Jeongwu Lee

Targeting MET and mTOR Synergistically Overcomes Adaptive Resistance in Glioblastoma

Yunzhan Li, Hanif Khan, Şeyma Demirsoy, Muhammad Younis et autres

Glioblastoma (GBM) is the most aggressive primary brain tumor with limited therapeutic options and extremely poor prognosis. Aberrant activation of the receptor tyrosine kinase MET drives tumor progression, therapeutic resistance, and reduced survival, particularly in the mesenchymal GBM subtype. Given its crucial …

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BNIP3-mTOR Signaling Mediates Resistance to MET Inhibition in Glioblastoma

Yunzhan Li, Hanif Khan, Şeyma Demirsoy, William Bernhardt et autres

ABSTRACT Glioblastoma (GBM) is an aggressive primary brain malignancy with poor prognosis due to rapid progression, extensive invasiveness, and intrinsic resistance to standard therapies. Aberrant activation of receptor tyrosine kinases (RTKs), particularly MET, drives tumor proliferation, invasion, and therapy resistance. Here, we …

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EZH2 Protects Glioma Stem Cells from Radiation-Induced Cell Death in a MELK/FOXM1-Dependent Manner

Sung-Hak Kim, Kaushal Joshi, Ravesanker Ezhilarasan, Toshia R. Myers et autres

The semaphorin 3A/neuropilin-1 pathway promotes clonogenic growth of glioblastoma via activation of TGF-β signaling

Hye-Min Jeon, Yong Jae Shin, Jaehyun Lee, Nakho Chang et autres

Glioblastoma (GBM) is the most lethal brain cancer with a dismal prognosis. Stem-like GBM cells (GSCs) are a major driver of GBM propagation and recurrence; thus, understanding the molecular mechanisms that promote GSCs may lead to effective therapeutic approaches. Through in vitro …

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Tissue factor is a critical regulator of radiation therapy-induced glioblastoma remodeling

Hye-Min Jeon, Jeong‐Yub Kim, Hee Jin Cho, Won Jun Lee et autres

Radiation therapy (RT) provides therapeutic benefits for patients with glioblastoma (GBM), but inevitably induces poorly understood global changes in GBM and its microenvironment (TME) that promote radio-resistance and recurrence. Through a cell surface marker screen, we identified that CD142 (tissue factor or …

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Supplementary Figure 6 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 120K, Supplemental data for Figure 5

Supplementary Methods from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 117K

Supplementary Table 1 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

XLS file - 42K, Candidate genes differentially required for expansion of G166-BTICs

Supplementary Figure 3 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 74K, BUB1B and other mitotic checkpoint genes are up-regulated in BTIC isolates and Ras- transformed astrocytes

Supplementary Figure 4 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 1.3MB, Examination of the effects of BUB1B knockdown on mitotic checkpoint activity

Supplementary Figure 5 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 1MB, Additional information showing cancer cells have added requirement on BUB1B for chromosome alignment and KT-MT attachment

Supplementary Figure 2 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells

Yulong Ding, Christopher G. Hubert, Jacob Herman, Philip Corrin et autres

PDF file - 133K, BTIC and NSC growth phenotypes resulting from knockdown of PLK1 and pharmacological inhibition of Aurora B kinase