Cheng-Jun Sui

Laparoscopic versus open distal pancreatectomy: A meta-analysis

OBJECTIVE Laparoscopic distal pancreatectomy (LDP) is a minimally invasive surgical technique. The aim of the present study was to evaluate the currently available literature and compare the short-term clinical outcomes of patients who underwent LDP for left-sided pancreatic pathology with patients who underwent traditional open surgery. METHODS A literature search was performed to identify and compare studies that reported the clinical outcomes of both LDP and open distal pancreatectomy (ODP). Pooled odds ratios (OR) and weighted mean differences (WMD) with 95% confidence intervals (95% CI) were calculated using either fixed-effects or random-effects models. RESULTS Nineteen nonrandomized controlled studies were identified that matched the selection criteria and reported the clinical outcomes of 1935 patients, of whom 805 underwent LDP and 1130 underwent ODP. Compared with open surgery, reports on laparoscopic resection indicate potentially favorable outcomes in terms of operative blood loss (WMD: -273.11; 95% CI: -404.61 to -141.61), the requirement of a blood transfusion (OR: 0.28; 95% CI: 0.11-0.71), postoperative time until oral intake (WMD: -1.19; 95% CI: -1.87 to -0.50), time to first flatus (WMD: -1.03, 95% CI: -1.93 to -0.12), length of hospital stay (WMD: -3.87, 95% CI: -5.06 to -2.68), and overall morbidity (OR: 0.70, 95% CI: 0.56-0.87). There were no differences in terms of the extent of oncologic clearance and postoperative mortality. CONCLUSION LDP results in a faster postoperative recovery and a comparable oncologic clearance in comparison with open surgery. Additional large trials are required to delineate the long-term clinical outcomes of patients diagnosed with malignant neoplasms who undergo either of these two surgeries.

Repeat hepatectomy for recurrent hepatocellular carcinoma: a local experience and a systematic review

BackgroundThis study aimed to assess the efficacy and safety of repeat hepatectomy for recurrent hepatocellular carcinoma (HCC).MethodsThirty-seven patients who underwent a curative repeat hepatectomy in our hospital were retrospectively studied. An extensive database literature search was performed to obtain for all relevant studies.ResultsIn our series, there were no perioperative deaths during repeat hepatectomy for recurrent HCC. Patients survival after repeat hepatectomy were similar to 429 patients undergoing initial hepatectomy. A computerized search of the Medline and PubMed databases found 29 retrospective studies providing relevant data in 1149 patients were included for appraisal and data extraction. After the repeat hepatectomy, postoperative morbidity ranged from 6.2% to 68.2% with a median per cohort of 23.5 per cent. There were 7 perioperative deaths (0.7 per cent of 993 for whom mortality data were provided). The overall median survival ranged from 21 to 61.5 months, with 1 -, 3 -, and 5-year survival of 69.0% to 100%, 21.0% to 87.0%, and 25.0% to 87.0%, respectively.ConclusionsRepeat hepatectomy can be performed safely and is associated with long-term survival in a subset of patients with recurrent HCC. However, the findings have to be carefully interpreted due to the lower level of evidence. A randomized controlled study is needed to compare repeat hepatectomy and other modalities for recurrent HCC.

MCM7 expression predicts post-operative prognosis for hepatocellular carcinoma

Dysregulation of minichromosome maintenance protein 7 (MCM7) was previously identified in multiple human malignancies. The clinical significance of MCM7 expression is yet to be delineated in patients with hepatocellular carcinoma (HCC).

Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429

Long noncoding RNAs (lncRNAs) have been reported to play pivotal roles in a variety of cancers. However, lncRNAs involved in hepatocellular carcinoma (HCC) initiation and progression remain largely unclear. In this study, we identified an lncRNA gradually increased during hepatocarcinogenesis (lncRNA-GIHCG) using publicly available microarray data. Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression. Furthermore, the biological functions of GIHCG on HCC are dependent on the silencing of miR-200b/a/429. Collectively, our results demonstrated the roles and functional mechanisms of GIHCG in HCC, and indicated GIHCG may act as a prognostic biomarker and potential therapeutic target for HCC.Key MessagelncRNA-GIHCG is upregulated in HCC and associated with poor survival of patients.GIHCG significantly promotes tumor growth and metastasis of HCC.GIHCG physically associates with EZH2.GIHCG upregulates H3K27me3 and DNA methylation levels on the miR-200b/a/429 promoter.GIHCG epigenetically silences miR-200b/a/429 expression.

