2, U2AF1, ZRSR2, SF3B1) were revealed. However, the clinical impact of these mutations on the outcomes of treatment of MDS patients with hypomethylating agents has not been described. PATIENTS AND METHODS: A total of 58 de novo MDS patients were
Inflammatory biomarkers, such as the neutrophil to lymphocyte ratio (NLR), lymphocyte to monocyte ratio (LMR), and Glasgow Prognostic Score (GPS) have been proposed to predict prognosis in diffuse large B-cell lymphoma (DLBCL). C-X-C motif ligand 10 (CXCL10) is a chemokine released from inflammatory cells in the tumor microenvironment and is known to promote tumor cell migration and invasion. In this study, we investigated the clinical impact of pretreatment serum level of CXCL10 on the prognost
Dermatofibrosarcoma protuberans (DFSP) is a very rare soft tissue sarcoma. DFSP often reveals a specific chromosome translocation, t(17;22)(q22;q13), which results in the fusion of collagen 1 alpha 1 (COL1A1) gene and platelet-derived growth factor-B (PDGFB) gene. The COL1A1-PDGFB fusion protein activates the PDGFB receptor and resultant constitutive activation of PDGFR receptor is essential in the pathogenesis of DFSP. Thus, blocking PDGFR receptor activation with imatinib has shown promising a
Abstract Background JAK2 expression and activity increased in classical Hodgkin lymphoma (HL) and primary mediastinal large B-cell lymphoma (PMBCL) because both of them were reported to have chromosome 9p24.1/JAK2 amplification. Thus, JAK2 has been suggested as a potential therapeutic target in both disease having similar clinical and genetic features, and a previous in vitro and in vivo study showed cHL and PMBCL with JAK2 amplification were sensitive to JAK2 inhibition. However, the efficacy o
Survivin is an inhibitor of apoptosis and is upregulated by Epstein-Barr virus (EBV) latent genes. Given the frequent association of EBV with lymphoid malignancies, survivin is expected to have prognostic value in diffuse large B-cell lymphoma (DLBCL). Thus, we measured the pretreatment serum level of survivin in DLBCL patients and analyzed its association with survival outcome and EBV status, as represented by EBV-encoded RNA (EBER) in DLBCL. Pretreatment serum survivin level was measured in pa
Research Areas
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