Fully-covered metal stent for the treatment of post-percutaneous transhepatic biliary drainage (PTBD) obstruction due to a blood clot in the common bile duct: a case report.

AIM: This study aimed to report a case of a fully-covered metal stent for the treatment of post-Percutaneous Transhepatic Biliary Drainage (PTBD) obstruction caused by a blood clot in the common bile duct (CBD). CASE PRESENTATION: The case involved a 75-year-old man who had a history of recurring upper abdominal pain and jaundice. The result of an abdominal computerized tomography showed a stricture in the CBD. After PTBD, bleeding in the tube of PTBD was noted. The bleeding sites were detected using superselective hepatic arteriography. After the bleeding was stopped, Endoscopic Retrograde Cholangiopancreatography (ERCP) was performed to insert a fully-covered metal stent to extract the blood clot. Five months later, He was performed whipple procedure successfully and the pathology shows adenocarcinoma (cholangicarcinoma). This was the first case reported in China. CONCLUSIONS: The complications related to post-PTBD obstruction, which was caused by a blood clot in the CBD, might lead to serious health issues or even death. The blood clot could be diagnosed according to laboratory and clinical data, particularly imaging. Digital subtraction angiography (DSA) and ERCP were necessary and effective for the patient in the present case. Successfully placement of a fully-covered stent could relieve jaundice. The residual thrombus was easily extracted through the stent. This was important for the preparation of the coming procedure.

Obesity promotes gastric cancer metastasis via diacylglycerol acyltransferase 2-dependent lipid droplets accumulation and redox homeostasis.

Experimental and molecular epidemiological studies indicate important roles for adipose tissue or high-fat diet (HFD) in tumor growth and metastasis. Gastric cancer (GC) possesses a metastatic predilection for the adipocyte-rich peritoneum. However, the precise molecular relevance of HFD in the peritoneal metastasis of GC remains unclear. Here, we showed that HFD causes obvious fat accumulation and promotes peritoneal dissemination of GC in vivo. Peritoneum-derived adipocytes induces robust lipid droplet (LD) accumulation and fatty acid oxidation in GC cells through transcriptional upregulation of DGAT2 in a C/EBPα-dependent manner and prevents anoikis during peritoneal dissemination. Treatment of GC cells with FAs or coculture with adipocytes induces intracellular formation of LDs and production of NADPH to overcome oxidative stress in vitro. Importantly, overexpression of DGAT2 was identified as an independent predictor of poor survival that promotes lung and peritoneal metastasis of GC, and genetic or pharmacological inhibition of DGAT2, via disruption of lipid droplet formation in a lipid-rich environment, enhances the sensitivity of GC to anoikis in vitro and inhibits peritoneal metastasis in vivo. Overall, our findings highlight the notion that DGAT2 may be a promising therapeutic target in GC with peritoneal implantation and provide some evidence for uncovering the link between obesity and tumor metastasis.

Proliferative ductular reactions correlate with hepatic progenitor cell and predict recurrence in HCC patients after curative resection.

BACKGROUND: Ductular reactions (DRs) are well documented in many acute and chronic liver disease.The DRs are thought to be the transit amplifying cells deriving from activation of the stem/progenitor cell compartments of the liver. The aim of this study was to examine the presence of proliferative index of DR (PI-DR) and HPC markers' expression in HCCs after curative hepatectomy, as well as their relationship with clinicopathological features and prognosis. RESULTS: Tissue microarray with peritumoral and intratumoral tissue samples of 120 HCCs after hepatectomy was analysed for peritumoral expression of proliferating cell nuclear antigen for PI-DR. Peritumoral and intratumoral expression status of HPC markers including EpCAM, OV6, CD133 and c-kit were also examined by immunohistochemistry. TMA analysis of HCCs revealed that peritumoral PI-DR strongly correlated with the degree of inflammation and fibrosis. The peritumoral PI-DR positively correlated with peritumoral HPC markers EpCAM, OV6, CD133 and c-kit expression. Moreover, there were highly significant correlations between peritumoral PI-DR and intratumoral HPC markers EpCAM, OV6, CD133 and c-kit expression. Further, multivariate analysis showed that peritumoral PI-DR was the independent prognostic factor for overall survival (HR; 3.316, P < 0.001), and peritumoral PI-DR had a better power to predict disease-free survival (HR; 2.618, P < 0.001). CONCLUSIONS: Peritumoral PI-DR, as a valid surrogate for peritumoral and intratumoral expression of HPC markers, could be served as a potential prognostic marker for recurrence and survival in HCC after hepatectomy.

