Diffuse midline glioma in children, and glioblastoma in adults, are the most lethal primary malignancy in the central nervous system, with a dismal prognosis. Despite over a century of research, curative treatment remains elusive. Surgery, radiation, and chemotherapy make up the core of standard therapeutic regimens today, but rarely improve outcomes with more than a few months. Therapeutic failure could be attributed to the diffuse and invasive nature of this disease, coupled with a lack of therapeutic compounds, and acquired resistance to treatment compounds through multiple driver mutations. Advancements in molecular pathology have recently shown that epigenetic modifications influence glioma proliferation, invasion, and metastasis, as well as prognosis, interacting closely in the occurrence and progression of this disease. Glioma development and epigenetic phenomena, such as DNA methylation, chromatin remodelling, histone modifications and abnormal microRNA, are closely related, and as such, targeting these changes offer new hope in finding a cure.
Due to the complicated heterogeneous pathogenesis of glioma, epigenetic applications to glioma clinical treatment are still limited. “Omics’’ have advanced our understanding of the cancer epigenome, and as such, multiple genes and enzymes that regulate epigenetic modifications have become new targets for glioma treatment strategies. The reversibility and plastic nature of epigenetic modifications would enable the resetting of the cancer epigenome, making them prospective druggable targets for anticancer strategies. Targeting these alterations to exploit glioma vulnerabilities that could lead to novel therapeutics and the potential for personalised cancer medicine in treating paediatric and adult gliomas.
With this research topic, we aim to shed light on the most recent advances on the epigenetics of gliomas, how these processes promote glioma growth and progression, and ways in which they can be regulated to synchronise with current treatment modalities for the benefit of the patient.
Basic biology, translational and clinical submissions investigating epigenetic therapeutic targets in paediatric and adult high-grade gliomas will be considered for this research topic, focusing on, but not limited to:
• Glioma-specific epigenetic abnormalities
• How epigenetic modifications influence glioma progression
• How dysregulation of epigenetic processes promotes treatment resistance
• Novel epigenetic targets inhibiting disease progression
• Synergistic treatment and innovative drug modalities targeting epigenetic modifications
• Abnormalities in genes involved in cell cycle regulation or tumour suppressor genes that could lead to glioma occurrence
• Exploring the regulation and function of DNA methylation in glioma cells
• Strategies promoting epithelial to mesenchymal transition (EMT) in glioma
• Chromatin remodelling and transcription regulation in gliomas
• Oncology biomarkers and prediction of therapeutic resistance
Note: Manuscripts that are solely in silico/bioinformatic without either validation in actual clinical tumor samples from patients or functional validation in at least 2 cells lines in vitro or in vivo are not considered in scope
Conflict of interest declaration: Dr. Ziegler reports consulting & advisory board fees from Astra Zeneca, Novartis, Alexion, Day One, Accendatech, FivepHusion, Bayer and Amgen..
Diffuse midline glioma in children, and glioblastoma in adults, are the most lethal primary malignancy in the central nervous system, with a dismal prognosis. Despite over a century of research, curative treatment remains elusive. Surgery, radiation, and chemotherapy make up the core of standard therapeutic regimens today, but rarely improve outcomes with more than a few months. Therapeutic failure could be attributed to the diffuse and invasive nature of this disease, coupled with a lack of therapeutic compounds, and acquired resistance to treatment compounds through multiple driver mutations. Advancements in molecular pathology have recently shown that epigenetic modifications influence glioma proliferation, invasion, and metastasis, as well as prognosis, interacting closely in the occurrence and progression of this disease. Glioma development and epigenetic phenomena, such as DNA methylation, chromatin remodelling, histone modifications and abnormal microRNA, are closely related, and as such, targeting these changes offer new hope in finding a cure.
Due to the complicated heterogeneous pathogenesis of glioma, epigenetic applications to glioma clinical treatment are still limited. “Omics’’ have advanced our understanding of the cancer epigenome, and as such, multiple genes and enzymes that regulate epigenetic modifications have become new targets for glioma treatment strategies. The reversibility and plastic nature of epigenetic modifications would enable the resetting of the cancer epigenome, making them prospective druggable targets for anticancer strategies. Targeting these alterations to exploit glioma vulnerabilities that could lead to novel therapeutics and the potential for personalised cancer medicine in treating paediatric and adult gliomas.
With this research topic, we aim to shed light on the most recent advances on the epigenetics of gliomas, how these processes promote glioma growth and progression, and ways in which they can be regulated to synchronise with current treatment modalities for the benefit of the patient.
Basic biology, translational and clinical submissions investigating epigenetic therapeutic targets in paediatric and adult high-grade gliomas will be considered for this research topic, focusing on, but not limited to:
• Glioma-specific epigenetic abnormalities
• How epigenetic modifications influence glioma progression
• How dysregulation of epigenetic processes promotes treatment resistance
• Novel epigenetic targets inhibiting disease progression
• Synergistic treatment and innovative drug modalities targeting epigenetic modifications
• Abnormalities in genes involved in cell cycle regulation or tumour suppressor genes that could lead to glioma occurrence
• Exploring the regulation and function of DNA methylation in glioma cells
• Strategies promoting epithelial to mesenchymal transition (EMT) in glioma
• Chromatin remodelling and transcription regulation in gliomas
• Oncology biomarkers and prediction of therapeutic resistance
Note: Manuscripts that are solely in silico/bioinformatic without either validation in actual clinical tumor samples from patients or functional validation in at least 2 cells lines in vitro or in vivo are not considered in scope
Conflict of interest declaration: Dr. Ziegler reports consulting & advisory board fees from Astra Zeneca, Novartis, Alexion, Day One, Accendatech, FivepHusion, Bayer and Amgen..
