Sungkyunkwan University · 医学
Professor Jung Yong Hong's research lab specializes in translational oncology, focusing on molecular mechanisms and targeted therapies in hematologic malignancies and rare solid tumors. The lab investigates splicing factor mutations in myelodysplastic syndromes, claudin 18.2 expression in epithelial cancers, and the tumor microenvironment's role in lymphoma prognosis. Key research directions include identifying biomarkers for treatment response, understanding resistance mechanisms to targeted agents like imatinib in dermatofibrosarcoma protuberans, and exploring inflammatory biomarkers such as CXCL10 in diffuse large B-cell lymphoma.
Figures are computed from collected data and may differ slightly.
NCT#03163992 (first posted: May 23, 2017).
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.
In the present analysis of 58 Korean MDS patients, mutations in the splicing machinery genes SRSF2, U2AF1 and ZRSR2 were detected in 5 (8.6%), 10 (17.2%) and 6 (10.3%) patients, respectively, and the incidence of SRSF2 mutation was lower than those of previous series. The overall response rates (ORRs) including complete remission (CR), partial response (PR), and marrow CR (mCR) were 42.9% in the spliceosome wild-type (WT) group and 46.7% in the spliceosome-mutated group (p>0.999). The median OS
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
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
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
Further research is anticipated, as follows: first, identifying geographical/ethnical differences in gene expression profiles and CD30 coexpression in EBV-positive DLBCL of the elderly; second, feasibility of the revision of the current disease entity confined to elderly patients; and third, novel therapeutic approaches targeting CD30 and the NF-κB and JAK/STAT pathways in EBV-positive DLBCL of the elderly.
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