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Dooley S et al. - Consequently and most importantly, the oncogenic potential of recent therapeutic approaches against profibrogenic TGF-beta effects needs to be carefully delineated and a cancer therapy with specific targets disrupting the TGF-beta signaling cascade may be envisioned. In line with this concept, the authors and others found overexpression of TGF-beta antagonist Smad7 in the majority of HCC samples, providing a mechanism for hepatocytes to escape TGF-beta-dependent growth control in the process of cancerogenesis.

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