کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3063509 | 1187519 | 2008 | 11 صفحه PDF | دانلود رایگان |

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.
Journal: Journal of Clinical Neuroscience - Volume 15, Issue 8, August 2008, Pages 845–855