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- W2018421775 abstract "Hepatocellular carcinomas (HCCs) constitute a therapeutic challenge with mostly unfavorable outcome. This may reflect our incomplete understanding of disease pathogenesis, e.g. the elucidation of tumorigenic signaling pathways. Knowledge gathered hitherto focuses on genetic alterations that result in the loss of tumor suppressor functions as well as amplification and mutation of cancer genes. Further evidence points to a decisive role of cytostatic and apoptotic functions mediated on hepatocytes by transforming growth factor (TGF)-β. These effects are critical for the control of liver mass with loss of TGF-β activities resulting in hyperproliferative disorders and cancer. This concept is based on studies that describe a bipartite role of TGF-β with tumor suppressor functions at early stages of liver damage and regeneration, whereas during cancer progression TGF-β may turn from a tumor suppressor to a tumor promoter that exacerbates invasive and metastatic behavior. Consequently and most importantly, the oncogenic potential of recent therapeutic approaches against profibrogenic TGF-β effects needs to be carefully delineated and a cancer therapy with specific targets disrupting the TGF-β signaling cascade may be envisioned. In line with this concept, we and others found overexpression of TGF-β antagonist Smad7 in the majority of HCC samples, providing a mechanism for hepatocytes to escape TGF-β-dependent growth control in the process of cancerogenesis." @default.
- W2018421775 created "2016-06-24" @default.
- W2018421775 creator A5050024715 @default.
- W2018421775 creator A5054147665 @default.
- W2018421775 creator A5058204085 @default.
- W2018421775 date "2009-01-01" @default.
- W2018421775 modified "2023-09-26" @default.
- W2018421775 title "Hypotheses on the Role of Transforming Growth Factor-β in the Onset and Progression of Hepatocellular Carcinoma" @default.
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