Glioblastoma(GBM)remains the most aggressive and lethal brain tumor in adults and poses significant challenges to patient survival.This review provides a comprehensive exploration of the molecular and genetic landscap...Glioblastoma(GBM)remains the most aggressive and lethal brain tumor in adults and poses significant challenges to patient survival.This review provides a comprehensive exploration of the molecular and genetic landscape of GBM,focusing on key oncogenic drivers,such as epidermal growth factor receptor(EGFR),platelet-derived growth factor receptor(PDGFR),and the PI3K/AKT/mTOR pathway,which are critical for tumorigenesis and progression.We delve into the role of epigenetic alterations,including DNA methylation and histone modifications,in driving therapy resistance and tumor evolution.The tumor microenvironment is known for its pivotal role in immune evasion,with tumor-associated macrophages,myeloid-derived suppressor cells,and regulatory T cells creating an immunosuppressive niche that sustains GBM growth.Emerging therapies,such as immunotherapies,oncolytic viral therapies,extracellular vesicle-based approaches,and non-coding RNA interventions,are highlighted as promising avenues to disrupt GBM pathogenesis.Advances in precision medicine and innovative technologies,including electric field therapy and locoregional treatments,are discussed for their potential to overcome the blood‒brain barrier and treatment resistance.Additionally,this review underscores the importance of metabolic reprogramming,particularly hypoxia-driven adaptations and altered lipid metabolism,in fueling GBM progression and influencing the therapeutic response.展开更多
Dear Editor,Pathogenic fungi often undergo rapid morphological transitions to adapt to dynamic environments during infections and in natural habitats(Biswas et al.,2007;Prasad and Tippana,2023).These phenotypic transi...Dear Editor,Pathogenic fungi often undergo rapid morphological transitions to adapt to dynamic environments during infections and in natural habitats(Biswas et al.,2007;Prasad and Tippana,2023).These phenotypic transitions are primarily driven by environmental cues through nongenetic alterations,including epigenetic,transcriptional,and post-transcriptional modifications(Biswas et al.,2007).展开更多
文摘Glioblastoma(GBM)remains the most aggressive and lethal brain tumor in adults and poses significant challenges to patient survival.This review provides a comprehensive exploration of the molecular and genetic landscape of GBM,focusing on key oncogenic drivers,such as epidermal growth factor receptor(EGFR),platelet-derived growth factor receptor(PDGFR),and the PI3K/AKT/mTOR pathway,which are critical for tumorigenesis and progression.We delve into the role of epigenetic alterations,including DNA methylation and histone modifications,in driving therapy resistance and tumor evolution.The tumor microenvironment is known for its pivotal role in immune evasion,with tumor-associated macrophages,myeloid-derived suppressor cells,and regulatory T cells creating an immunosuppressive niche that sustains GBM growth.Emerging therapies,such as immunotherapies,oncolytic viral therapies,extracellular vesicle-based approaches,and non-coding RNA interventions,are highlighted as promising avenues to disrupt GBM pathogenesis.Advances in precision medicine and innovative technologies,including electric field therapy and locoregional treatments,are discussed for their potential to overcome the blood‒brain barrier and treatment resistance.Additionally,this review underscores the importance of metabolic reprogramming,particularly hypoxia-driven adaptations and altered lipid metabolism,in fueling GBM progression and influencing the therapeutic response.
基金supported by the National Key Research and Development Program of China(2022YFC2303000,2021YFC2300400)the National Natural Science Foundation of China(31930005,82272359,32170194,32170193,82202546)the China Postdoctoral Science Foundation(2023M730684,2022M720804)。
文摘Dear Editor,Pathogenic fungi often undergo rapid morphological transitions to adapt to dynamic environments during infections and in natural habitats(Biswas et al.,2007;Prasad and Tippana,2023).These phenotypic transitions are primarily driven by environmental cues through nongenetic alterations,including epigenetic,transcriptional,and post-transcriptional modifications(Biswas et al.,2007).
