Glioma, as a primary intracranial tumor, is also the most common malignant brain tumor, leading to significant morbidity and mortality. Despite significant research advances in molecular mechanisms, diagnostics, and therapeutic approaches, their survival rate remains low. The immune microenvironment of glioma is highly heterogeneous, which is closely related to the occurrence and development of glioma and the effect of anti-tumor immunotherapy. Glioma cells secrete a variety of chemokines, cytokines, and growth factors that promote the infiltration of various immune cells, such as macrophages, myeloid-derived suppressor cells, CD4+ T cells, and Treg into the microenvironment. These cytokines and chemokines, as well as their interactions with extracellular matrix components, reprogram infiltrating immune cells to acquire different functional phenotypes, thereby directing the immune system to promote glioma progression and facilitate anti-immunotherapy.

Previous studies on the molecular mechanism of glioma have revealed the molecular features associated with different types of glioma, and the diversity of molecular subtypes is often related to patient treatment and prognosis. IDH-WT glioblastomas usually contain higher levels of EGFR amplification, TERT promoter mutations, and PTEN deletion. MGMT promoter methylation was observed in approximately half of the IDH-WT glioblastomas, which showed better prognosis and response to therapy. The molecular features of low-grade gliomas in pediatrics and adults are different; low-grade gliomas in pediatrics are thought to carry FGFR1 and BRAF mutations; low-grade gliomas in adults are characterized by IDH1/2 and ATRX mutations, sometimes accompanied by 1p/19q codeletions. These molecular features can be used to improve the classification of gliomas, guide individualized treatment and improve prognosis, but current standard treatments are only effective for patients with MGMT promoter methylation. Therefore, studying the molecular mechanisms of gliomagenesis and the regulation of the glioma microenvironment would not only help to better understand the mechanisms of glioma development but also help to improve the sensitivity of glioma chemotherapy as well as develop precise targeted therapy and immunotherapy strategies.

Accumulating evidence indicates that the unraveling of tumor molecular mechanisms and the remodeling of the immune microenvironment play crucial roles in the development of glioma. This Research Topic aims to reveal the mechanism of the heterogeneity of the glioma immune microenvironment and the mechanism that affects glioma progression and treatment resistance including low-grade gliomas in pediatrics and adults, so as to develop methods that could target the expression of glioma molecular markers and regulate the remodeling of the immune microenvironment, and ultimately provide valuable references for enhancing the immunotherapy, targeted therapy and chemotherapy sensitivity of glioma. We welcome submissions covering adult and pediatric gliomas, as well as low-grade gliomas among them. These may include but are not limited to the following:

1) Molecular heterogeneity of glioma immune microenvironment in adults
2) Molecular heterogeneity of glioma immune microenvironment in pediatrics
3) Novel molecular mechanisms in glioma diagnosis, treatment, drug resistance, recurrence, and prognosis monitoring
4) Novel molecules and relevant mechanisms involved in glioma immunotherapy response and/or sensitivity
5) Novel biomarkers based on new technologies or methods to predict response to immunotherapy in glioma patients

Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Research Topic.

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