Publications by authors named "Geng-Qiang Ling"
Early brain injury (EBI)‑induced neuronal apoptosis is primarily responsible for the subsequent complications of aneurysmal subarachnoid hemorrhage (aSAH), which may increase the risk of mortality in patients with aSAH. c‑Jun N‑terminal kinase (JNK) has been demonstrated to be a promoter of EBI‑induced cell apoptosis, although the mechanism has yet to be fully elucidated. The present study aimed to explore whether the role of JNK1 is associated with tumor protein p53 (p53), which is one of the most important factor that triggers cell apoptosis.
View Article and Find Full Text PDFArticle Synopsis
- Traditional antiangiogenic therapy for glioblastoma multiforme (GBM) is less effective, potentially due to vasculogenic mimicry (VM) linked to cancer stem-like cells (SLCs).
- All-trans retinoic acid (ATRA) can differentiate these SLCs and has shown promise in reducing their harmful properties in other cancers.
- In this study, ATRA was found to enhance differentiation markers and reduce proliferation, invasiveness, and VM formation abilities in U87 glioblastoma SLCs, indicating it could be a novel treatment option for GBM.
Article Synopsis
- Vasculogenic mimicry (VM) is a process where tumor cells form their own tubular structures to supply nutrients and oxygen, aiding tumor growth in malignant tumors.
- A study found VM in 22% of medulloblastoma tissues, with its presence linked to specific molecular markers and lower microvessel density, suggesting it complements blood supply.
- Patients with VM exhibited shorter overall survival, establishing VM as a significant independent prognostic factor for survival in medulloblastoma cases.
Article Synopsis
- Immunotoxins show potential as an alternative treatment for brain cancers like gliomas, but they struggle to effectively penetrate tumor tissue.
- This study explores using human bone marrow-derived mesenchymal stem cells (hMSCs) to deliver EphrinA1-PE38, an immunotoxin targeting the EphA2 receptor prevalent in gliomas.
- Results demonstrated that engineered hMSCs can express and release the immunotoxin, leading to effective tumor growth inhibition in a glioma model, highlighting gene therapy's promise for treating these tumors.