Dohyun Nam
Sungkyunkwan University · Medicine
About the Lab
Professor Dohyun Nam's research lab focuses on advancing personalized cancer therapy, particularly for glioblastoma (GBM), by developing patient-derived preclinical models and dissecting the molecular mechanisms driving tumor progression and treatment resistance. The lab investigates key signaling pathways such as MET and Wnt/β-catenin in glioblastoma stem cells (GSCs), with an emphasis on the tumor microenvironment's role in promoting malignancy, including necrosis-induced mesenchymal transition. Innovative platforms, including microfluidic chips for high-throughput drug screening, are developed to overcome translational challenges in precision oncology.
Research Overview
Research Output Trend
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Selected Papers
15Frequent discrepancies between preclinical and clinical results of anticancer agents demand a reliable translational platform that can precisely recapitulate the biology of human cancers. Another critical unmet need is the ability to predict therapeutic responses for individual patients. Toward this goal, we have established a library of orthotopic glioblastoma (GBM) xenograft models using surgical samples of GBM patients. These patient-specific GBM xenograft tumors recapitulate histopathologica
BACKGROUND: The authors investigated whether expression of c-Met protein in glioblastomas is associated with overall survival and biologic features representing tumor invasiveness in patients with glioblastomas. METHODS: Paraffin-embedded specimens of glioblastomas from 62 patients treated in a single institution were assessed by immunohistochemical (IHC) analysis of c-Met expression. On the basis of the clinical data for these patients, the association between c-Met expression and clinicobiolog
Glioblastomas multiforme (GBM) contain highly tumorigenic, self-renewing populations of stem/initiating cells [glioblastoma stem cells (GSC)] that contribute to tumor propagation and treatment resistance. However, our knowledge of the specific signaling pathways that regulate GSCs is limited. The MET tyrosine kinase is known to stimulate the survival, proliferation, and invasion of various cancers including GBM. Here, we identified a distinct fraction of cells expressing a high level of MET in h
These data suggest that Wnt/β-catenin signaling is a key downstream effector of MET signaling and contributes to the maintenance of GSC and GBM malignancy.
Contemporary cancer therapy refers to treatment based on genetic abnormalities found in patient's tumor. However, this approach is faced with numerous challenges, including tumor heterogeneity and molecular evolution, insufficient tumor samples available along with genetic information linking to clinical outcomes, lack of therapeutic drugs containing pharmacogenomic information, and technical limitations of rapid drug efficacy tests with insufficient quantities of primary cancer cells from patie
Research Areas
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