No serious complications occurred in either group. Conclusions: 

In this retrospective and small case series, guidewire cannulation after needle-knife fistulotomy increased the success rate of selective bile duct cannulation in patients with difficult bile duct access. “
“Cyclin G1 deficiency is associated with reduced Metformin in vitro incidence of carcinogen-induced hepatocellular carcinoma (HCC), but its function in HCC progression remains obscure. We report a critical role of cyclin G1 in HCC metastasis. Elevated expression of cyclin G1 was detected in HCCs (60.6%), and its expression levels were even higher in portal vein tumor thrombus. Clinicopathological analysis revealed a close correlation of cyclin G1 expression with distant metastasis and poor prognosis of HCC. Forced expression of cyclin G1 promoted epithelial-mesenchymal transition (EMT) and metastasis of HCC cells in vitro and in vivo. Cyclin G1 overexpression enhanced Akt activation through interaction with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]), which led to subsequent phosphorylation of glycogen

synthase kinase-3β (GSK-3β) and stabilization of Snail, a critical EMT mediator. ITF2357 clinical trial These results suggest that elevated cyclin G1 facilitates HCC metastasis by promoting EMT via PI3K/Akt/GSK-3β/Snail-dependent pathway. Consistently, we have observed a significant correlation between cyclin G1 expression and p-Akt levels in a cohort of HCC patients, and found that combination of these two parameters is a more powerful predictor of poor prognosis. Conclusions: Cyclin G1 plays a pivotal role in HCC metastasis and may serve as a novel prognostic biomarker and therapeutic target. (HEPATOLOGY 2012;55:1787–1798) Cyclin G1 was first

identified serendipitously in screening for Src kinase family in rat fibroblasts.1 It has been categorized as a cyclin on account of possessing a well-conserved cyclin box, although it lacks a destruction box or PEST (Pro, Glu, Ser and Thr)-rich sequences that are responsible for cyclin degradation.1 Cyclin G1 has been well documented as a p53-responsive gene and could be transcriptionally activated by p53 or p73.2, 3 In fact, p53 is the Ergoloid major factor regulating cyclin G1 expression upon DNA damage.4 Cyclin G1 was reported to interact with the B′ regulatory subunit of protein phosphatase 2A, which in turn dephosphorylated MDM2 followed by p53 degradation.5 A feedback regulation of p53 by cyclin G1 was also observed in cyclin G1-null mouse embryo fibroblasts, which exhibited increased p53 levels.6, 7 Additionally, cyclin G1 was found to interact with certain proteins involved in cell cycle regulation, such as cyclin G–associated kinase and cyclin-dependent kinase 5, but the physiologic significance of these interactions remains elusive.8 Cyclin G1–deficient mice have been reported to be viable without any apparent phenotype.