ArticleFrontiers in oncology2024
GQIcombi application to subdue glioma via differentiation therapy.
Article in Frontiers in oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Aptamers Structure Flexibility Is Crucial to EGFR Inhibition Function.Pharmaceuticals (Basel, Switzerland) · 2026Article
- ZEB1 and Uveal Melanoma Invasiveness.International journal of molecular sciences · 2025Article
- Real-Time Kinetics of Internalization of Anti-EGFR DNA Aptamers and Aptamer Constructs into Cells Derived from Glioblastoma Patients as Indicated by Doxorubicin.International journal of molecular sciences · 2025Article
- N-Glycoside of Indolo[2,3-Pharmaceuticals (Basel, Switzerland) · 2024Article
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9 authors.
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Abstract
Current therapy protocols fail to cure high-grade gliomas and prevent recurrence. Therefore, novel approaches need to be developed. A re-programing of glioma cell fate is an alternative attractive way to stop tumor growth. The two-step protocol applies the antiproliferative GQ bi-(AID-1-T) and small molecule inducers with BDNF to trigger neural differentiation into terminally differentiated cells, and it is very effective on GB cell cultures. This original approach is a successful example of the "differentiation therapy". To demonstrate a versatility of this approach, in this publication we have extended a palette of cell cultures to gliomas of II, III and IV Grades, and proved an applicability of that version of differential therapy for a variety of tumor cells. We have justified a sequential mode of adding of GQIcombi components to the glioma cells. We have shown a significant retardation of tumor growth after a direct injection of GQIcombi into the tumor in rat brain, model 101/8. Thus, the proposed strategy of influencing on cancer cell growth is applicable to be further translated for therapy use.
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