- Blood properties and coagulation
- Glioma Diagnosis and Treatment
- Nuclear Receptors and Signaling
- RNA Research and Splicing
- Macrophage Migration Inhibitory Factor
- Medical Imaging Techniques and Applications
- Nicotinic Acetylcholine Receptors Study
- Hepatocellular Carcinoma Treatment and Prognosis
- DNA Repair Mechanisms
- Cancer Mechanisms and Therapy
- RNA Interference and Gene Delivery
- Neurogenesis and neuroplasticity mechanisms
- Nuclear Structure and Function
- MRI in cancer diagnosis
- Drug Transport and Resistance Mechanisms
- Biochemical Analysis and Sensing Techniques
- Smoking Behavior and Cessation
- Axon Guidance and Neuronal Signaling
- Phagocytosis and Immune Regulation
- Signaling Pathways in Disease
National Cancer Center
2017-2024
National Cancer Center
2022
Abstract Diffuse infiltration is the main reason for therapeutic resistance and recurrence in glioblastoma (GBM). However, potential targeted therapies GBM stem-like cell (GSC) which responsible invasion are limited. Herein, we report Insulin-like Growth Factor-Binding Protein 5 (IGFBP5) a ligand Receptor tyrosine kinase like Orphan 1 (ROR1), as promising target GSC invasion. Using GSC-derived brain tumor model, GSCs were characterized into invasive or non-invasive subtypes, RNA sequencing...
Necrosis is a hallmark of glioblastoma (GBM) and responsible for poor prognosis resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) upregulated in perinecrotic region triggered mesenchymal (MES) transdifferentiation glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPβ, TAZ, STAT3. TGM2 expression was...
As the clinical failure of glioblastoma treatment is attributed by multiple components, including myelin-associated infiltration, assessment molecular mechanisms underlying such process and identification infiltrating cells have been primary objectives in research. Here, we adopted radiogenomic analysis to screen for functionally relevant genes that orchestrate glioma cell infiltration through myelin promote aggressiveness. The receptor Nogo ligand (NgR1) was selected as top candidate...
Radiation therapy is among the most essential treatment methods for glioblastoma multiforme (GBM). Radio-resistance and cancer stem cell properties can cause therapeutic resistance, heterogeneity, poor prognoses in association with GBM. Furthermore, GBM subtype transition from proneural to malignant mesenchymal after radiation also accounts high resistance conventional treatments. Here, we demonstrate that inhibition of macrophage migration inhibitory factor (MIF) D-dopachrome tautomerase...
Leucine-rich repeat kinase 2 (LRRK2), a large GTP-regulated serine/threonine kinase, is well-known for its mutations causing late-onset Parkinson's disease. However, the role of LRRK2 in glioblastoma (GBM) carcinogenesis has not yet been fully elucidated. Here, we discovered that was overexpressed 40% GBM patients, according to tissue microarray analysis, and high expression correlated with poor prognosis patients. stemness factors were highly expressed various patient-derived stem cells,...
Introduction Recently, electric cigarettes with liquid (e-liquid) were introduced as an alternative to tobacco smoking. They promoted possible cessation aids and considered be potentially less harmful than traditional tobacco-based cigarettes. However, there is little information on the toxicants present in e-liquids their carcinogenic effects. Methods Western blot analysis was performed identify protein levels of cancer progression related signal transducers. Patient-derived brain tumor...
To correlate 18F-FDG uptake on PET/CT with patterns of arterial and portal perfusion multi-detector CT (MDCT) in patients hepatocellular carcinoma (HCC) to assess the value variables from MDCT predicting histological grades overall survival.We retrospectively analyzed 66 HCC who underwent surgical treatment. Tumor peak standard (SUV) was divided by mean liver SUV (T/LSUV). The tumor Hounsfield unit (HU) HU calculated for (T/LHU-A) phases (T/LHU-P). All were into three groups: I, T/LHU-A ≤l...
Abstract A significant hurdle in treating glioblastoma (GBM) is addressing the development of drug resistance. In this study, role Family Sequence Similarity 20, Member C (Fam20C) as a central player bevacizumab resistant GBM mouse model investigated. vivo analyses confirm that Fam20C upregulation accelerates resistance and correlates with tumor progression. Proteomic conditioned media cell lysates subsequent to knockout (KO) cells reveal regulatory both intracellular extracellular aspects...
<p>Supplementary Figure 1 related to 1. TGM2 is highly expressed in the necrotic region of MES GBM. Supplementary 2 2. regulates stemness MES, PN, and CL GSCs. 3 4. A negative correlation between C/EBPβ GADD153.</p>
<p>Supplementary Figure 1 related to 1. TGM2 is highly expressed in the necrotic region of MES GBM. Supplementary 2 2. regulates stemness MES, PN, and CL GSCs. 3 4. A negative correlation between C/EBPβ GADD153.</p>
<div>Abstract<p>Necrosis is a hallmark of glioblastoma (GBM) and responsible for poor prognosis resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) upregulated in perinecrotic region triggered mesenchymal (MES) transdifferentiation glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPβ, TAZ,...
<div>Abstract<p>Necrosis is a hallmark of glioblastoma (GBM) and responsible for poor prognosis resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) upregulated in perinecrotic region triggered mesenchymal (MES) transdifferentiation glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPβ, TAZ,...