Our study suggests that miR-122, a tumor suppressor microRNA affecting hepatocellular carcinoma intrahepatic metastasis by angiogenesis suppression, exerts some of its action via regulation of ADAM17. Restoration of miR-122 has a far-reaching effect on the cell. Using the concomitant down-regulation of its targets, including ADAM17, a rational therapeutic strategy based on miR-122 may prove to be beneficial for patients with hepatocellular carcinoma.
In addition, data from tumor xenografts and human cancer specimens indicate that AGO1-mediated translational desuppression of VEGF may be associated with tumor angiogenesis and poor prognosis. These findings provide evidence for an angiogenic pathway involving HRMs that target AGO1 and suggest that this pathway may be a suitable target for anti-or proangiogenesis strategies.
A total of 238 patients who received curative hepatic resections during the last 10 yr were observed to search for the risk factors linked to early tumor recurrence of human hepatocellular carcinoma after hepatectomy. The results revealed that tumor size, tumor appearance and DNA ploidy were the factors in predicting tumor recurrence after resection for hepatocellular carcinoma. Patients with a tumor size less than or equal to 5 cm or a tumor appearance of the solitary type had better disease-free survival than did those with a tumor size greater than 5 cm or a tumor appearance of multiple/daughter nodule types (p < 0.05). Although patients with pattern III (aneuploid with > or = 2 G0/G1 peaks) hepatoma had fewer statistically significant differences (p = 0.19) than did those with pattern I (diploid) or pattern II (aneuploid with single G0/G1 peak) tumors in predicting tumor recurrence, they did have poorer results in terms of the overall survival rate (p < 0.05). We conclude that patients with hepatocellular carcinoma having the aforementioned risk factors should be observed closely.
In patients with HCC, the preoperative serum IL-10 level is related to the clinical outcome. IL-10 may play an important role in the progression of HCC.
This work provides just a model, but a strong one, for quantitative assessments of ethanol metabolism in the human liver and stomach. The results indicate that the hepatic-alcohol clearance of ADH1B*2 individuals is higher than that of the ADH1B*1 and those of the ADH1B*3 versus the ADH1B*1 vary depending on sinusoidal ethanol levels. The maximal capacity for potential alcohol first-pass metabolism in the liver is greater than in the stomach.
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