[Staging the severity of liver cirrhosis and decision of surgical treatment for hepatocellular carcinoma: Tongji experience].

Liver resection is the mainstay of treatment for patients with hepatocellular carcinoma (HCC). Most of HCC patients are associated with varied degrees of liver cirrhosis.Severity of liver cirrhosis adversely affects the outcomes of liver resection, and also plays a vital role in making an appropriate surgical strategy for HCC.In current surgical practice for HCC, liver function and functional reserve are the focus of preoperative evaluation. Liver cirrhosis is still widely regarded as an one-stage entity. The pathological severity of liver cirrhosis is largely ignored. As neither liver function nor functional reserve can reflect the pathological severity of liver cirrhosis when liver function is at the stage of compensation. Preoperative evaluation on the severity of cirrhosis has not been established in a surgical setting.Thus, there is an urgent need to stage the severity of cirrhosis in surgical practice in order to make more precise surgical modalities for individual patients.This article mainly introduces the ongoing research progress in staging the severity of liver cirrhosis while treating HCC at Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, and emphasizes the importance of staging the severity of cirrhosis in surgical treatment of HCC.

Therapeutic efficacy of percutaneous microwave coagulation versus liver resection for single hepatocellular carcinoma ≤3 cm with Child-Pugh A cirrhosis.

AIMS: This study aimed to compare the therapeutic efficacy of liver resection (LR) and percutaneous microwave coagulation therapy (PMCT) for single hepatocellular carcinoma ≤3 cm (HCC) in cirrhotic livers. METHODS: In this study, 190 patients with single HCC ≤3 cm and Child-Pugh A cirrhosis were retrospectively reviewed. Among these patients, 122 patients underwent LR, and 68 patients received PMCT. The therapeutic efficacy and complications were compared between the two procedures. RESULTS: There was no treatment-related hospital mortality in either group. Major complications were significantly more frequent in the LR group compared to the PMCT group (22.1% vs 5.9%, p = 0.004). The 1-, 3-, and 5-year OS rates for the LR group and PMCT group were 98.4%, 93.6%, 55.2% and 97.1%, 87.7%, 51%, respectively. There was no significant difference in OS rates between the LR group and PMCT group (p = 0.153). The 1-, 3-, and 5-year DFS rates were 96.7%, 70.5% and 43.7%, respectively, in the LR group, which were significantly higher compared to the PMCT group (92.6%, 50.5% and 26.3%, p = 0.006). Subgroup analyses revealed that HCC patients with portal hypertension (PH), OS and DFS were similar between the two groups. CONCLUSIONS: LR may provide better DFS and lower recurrence rates than PMCT for single HCC ≤3 cm and Child-Pugh A cirrhosis. For HCC patients with PH, PMCT may provide therapeutic effects that are similar to LR.

MiR-216b is involved in pathogenesis and progression of hepatocellular carcinoma through HBx-miR-216b-IGF2BP2 signaling pathway.

This study aims to investigate the expression status of miRNA-216b in familial hepatocellular carcinoma (HCC) and the correlation between miRNA-216b expression and pathogenesis, as well as the progression of HCC. The expression profile of miRNAs in plasma of peripheral blood between HCC patients with HCC family history and healthy volunteers without HCC family history was determined by microarray. Using real-time quantitative PCR to detect the expression in paired tissues from 150 patients with HCC, miR-216b was selected as its expression value in HCC patients was significantly lower compared with healthy volunteers. Next, miR-216b expression and the clinicopathological features of HCC were evaluated. The effect of miR-216b expression on tumor cells was investigated by regulating miR-216b expression in SMMC-7721 and HepG2 in vitro and in vivo. Finally, we explored mRNA targets of miR-216b. In 150 HCC, 37 (75%) tumors showed reduced miR-216b expression comparing with their adjacent liver tissues. The decreased expression of miR-216b was significantly correlated with tumor volume (P=0.044), HBV infection (P=0.026), HBV DNA quantitative (P=0.001) and vascular invasion (P=0.032). The 5-year disease-free survival and overall rates after liver resection in low expression and high expression groups of miR-216b are 62% and 54%, 25% and 20%, respectively. MiR-216b overexpression inhibited cell proliferation, migration and invasion, and miR-216b inhibition did the opposite. The expression of hepatitis B virus x protein (HBx) has tight correlation with downregulation of miR-216b. Furthermore, miR-216b downregulated the expression of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and exerted its tumor-suppressor function through inhibition of protein kinase B and extracellular signal-regulated kinase signaling downstream of IGF2. MiR-216b inhibits cell proliferation, migration and invasion of HCC by regulating IGF2BP2 and it is regulated by HBx.