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BackgroundAll patients with liver cirrhosis are recommended to undergo an evaluation of esophageal varices (EV) to assess their risk of bleeding. Predicting the presence of EV through non-invasive means may reduce a large number of unnecessary endoscopies. This study was designed to develop a predictive model for varices in patients with Hepatitis B virus-related cirrhosis.MethodsThe retrospective analysis was performed in 146 patients with Hepatitis B virus-related cirrhosis. The data were assessed by univariate analysis and a multivariate logistic regression analysis. In addition, the receiver operating characteristic curves were also applied to calculate and compare the accuracy of the model and other single parameters for the diagnosis of esophageal varices.ResultsWe found the prevalence of EV in patients with Hepatitis B virus-related cirrhosis to be 74.7%. In addition, platelet count, spleen width, portal vein diameter and platelet count/spleen width ratio were significantly associated with the presence of esophageal varices on univariate analysis. A multivariate analysis revealed that only the spleen width and portal vein diameter were independent risk factors. The area under the receiver operating characteristic curve of regression function (RF) model, which was composed of the spleen width and portal vein diameter, was higher than that of the platelet count. With a cut-off value of 0.3631, the RF model had an excellent sensitivity of 87.2% and an acceptable specificity of 59.5% with an overall accuracy of 80.1%.ConclusionOur data suggest that portal vein diameter and spleen width rather than platelet count may predict the presence of varices in patients with Hepatitis B virus-related cirrhosis, and that the RF model may help physicians to identify patients who would most likely benefit from screenings for EV.

PurposeThe influence of X-inactive specific transcript (XIST) and X-chromosome inactivation associated long non-coding RNAs (lncRNAs) just proximal to XIST (JPX) on hepatocellular carcinoma (HCC) remains controversial in light of previous reports, which the present study aimed to verify.Materials and MethodsThe DIANA lncRNA-microRNA (miRNA) interaction database was used to explore miRNA interactions with JPX or XIST. JPX, XIST, and miR-155-5p expression levels in paired HCC specimens and adjacent normal tissue were analyzed by RT-qPCR. Interaction between XIST and miR-155-5p was verified by dual luciferase reporter assay. Expression levels of miR-155-5p and its known target genes, SOX6 and PTEN, were verified by RT-qPCR and Western blot in HepG2 cells with or without XIST knock-in. The potential suppressive role of XIST and JPX on HCC was verified by cell functional assays and tumor formation assay using a xenograft model.ResultsJPX and XIST expression was significantly decreased in HCC pathologic specimens, compared to adjacent tissue, which correlated with HCC progression and increased miR-155-5p expression. Dual luciferase reporter assay revealed XIST as a direct target of miR-155-5p. XIST knock-in significantly reduced miR-155-5p expression level and increased that of SOX6 and PTEN, while significantly inhibiting HepG2 cell growth in vitro, which was partially reversed by miR-155-5p mimic transfection. JPX knock-in significantly increased XIST expression and inhibited HepG2 cell growth in vitro or tumor formation in vivo in a XIST dependent manner.ConclusionJPX and XIST play a suppressive role in HCC. JPX increases expression levels of XIST in HCC cells, which suppresses HCC development by sponging the cancer promoting miR-155-5p.

TIPS was confirmed to improve ascites control in both the short term and the long term. Although HE frequently appeared in the TIPS group, patients with better hepatic and renal function survived longer when they were treated with TIPS. Serum bilirubin and urine sodium could be used as pre-TIPS predictors for patient survival. Portal pressure gradient reduction values could be used as post-TIPS predictors of survival.

OBJECTIVE:To identify microRNA expression patterns associated with the lymph node metastasis of colon cancer. METHODS:MicroRNA were isolated from six frozen non-cancerous surrounding colonic tissues derived from stage II-III colon cancer patients with (n = 3) and without (n = 3) lymph node metastasis. We compared the microRNA expression profiles of the six non-cancerous colonic tissues from two colon cancer patient groups; those with confirmed lymph node metastasis, termed the lymph node positive group, and those without detectable lymph node metastasis, termed the lymph node negative group. MicroRNA expression was analyzed with Agilent microarrays containing 723 human microRNA probes. We validated the expression level of differentially expressed microRNA using quantitative real-time PCR analysis. RESULTS:Two microRNA (hsa-miR-129*, hsa-miR-137) were differentially expressed in the lymph node positive group compared with the lymph node negative group. The expression level of hsa-miR-137 was quantified via quantitative real-time PCR analysis for validation. Hsa-miR-137 expression was significantly upregulated nearly 6.6-fold in lymph node positive specimens (P = 0.036). The quantitative real-time PCR result correlates with the microarray finding. CONCLUSION:The non-cancerous colonic tissues from colon cancer patients with lymph node metastasis have a significantly different microRNA expression profile compared to that from colon cancer patients without lymph node metastasis. The differentially expressed microRNA could have relevance to the lymph node metastasis of colon cancer and may provide a simple profiling method to assist in identifying patients with lymph node metastasis. Besides, these data might offer new ideas for preventing and controlling lymphatic metastasis in colon cancer.KEY WORDS: adjacent non-cancerous colonic tissue, colon cancer, hsa-miR-137, lymph node metastasis, microRNA expression profile.