The caudate lobectomy combined with an additional partial hepatectomy is preferred because this approach is technically less demanding and offers an adequate surgical margin.

Abstract. Hilar cholangiocarcinoma is often unresectable at the time of the initial diagnosis, and the provision of a definite palliative benefit is important in patients with unresectable hilar cholangiocarcinoma. The aim of the present study was to evaluate the safety of percutaneous biliary stenting and to analyze whether percutaneous biliary stenting combined with radiotherapy (RT) prolonged the stent patency and survival time of patients. In total, the cases of 38 patients with unresectable hilar cholangiocarcinoma that underwent percutaneous biliary stenting at the Navy General Hospital were retrospectively reviewed in the present study. Uncovered metallic stenting (UMS) combined with RT was administered to 25 patients, and UMS alone was administered to 13 patients. The records of early complications subsequent to percutaneous biliary stenting were collected, and the stent patency and survival times of patients were analyzed and compared between the two groups. The technical success rate of the procedure was 100% and the successful drainage rate was 86.8%. The overall early complication rate was 15.8% and the procedure-associated mortality rate was 2.6%. The median stent patency was 326 days in the UMS+RT group and 196 days in the UMS group (P= 0.022). The UMS+RT group (median, 367 days) demonstrated a longer survival time compared with the UMS group (median, 267 days; P= 0.025). Percutaneous biliary stenting offers a safe and effective method for the palliative treatment of patients with unresectable hilar cholangiocarcinoma, and percutaneous biliary stenting combined with RT may prolong stent patency and patient survival time.

AIMTo determine a panel of serum microRNAs (miRNAs) that could be used as novel biomarkers for diagnosis of hepatocellular carcinoma (HCC).METHODSWe initially screened 9 out of 754 serum miRNAs by TaqMan Low Density Array in two pooled samples respectively from 35 HCC and 35 normal controls, and then validated individually by RT-qPCR in another 114 patients and 114 controls arranged in two phases. The changes of the selected miRNAs after operation and their prognostic value were examined.RESULTSmiR-375, miR-10a, miR-122 and miR-423 were found to be significantly higher in HCC than in controls (P < 0.0001), and the area under the receiver-operating-characteristic curve for the 4-miRNA panel was 0.995 (95%CI: 0.985-1). All the four miRNAs were significantly reduced after surgical removal of the tumors (P < 0.0001), while still higher than normal controls (at least P < 0.05)CONCLUSIONThe four serum miRNAs (miR-375, miR-10a, miR-122 and miR-423) could potentially serve as novel biomarkers for the diagnostic and prognostic of HCC.

Abstract. Gemcitabine (GEM) is one of the first-line drugs in the treatment of gallbladder cancer (GBC), although the therapeutic effect is not sustained due to resistance to the drug over time. Maslinic acid (MA) has been shown to inhibit transcription factor nuclear factor-κB (NF-κB), resulting in the suppression of survival signaling. The authors of the present study investigated whether MA enhanced the antitumor activity of GEM in GBC. Anti-proliferative effects of MA, GEM and MA + GEM were assessed using the MTT assay. Apoptosis was assessed using Annexin V and by western blot analysis of various mediators of apoptosis. Xenograft tumors of EH-GB2 GBC cells were established in athymic nude mice and were monitored following treatment with MA, GEM and MA + GEM. Immunohistochemistry of the tumors was used to examine various survival proteins. MA inhibited the in vitro proliferation of various GBC cell lines and potentiated the apoptosis and cell invasion inhibition induced by GEM. Western blot analysis showed that the combination of MA and GEM inhibited constitutive NF-κB activation and NF-κB-regulated gene products, including cyclin D1, Bcl-2, Bax, MMP-2 and MMP-9, to a greater extent. In vivo, the group that was treated with MA + GEM showed significant reductions in tumor volume and a decreased expression of NF-κB-regulated gene products. In conclusion, the results suggest that MA potentiates the antitumor effects of GEM in human GBC cell lines by suppressing the activation of NF-κB and its dowstream gene products, which are involved in survival signaling. IntroductionGallbladder cancer (GBC) is the most common cancer of the bile duct system and is the fifth most lethal cancer of the digestive system (1). The incidence of GBC in China, Thailand, Chile and Northern India is higher when compared with the United States and European countries (2). At present, radical surgical resection is the most effective treatment of GBC. However, for the majority of patients, surgery is not curative because of late detection and/or early, regional or distant metastasis. Additionally, few patients experience complete responses to chemotherapy, mainly due to chemoresistance. Thus, identifying novel approaches to enhance the antitumor effects of chemotherapeutic drugs and reduce chemoresistance are imperative.Maslinic acid (MA), a pentacyclic triterpene acid, is widely present in dietary plants, especially in olive fruit skins and hawthorn berries (3). The compound has attracted much interest due to its proven pharmacological safety and its many biological activities, including anticancer such as anti-inflammation (2), anti-viral (4,5), anti-oxidation (6), anti-diabetogenic (7), anticolonic cancer (8,9) and anti-astrocytoma (10) activities. MA has been shown to potentiate the anticancer activity of TNF-α in pancreatic cancer cells through the inhibition of nuclear factor-κB (NF-κB) survival signaling pathways (11).NF-κB is a transcriptional activator that has been extensively studied for its role in controlling the expression of...

Cholangiocarcinoma (CCA) is one of the most common hepatic and biliary malignancies, accounting for about 3% of all gastrointestinal tumors. GATA5 is a transcription factor capable of suppressing the development of various human cancer types. Transcriptional inactivation and CpG island (CGI) methylation of GATA3 and GATA5, two members of the GATA family of transcription factors, have been observed in some human cancers. But whether high-density CGI methylation of GATA5 is associated with the clinical course of CCA patients has not been clarified. Herein, we observed reduced expression of GATA5 in CCA tissues compared with noncancerous tissues. Treatment with the demethylating agent 5-aza-2'-deoxycytidine restored GATA5 expression in CCA cell lines. Furthermore, GATA5 expression was downregulated after treatment with IL-6 in human intrahepatic biliary epithelial cells. Upregulated GATA5 inhibited CCA cell growth and metastasis. Mechanistically, GATA5 suppressed CCA cell growth and metastasis via Wnt/β-catenin pathway. Specific β-catenin inhibitor or siRNA abolished the discrepancy of the proliferation and metastasis capacity between GATA5-overexpression CCA cells and their control cells, which further confirmed that Wnt/β-catenin was required in GATA5-inhibited CCA cell growth and metastasis.