BackgroundAn elevated preoperative neutrophil-to-lymphocyte ratio (NLR) has been reported to be a prognostic factor for hepatocellular carcinoma (HCC) patients after treatment. However, the clinical implication of postoperative NLR change remains unclear.Materials and MethodsFrom May 2005 to Aug 2008, a cohort of consecutive 178 small HCC patients treated with radiofrequency ablation (RFA) was retrospectively reviewed. The NLR was recorded within 3 days before and 1 month after RFA. Baseline characteristics, overall survival (OS) and recurrence free survival (RFS) were compared according to preoperative NLR and/or postoperative NLR change. Prognostic factors were assessed by multivariate analysis.ResultsCompared with preoperative NLR level, postoperative NLR decreased in 87 patients and increased in 91 patients after RFA. No significant differences were identified between two groups in commonly used clinic-pathologic features. The 1, 3, 5 years OS was 98.8%, 78.6%, 67.1% for NLR decreased group, and 92.2%, 55.5%, 35.4% for NLR increased group respectively (P<0.001); the corresponding RFS was 94.2%, 65.2%, 33.8% and 81.7%, 46.1%, 12.4% respectively (P<0.001). In subgroup analysis, the survival of patients with lower or higher preoperative NLR can be distinguished more accurate by postoperative NLR change. Multivariate analysis showed that postoperative NLR change, but not preoperative NLR, was an independent prognostic factor for both OS (P<0.001, HR = 2.39, 95%CI 1.53–3.72) and RFS (P = 0.003, HR = 1.69, 95%CI 1.87–8.24).ConclusionThe postoperative NLR change was an independent prognostic factor for small HCC patient undergoing RFA, and patients with decreased NLR indicated better survival than those with increased NLR.

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Serum levels of KL-6 were elevated in ILD patients with severe respiratory function compared to those without. The rate of poor prognosis and mortality was associated with increased biomarker concentrations. Sequential measurements of biomarkers could be valuable in disease monitoring and evaluations in clinical management.

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The aims of this study were to compare the prognostic ability of inflammation-based prognostic scores including the Glasgow Prognostic Score (GPS), the modified Glasgow Prognostic Score (mGPS), neutrophil to lymphocyte ratio, prognostic index, and prognostic nutritional index (PNI) for patients with hepatocellular carcinoma (HCC) undergoing hepatectomy, and to propose the combination of staging systems and inflammation scores to improve the prognostic power. Data for 349 patients who underwent hepatectomy as initial treatment for HCC between 2008 and 2009 were retrieved from a prospective database. The association of inflammation scores with clinicopathological variables and overall survival (OS) was analyzed, and the concordance index (C-index) was calculated to compare the predictive ability of each inflammation scores and staging systems including Barcelona Clinic Liver Cancer (BCLC) and Cancer of the Liver Italian Program (CLIP) scores. The median follow-up period was 39 months, the 1, 2, and 3 year OS was 75.4, 67.0, and 59.0 %, respectively, and the median OS was 39 months. All inflammation scores, except PNI, were associated with tumor size, major/microvascular invasion and clinical stages, and the GPS and mGPS had a higher C-index (0.608). Multivariate analysis showed that the GPS, BCLC, and CLIP were independently associated with OS. The combined GPS and CLIP (C-index = 0.705) were superior to CLIP alone (C-index = 0.686) or the GPS alone in prognostic ability. The prognostic ability of the GPS is superior to other inflammation scores for patients undergoing hepatectomy as initial treatment for HCC. Combining GPS and CLIP improved the prognostic power.

Cancer stem cells (CSCs) are cancer-initiating cells that are not only a source of tumorigenesis but also the cause of tumour progression, metastasis and therapy resistance. EBV-associated gastric cancer (EBVaGC) is a distinct subtype of gastric cancer with unique clinicopathological and molecular features. However, whether CSCs exist in EBVaGC, and the tumorigenic mechanism of EBV, remains unclear. Here, NOD/SCID mice were injected subcutaneously with the EBVaGC cell line SNU719 and treated with 5-fluorouracil weekly. Successive generations of xenografts yielded a highly malignant EBVaGC cell line, SNU-4th, which displays properties of CSCs and mainly consists of CD44 + CD24 À cells. In SNU-4th cells, an EBV-encoded circRNA, ebv-circLMP2A, expression increased and plays crucial roles in inducing and maintaining stemness phenotypes through targeting miR-3908/ TRIM59/p53 axis. Additionally, high expression of ebv-circLMP2A is significantly associated with metastasis and poor prognosis in patients with EBVaGC. These findings not only provide evidence for the existence of CSCs in EBVaGC and elucidate the pathogenic mechanism of ebv-circLMP2A in EBVaGC, but also provide a promising therapeutic target for EBVaGC.

Background: Circular RNAs (circRNAs) are considered as key regulators of cancer biology. Recently, cMTO1 (a circRNA derived from MTO1 gene, hsa_circ_0007874) has been demonstrated to act as a tumor suppressor in hepatocellular carcinoma (HCC). However, the roles of cMTO1 in liver fibrosis are largely unknown. Methods: Expressions and roles of cMTO1 were examined in vivo and in vitro during liver fibrosis. The interaction between microRNA-181b-5p (miR-181b-5p) and cMTO1 was analyzed by luciferase activity assays and pull down assays. Results: cMTO1 was shown to be reduced in the liver from patients with cirrhosis. In addition, cMTO1 was down-regulated in the mouse fibrotic livers as well as activated hepatic stellate cells (HSCs). Restoring of cMTO1 led to a reduction in HSC proliferation. Results of immunofluorescence analysis showed that cMTO1 suppressed the expressions of α-SMA and type I collagen. cMTO1 was found to be expressed in the cytoplasm of HSCs. Further studies confirmed that cMTO1 and miR-181b-5p were colocated in the cytoplasm. Interestingly, there was an interaction between cMTO1 and miR-181b-5p. Results of luciferase reporter assays and pull down assays confirmed that miR-181b-5p could bind to cMTO1. cMTO1-inhibited HSC activation was blocked down by miR-181b-5p or PTEN. Meanwhile, PTEN was a target of miR-181b-5p. Conclusion: cMTO1 inhibits HSC activation, at least in part, through miR-181b-5pmediated PTEN expression. Our results also suggest that cMTO1 may be a novel therapeutic target in liver fibrosis.