About this Research Topic
For a long time, cancer has been perceived as a cell autonomous disease caused dominantly by transformed cells and thus, substantial part of current research is concentrated on genetic and epigenetic changes in cancer cells. However, cancer behavior, although driven by mutated cells, depends critically on dynamic interactions with their surroundings. It has been suggested that the initiation of tumors is unavoidable, but their progression to malignancy can and should be controllable. However, once tissue homeostasis is lost, the altered microenvironment can itself become a potent tumor promoter. Cancer microenvironment varies in its composition in individual patients, but also vastly within the tumor itself. The major pro-tumor stimuli in glioma microenvironment triggers growth, local immunosuppression, angiogenesis, and invasion. Growth and invasive behavior cause substantial changes in the structure and properties of afflicted tissues resulting in perpetuation of the pathological processes. Local immunosuppression in glioma may be mediated by tumour cells themselves as well as by recruitment of additional elements of innate and adaptive immune system, forming an immunologically privileged tissue where neoantigens from the developing tumor cells are tolerated.
Invasion of glioma, typically occurring in conditions of local hypoxia, is associated with unbalance of proteolytical homeostasis, epithelial-mesenchymal transition and extensive aberrant neovascularization. Untangling of the active crosstalk among multiple cell types participating in the glioma microenvironment, including tumour activated myeloid cells, cancer-associated fibroblasts and other microenvironmental components, is a critical prerequisite to design strategies for an effective modification of the pro- and anti-tumorigenic forces within the glioma bulk and may help to improve patient prognosis.
Thus, this Research Topic focuses on “general” hallmarks of transformed cells, specific features of stromal cells and extracellular matrix, multilateral cell-to-cell communication and aberrant neovascularization and immunosuppression, which jointly contribute to dysregulated glioma growth, invasiveness and recurrence in the very specific "inner space" of the central nervous system.
To offer a wide spectrum of cutting-edge information, the articles included in the collection will be prepared by biochemists, medicinal chemists, molecular, and cell biologists. We invite both Original Research and Review Articles, covering topics such as:
· Genetic and epigenetic features of glioma cells
· Functions of non-coding RNAs in gliomas
· Cell-to-cell communication and signal transduction pathways associated with gliomagenesis
· Cellular composition and dynamics of glioma microenvironment; stem cells, transformed cells, stromal cells
· Composition of the glioma extracellular microenvironment with respect to the extracellular matrix and representation of regulatory molecules, such as cytokines, chemokines and proteases and their possible diagnostic and/or therapeutic targeting
· Apoptosis and autophagy in glioma
Keywords: Glioma, Glioblastoma, Tumor microenvironment
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.