Seong-Doo Hong
Seoul National University · 医学
研究室紹介
Professor Seong-Doo Hong's research lab specializes in oral and maxillofacial oncology, focusing on the molecular mechanisms underlying odontogenic tumors and oral squamous cell carcinoma (OSCC). The lab investigates key signaling pathways—particularly the MAPK/ERK pathway—through the identification of driver mutations such as BRAF V600E, and explores targeted therapeutic strategies using agents like norcantharidin (NCTD). Research also emphasizes tumor suppressor genes like SOX7 and their prognostic implications in OSCC. The lab integrates molecular pathology, immunohistochemistry, and in vitro/in vivo functional assays to translate basic findings into clinical applications.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15BACKGROUND: The Akt/PKB family of kinases is frequently activated in human cancers, including oral squamous cell carcinoma (OSCC). Akt-induced epithelial-to-mesenchymal transition (EMT) involves downregulation of E-cadherin, which appears to result from upregulation of the transcription repressor Snail. Recently, it was proposed that carcinoma cells, especially in metastatic sites, could acquire the mesenchymal-to-epithelial reverting transition (MErT) in order to adapt the microenvironments and
BACKGROUND: BRAF V600E mutations are activating mutations that have recently been detected in ameloblastoma. However, their prevalence has not been reported in East Asian patients with ameloblastoma and their clinicopathological significance remains unclear. In this study, we examined the prevalence and clinicopathological significance of BRAF V600E mutations in Korean patients with ameloblastoma. In addition, we investigated the relationship between BRAF V600E mutations and epithelial-mesenchym
Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral cavity, remains a lethal disease in over 50% of cases diagnosed annually, due mostly to late detection of this cancer in its advanced stages despite the easy accessibility of the oral cavity for regular examinations. Cripto-1 is a member of the epidermal growth factor (EGF)-CFC protein family and is involved in the activation of several different signaling pathways during embryonic development and cellular transformation
BACKGROUND: Multiple calcifying hyperplastic dental follicles (MCHDF) is a rare disorder that is characterized by multiple impacted teeth and enlarged dental follicles that include calcifications. The current lack of information characterizing MCHDF impedes clinicians from making prompt differential diagnoses. We describe five cases of MCHDF and analyze their clinical and histopathological features in an effort to compare MCHDF with hyperplastic dental follicles (HDF) of singly impacted teeth. M
BACKGROUND: Oral squamous cell carcinomas (OSCCs) are characterized by a high degree of local invasion and a high rate of metastases to cervical lymph nodes. Downregulation of CXCR-4 by siRNA inhibits invasion and growth of breast and colon cancer cells. However, there have been no reports on the downregulation of CXCR-4 by small interfering RNA (siRNA) in oral cancer cells. METHODS: We generated two stable CXCR-4-knockdown clones (KBsi and KOSCC-25Bsi) from the KB and KOSCC-25B OSCC cell lines
BACKGROUND: Although immunohistochemistry (IHC) along with molecular tests has been investigated in ameloblastoma for BRAF V600E detection, VE1 IHC has not been studied in odontogenic carcinomas (OCs) and benign mixed epithelial and mesenchymal odontogenic tumours (BMOTs). Here, we performed BRAF V600E mutation analysis, examined the expression pattern of VE1 IHC, and comparatively evaluated the performance of two VE1 antibodies in ameloblastomas, OCs and BMOTs. METHODS: BRAF V600E detection was
Norcantharidin (NCTD), a demethylated analog of cantharidin isolated from blister beetles, has been used as a promising anticancer agent; however, the underlying function of NCTD against human oral squamous cell carcinoma (OSCC) has not been fully understood. Here, this study was aimed to investigate the apoptotic effect and molecular targets of NCTD in human OSCC in vitro and in vivo. The anticancer effects of NCTD and its related molecular mechanisms were evaluated by trypan blue exclusion ass
Abstract Although several types of odontogenic tumors share the same mutations in MAPK pathway genes, their effects on MAPK activation remain unclarified. This study aimed to evaluate the associations between these mutations and ERK phosphorylation in ameloblastoma and mixed odontogenic tumors (MOTs) and to analyze the expression pattern of phosphorylated ERK (p‐ERK) for determining the involvement of MAPK activation in the development and progression of odontogenic tumors. Forty‐three odontogen