홍성두 교수
Seong-Doo Hong
서울대학교 치의학과 · 의학
연구실 소개
홍성두 교수의 연구실은 구강악세포종양 및 치아유래 종양의 분자 기전을 규명하고, 특히 MAPK 신호전달 경로의 변동이 종양 발생 및 진행에 미치는 영향을 중심으로 연구를 진행하고 있습니다. BRAF V600E 돌연변이와 EMT(상피세포-중간엽세포 전환)의 독립적 역할, 그리고 항암제인 노르카나타이드(NCTD)의 Apoptosis 유도 및 전이 억제 기전에 대한 기초 연구를 통해 정밀의료 기반의 치료 전략 개발을 목표로 하고 있습니다. 특히 구강암, 땀샘암, 치아유래 종양 등 다양한 종양 모델을 이용한 in vitro 및 in vivo 실험을 통해 약물의 작용 기전을 규명하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
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
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