Identification and differential expression of human carcinoma-associated antigens in hepatocellular carcinoma tissues.

This study was designed to identify and verify hepatocellular carcinoma (HCC)-associated human carcinoma antigens (HCAs) that may be useful as tumor markers for HCC. We found that BCE075 and BCD021 anti-HCA antibodies were immunostained in the liver tissue samples and showed specific staining. Their expression was increased in HCC compared with normal liver tissues (P = 0.008). Immunoprecipitation and mass spectrometry analyses of the proteins precipitated by these two antibodies were identified to be cytoskeleton-associated protein 4 (CLIMP63) and brain-type glycogen phosphorylase (PYGB). This study demonstrated that HCC tissues expressed specific HCA glycoproteins, suggesting that our mouse monoclonal anti-HCA antibodies could be useful for immunohistochemical analysis of HCA expression as potential biomarkers for HCC diagnosis.

Endoscopic stenting for post-transplant biliary stricture: usefulness of a novel removable covered metal stent.

BACKGROUND: Endoscopic management of biliary anastomotic stricture (AS) following liver transplantation (LT) remains challenging. There are no dedicated self-expandable metal stents (SEMS) for this setting. METHODS: A short fully covered SEMS (FCSEMS) with a retrieval suture was designed. Between July 2008 and June 2010, 13 patients with post-LT AS had this FCSEMS placed endoscopically, keeping the whole stent inside the bile duct across the AS with the retriever out of the papilla. The stents were removed by forceps under endoscopy according to a schedule. Technical success, complications, AS resolution and the outcome for the patients were observed. RESULTS: Placement of the FCSEMS was successful on the first attempt in all patients. One patient with complicated infection did not respond to the stenting therapy and underwent stent retrieval ahead of schedule. Others kept well during stenting for a mean (SD) duration of 5.4 (1.7) months (range 2-8) without stent migration. All stents were removed successfully without great difficulty. AS resolution was obtained in all 12 patients, who were closely followed up for a mean (SD) time of 12.1 (8.0) months (range 1-26.5) after stent removal. Stricture recurrence occurred in one, who underwent a successful re-intervention with a second FCSEMS. Others remain free from symptoms and have normal liver function up to now. CONCLUSIONS: Endoscopic treatment of post-LT AS using a removable FCSEMS is technically feasible, safe, and effective. This dedicated method may play an increasing role in the future management of benign biliary strictures.

Oncogenic potential of retinoic acid receptor-gamma in hepatocellular carcinoma.

Retinoic acid receptors (RAR; alpha, beta, and gamma), members of the nuclear receptor superfamily, mediate the pleiotropic effects of the vitamin A metabolite retinoic acid (RA) and derivatives (retinoids) in normal and cancer cells. Abnormal expression and function of RARs are often involved in the growth and development of cancer. However, the underlying molecular mechanisms remain largely elusive. Here, we report that levels of RARgamma were significantly elevated in tumor tissues from a majority of human hepatocellular carcinoma (HCC) and in HCC cell lines. Overexpression of RARgamma promoted colony formation by HCC cells in vitro and the growth of HCC xenografts in animals. In HepG2 cells, transfection of RARgamma enhanced, whereas downregulation of RARgamma expression by siRNA approach impaired, the effect of RA on inducing the expression of alpha-fetoprotein, a protein marker of hepatocarcinogenesis. In studying the possible mechanism by which overexpression of RARgamma contributed to liver cancer cell growth and transformation, we observed that RARgamma resided mainly in the cytoplasm of HCC cells, interacting with the p85alpha regulatory subunit of phosphatidylinositol 3-kinase (PI3K). The interaction between RARgamma and p85alpha resulted in activation of Akt and NF-kappaB, critical regulators of the growth and survival of cancer cells. Together, our results show that overexpression of RARgamma plays a role in the growth of HCC cells through nongenomic activation of the PI3K/Akt and NF-kappaB signaling pathways.