Donggeon Kim

Sema3A binds to its receptor neuropilin-1 (NRP1) and facilitates an interaction between NRP1 and TGF-β receptor 1 (TGF-βR1), which in turn leads to activation of canonical TGF-β signaling in both GSCs and NPCs. TGF-β signaling enhances self-renewal and survival of GBM tumors through induction of key stem cell factors, but it evokes cytostatic responses in NPCs. Blockage of the Sema3A/NRP1 axis via shRNA-mediated knockdown of Sema3A or NRP1 impeded clonogenic growth and TGF-β pathway activity in… 더보기

Sema3A binds to its receptor neuropilin-1 (NRP1) and facilitates an interaction between NRP1 and TGF-β receptor 1 (TGF-βR1), which in turn leads to activation of canonical TGF-β signaling in both GSCs and NPCs. TGF-β signaling enhances self-renewal and survival of GBM tumors through induction of key stem cell factors, but it evokes cytostatic responses in NPCs. Blockage of the Sema3A/NRP1 axis via shRNA-mediated knockdown of Sema3A or NRP1 impeded clonogenic growth and TGF-β pathway activity in GSCs and inhibited tumor growth in vivo. 더보기 취소

Identified molecular characteristics associated with temozolomide (TMZ) resistance in primary isocitrate dehydrogenase wild-type glioblastoma (GBM) patients. They used patient-derived glioma stem-like cells to develop a machine learning model that predicts TMZ response from genomic and transcriptomic signatures. They validated their findings with multi-sector sequencing analysis and showed highly heterogeneous TMZ-response patterns within each GBM patient. The model was developed into a… 더보기

Identified molecular characteristics associated with temozolomide (TMZ) resistance in primary isocitrate dehydrogenase wild-type glioblastoma (GBM) patients. They used patient-derived glioma stem-like cells to develop a machine learning model that predicts TMZ response from genomic and transcriptomic signatures. They validated their findings with multi-sector sequencing analysis and showed highly heterogeneous TMZ-response patterns within each GBM patient. The model was developed into a webserver for public use. The study highlights the potential clinical value of precision medicine approaches in treating GBM. 더보기 취소

SITC2020, Poster

In the present study, site-specific drug–conjugate technology was applied to develop an ADC using the human-mouse cross-reactive c-Met antibody and a prodrug pyrrolobenzodiazepine (PBD).

antagonizing MDK reduced the survival of GBM tumor spheres through the promotion of cell cycle arrest and the consequent apoptotic cell death caused by oxidative stress-induced DNA damage. We also identified PCBP4, a novel molecular predictor of resistance to anti-MDK treatment. Collectively, our results indicate that MDK inhibition is an important therapeutic option by suppressing GIC survival through the induction of ROS-mediated cell cycle arrest and apoptosis.