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The intertwined fates of inflammation and coagulation in glioma
Angela Cho1,2,3, Kelly J McKelvey1,2,3, Adrian Lee1,2,3
1The Brain Cancer Group, Bill Walsh Translational Cancer Research Laboratory, Kolling Institute, St Leonards, NSW, 2065, Australia.
Inflammation and coagulation are two intertwined pathways with evolutionary ties being traced back to the hemocyte, a single cell type in invertebrates that has functions in both the inflammatory and coagulation pathways. These systems have functioned together throughout evolution to provide a solid defence against infection, damaged cells and irritants. While these systems work in harmony the majority of the time, they can also become dysregulated or corrupted by tumours, enhancing tumour proliferation, invasion, dissemination and survival. This review aims to give a brief overview of how these systems work in harmony and how dysregulation of these systems aids in the development and progression of cancer, using glioma as an example.
Inflammation and coagulation are two intertwined pathways with evolutionary ties being traced back to the hemocyte, a single cell type in invertebrates that has functions in both the inflammatory and coagulation pathways. These systems have functioned together throughout evolution to provide a solid defence against infection, damaged cells and irritants. While these systems work in harmony the majority of the time, they can also become dysregulated or corrupted by tumours, enhancing tumour proliferation, invasion, dissemination and survival. This review aims to give a brief overview of how these systems work in harmony and how dysregulation of these systems aids in the development and progression of cancer, using glioma as an example.
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