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| http://dx.doi.org/10.5115/acb.23.159E | DOI Listing |
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Discovery of noncovalent diaminopyrimidine-based Inhibitors for glioblastoma via a dual FAK/DNA targeting strategy.
Eur J Med Chem
January 2025
School of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China. Electronic address:
Temozolomide, a widely used alkylating agent for glioblastoma treatment, faces significant challenges due to the development of resistance, which severely impacts patient survival. This underscores the urgent need for novel strategies to overcome this barrier. Focal adhesion kinase (FAK), an intracellular non-receptor tyrosine kinase, is highly expressed in glioblastoma cells and has been identified as a promising therapeutic target for anti-glioblastoma drug development.
View Article and Find Full Text PDFDevelopment and experimental validation of dephosphorylation-related biomarkers to assess prognosis and immunotherapeutic response in gliomas.
Front Immunol
January 2025
Department of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Background: Gliomas are common aggressive brain tumors with poor prognosis. Dephosphorylation-related biomarkers are in a void in gliomas. This study aims to construct a validated prognostic risk model for dephosphorylation, which will provide new directions for clinical treatment, prognostic assessment, and temozolomide (TMZ) resistance in glioma patients.
View Article and Find Full Text PDFFluorescent Polymer Nanocomposites as Novel Drug-Loading and Targeted Delivery Nanocarriers for Glioma Therapy by Modulating ERBB4.
J Fluoresc
December 2024
Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Gliomas are the most common type of tumor in the human central nervous system, characterized by high aggressiveness, elevated mortality, and poor prognosis. Therefore, developing new therapeutic strategies is crucial for improving glioma treatment. Temozolomide (TMZ) is widely used in glioma therapy due to its excellent ability to penetrate the blood-brain barrier.
View Article and Find Full Text PDFTonabersat enhances temozolomide-mediated cytotoxicity in glioblastoma by disrupting intercellular connectivity through connexin 43 inhibition.
Mol Oncol
December 2024
Department of Neurosurgery, University Hospital Bonn, Germany.
Glioblastoma cells rely on connexin 43 (Cx43)-based gap junctions (GJs) for intercellular communication, enabling them to integrate into a widely branched malignant network. Although there are promising prospects for new targeted therapies, the lack of clinically feasible GJ inhibitors has impeded their adoption in clinical practice. In the present study, we investigated tonabersat (TO), a blood-brain-barrier-penetrating drug with GJ-inhibitory properties, in regard to its potential to disassemble intercellular connectivity in glioblastoma networks.
View Article and Find Full Text PDFTemozolomide overcoming resistance to immune checkpoint inhibitors in relapsed/refractory metastatic melanoma? Insights from a single center series.
J Oncol Pharm Pract
November 2024
Lucy Curci Cancer Center, Eisenhower Health, Rancho Mirage, CA, USA.
There is a need to develop more effective salvage therapies for patients with relapsed melanoma of the skin. Research has shown that chemotherapy-induced cancer cell death may increase immunogenic antigen exposure, or upregulation of co-inhibitory ligands such as PD-L1, thereby augmenting immune checkpoint inhibitor (ICI) efficacy. In addition, chemotherapy preconditioning may lead to depletion of Tregs, known to suppress immune anti-melanoma responses.
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