| Literature DB >> 16286241 |
Abstract
When a cancer escapes the growth-inhibitory effects of TGF-beta secreted by cancer cells themselves or by cells in the local stroma, a further adverse outcome for the host is the associated TGF-beta-induced suppression of anticancer T cell immunity. In addition to the previously described dampening of T cell activation and proliferation, TGF-beta markedly and directly suppresses the transcription of genes encoding multiple key proteins of the "cytotoxic program" of CD8+ CTL, such as perforin and granzymes, cytotoxins that act through the granule exocytosis pathway. The findings described below suggest that TGF-beta and its signaling pathways will be major targets for novel cancer therapeutics.Entities:
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Year: 2005 PMID： 16286241 DOI： 10.1016/j.ccr.2005.10.018
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743