Quantification of serum hepatitis B surface antigen in predicting the response of pegylated interferon alfa-2a in HBeAg-positive chronic hepatitis B with prior lamivudine exposure.

AIMS: Majority of previous studies of pegylated interferon α-2a (PegIFNα-2a) forced on naïve chronic hepatitis B (CHB) patients, and the data of PegIFNα-2a in therapy of patients with prior exposure to nucleos(t)ide analogues is rare. This study aimed to investigate the predictive role of serum quantitative hepatitis B surface antigen (HBsAg) in predicting sustained response of PegIFNα-2a in HBeAg-positive CHB patients with prior lamivudine exposure. METHODS: Forty-six patients with prior lamivudine exposure received PegIFNα-2a for 12 months and followed-up for 6 months. The clinical features of responders and non-responders were compared, and the predictive role of quantitative HBsAg in predicting responders at the end of follow-up was evaluated. Responders were defined as an ALT normalization, HBeAg seroconversion and sustained virological response at the end of follow-up. RESULTS: In this cohort, only 26.1% (12/46) patients were responders. The baseline characteristics of the responders and non-responders were similar; however, the rates of ALT normalization, HBV DNA undetectability and HBeAg seroconversion were all significantly higher in responders than that in non-responders. During the treatment and follow-up, the HBsAg levels were all significantly lower in responders than that in non-responders. In predicting reponders, the serum HBsAg cutoff of 6000 IU/mL at months 6 had a positive predictive value of 73.3 and a negative predictive value of 96.8%, and with an area under the receiver operating characteristic curve of 0.869. CONCLUSION: The responders toward PegIFNα-2a in CHB patients with prior lamivudine exposure is not high, and serum HBsAg <6000 IU/Ml at months 6 of on-treatment had a high value to predict long-term outcomes of treatment.

A Prognostic Signature for Colon Adenocarcinoma Patients Based on m6A-Related lncRNAs.

N6-methyladenosine (m6A) modification is a common epigenetic modification. It is reported that lncRNA can be regulated by m6A modification. Previous studies have shown that lncRNAs associated with m6A regulation (m6A-lncRNAs) serve as ideal prognostic biomarkers. However, whether lncRNAs are involved in m6A modification in colon adenocarcinoma (COAD) needs further exploration. The objective of this study was to construct an m6A-lncRNAs-based signature for patients with COAD. We obtained the RNA sequencing data and clinical information from The Cancer Genome Atlas (TCGA). Pearson correlation analysis was employed to recognize lncRNAs associated with m6A regulation (m6A-lncRNAs). 24 prognostic m6A-lncRNAs was identified by univariate Cox regression analysis. Gene set enrichment analysis (GSAE) was used to investigate the potential cellular pathways and biological processes. We have also explored the relationship between immune infiltrate levels and m6A-lncRNAs. Then, a predictive signature based on the expression of 13 m6A-lncRNAs was constructed by the Lasso regression algorithm, including UBA6-AS1, AC139149.1, U91328.1, AC138207.5, AC025171.4, AC008760.1, ITGB1-DT, AP001619.1, AL391422.4, AC104532.2, ZEB1-AS1, AC156455.1, and AC104819.3. ROC curves and K M survival curves have shown that the risk score has a well-predictive ability. We also set up a quantitative nomogram on the basis of risk score and prognosis-related clinical characteristics. In summary, we have identified some m6A-lncRNAs that correlated with prognosis and tumor immune microenvironment in COAD. In addition, a potential alternative signature based on the expression of m6A-lncRNAs was provided for the management of COAD patients.

Pancreatic T/histiocyte-rich large B-cell lymphoma: A case report and review of literature.

Primary pancreatic lymphoma (PPL) is an extremely rare form of extranodal malignant lymphoma. The most common histological subtype of PPL is diffuse large B cell lymphoma (DLBCL). In rare cases, PPL can also present as follicular lymphoma, small lymphocytic lymphoma, and T cell lymphoma either of non-Hodgkin's lymphoma or of Hodgkin's lymphoma. T-cell/histiocyte-rich large B-cell lymphoma (T/HRBCL) is an uncommon morphologic variant of DLBCL with aggressive clinical course, it is predominantly a nodal disease, but extranodal sites such as bone marrow, liver, and spleen can be involved. Pancreatic involvement of T/HRBCL was not presented before. Herein, we report a 48-year-old male who was hospitalized with complaints of jaundice, dark brown urine, pale stools, and nausea. The radiological evaluation revealed a pancreatic head mass and, following operative biopsy, the tumor was diagnosed as T/HRBCL. The patient achieved remission after six cycles of CHOP chemotherapy. Therefore, T/HRBCL can be treated similarly to the stage-matched DLBCL and both of them get equivalent outcomes after chemotherapy.

Hepatoprotective effect of juglone on dimethylnitrosamine-induced liver fibrosis and its effect on hepatic antioxidant defence and the expression levels of α-SMA and collagen III.

The present study aimed to investigate the antifibrotic effects of juglone on dimethylnitrosamine (DMN)­induced fibrosis in rats. Juglone, which is a quinone, significantly decreased DMN­induced rat hepatic fibrosis, which was associated with increased superoxide dismutase (SOD) activity, decreased oxidative stress and reduced levels of α­smooth muscle actin (α­SMA) and collagen (Col) III in the liver. Serum levels of alanine aminotransferase, aspartate aminotransferase, hyaluronic acid, laminin, type III precollagen and type IV collagen were significantly reduced by treatment with juglone. Liver fibrosis was induced in male Sprague­Dawley rats by subcutaneous injections of DMN solution and hepatic fibrosis was assessed using Massons trichome staining. The expression levels of α­SMA and Col III were determined using immunohistochemical techniques. The activities of SOD and malondialdehyde in liver homogenates were also determined. The results suggested that juglone augmented the antioxidative capability of the liver, possibly by stimulating the activity of SOD, which promoted the inactivation of hepatic stellate cells (HSCs) and decreased the accumulation of extracellular matrix collagen in the liver, thereby alleviating hepatic fibrosis. Silymarin was used as a positive control for liver fibrosis protection. It was hypothesized that juglone alleviates or mitigates oxidative stress­mediated hepatic fibrosis by upregulating the expression of peroxisome proliferator­activated receptor γ and inhibiting the activation of HSC.