Article ID Journal Published Year Pages File Type
3063509 Journal of Clinical Neuroscience 2008 11 Pages PDF
Abstract

Since its discovery in the late 1970s considerable research has linked transforming growth factor-beta (TGF-β) to several human diseases such as fibrosis, auto-immunity and cancer. TGF-β acts initially as a growth inhibitory factor in early stages of tumour development. In contrast, as tumours evolve, they develop mechanisms to evade the growth-regulatory effects of TGF-β, resulting in greater tumour invasiveness, increased metastatic potential and inhibition of surrounding immune responses. However, although extensively studied, the molecular mechanisms that trigger tumour cells to “switch” from TGF-β-inhibited to TGF-β-promoted are still not fully understood. Contradictory studies that demonstrate opposite cellular effects mediated by TGF-β are abundant throughout the literature. This review summarizes the current molecular mechanisms involved in the tumour suppressive and tumour progressive characteristics of TGF-β in brain tumours. Potential therapeutic agents that target TGF-β and related proteins being evaluated against brain tumours is also discussed.

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