A let-7/Fas double-negative feedback loop regulates human colon carcinoma cells sensitivity to Fas-related apoptosis

Interferon-γ (IFN-γ) is considered essential for the regulation of anti-tumor reactions as it sensitizes Fas-related apoptosis in HT29 cells, but the mechanism is unclear. In the current study, our data demonstrated that IFN-γ stimulation and Fas activation suppressed Dicer processing and let-7 microRNA biogenesis, while let-7 microRNA strongly inhibited Fas expression by directly targeting Fas mRNA. Accordingly, our results indicate that Fas and let-7 microRNAs form a double-negative feedback loop in IFN-γ and Fas induced apoptosis in colon carcinoma cell line HT29, which may be an important synergistic mechanism in anti-tumor immune response. We also found that a let-7 microRNA inhibitor increased Fas expression and sensitized cells to Fas-related apoptosis, which may have future implications in colon carcinoma therapy.

Surgical outcome of hepatocellular carcinoma patients with biliary tumor thrombi

BackgroundTo investigate the surgical outcome of hepatocellular carcinoma (HCC) patients with biliary tumor thrombi (BTT).MethodsSurgical outcome of 27 HCC patients with BTT (group I) were compared with randomly selected HCC patients without BTT (group II; n = 270).ResultsOne patient in group I died of hepatic failure within 30 days after resection. The 1-, 3- and 5-year cumulative survival rates of group I were 70.3%, 25.9%, and 7.4%, respectively; these were significantly lower than those of group II (90.6%, 54.0%, and 37.7%) (P < 0.001). The rates of early recurrence (≤ 1 year) after resection were significantly higher in group I than group II (70.3% vs. 34.8%) (P < 0.001).ConclusionHCC patients with BTT had a worse prognosis after resection than those without BTT. Resection should be considered for these tumors given the lack of effective alternative therapies.

Risk factors for combined hepatocellular-cholangiocarcinoma: A hospital-based case-control study

AIM To identify risk factors contributing to the development of combined hepatocellular-cholangiocarcinoma (CHC) in China. METHODS One hundred and twenty-six patients with CHC and 4:1 matched healthy controls were interviewed during the period from February 2000 to October 2012. Logistic regression analysis was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for each risk factor. RESULTS Univariate analysis showed that the significant risk factors for CHC development were hepatitis B virus (HBV) infection, heavy alcohol consumption, a family history of liver cancer, and diabetes mellitus. Multivariate stepwise logistic regression analysis showed that HBV infection (OR = 19.245, 95%CI: 13.260-27.931) and heavy alcohol consumption (OR = 2.186, 95%CI: 1.070-4.466) were independent factors contributing to the development of CHC. CONCLUSION HBV infection and heavy alcohol consumption may play a role in the development of CHC in China.

Anatomical versus nonanatomical resection of colorectal liver metastases: a meta-analysis

PurposeThe purpose of the study was to compare anatomical resection (AR) versus nonanatomical resection (NAR) for colorectal liver metastases (CLM) with respect to perioperative and oncological outcomes.MethodsLiterature search was performed to identify comparative studies reporting outcomes for both AR and NAR for CLM. Pooled odds ratios (OR) and weighted mean differences (WMD with 95% confidence intervals (95% CI) were calculated using either the fixed effects model or random effects model.ResultsSeven nonrandomized controlled studies matched the selection criteria and reported on 1,662 subjects, of whom 989 underwent AR, and 673 underwent NAR for CLM. Compared with the perioperative results, NAR reduced the operation time (WMD, 0.39; 95% CI, 1.97–79.17) and blood transfusion requirement (OR, 2.98; 95% CI, 1.87–4.74), whereas postoperative morbidity and mortality were similar between the two groups. With respect to oncologic outcomes, there was no significant difference in surgical margins, overall survival and disease-free survival between the two groups.ConclusionsNAR is a safe procedure for CLM and does not compromise oncological outcomes. However, the findings have to be carefully interpreted due to the lower level of evidence.

Methylation patterns of estrogen receptor α promoter correlate with estrogen receptor α expression and clinicopathological factors in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is the seventh most common type of cancer; notably, the incidence of HCC is four to eight times higher in men than women. Previous studies reported that the estrogen receptor (ER) signaling pathway is involved in the pathogenesis of HCC, although the extent of its involvement is unclear due to several conflicting reports. In the present study, tumor and paired adjacent non-cancerous tissues from 157 HCC patients were collected. Transcriptome sequencing and real-time quantitative polymerase chain reaction were used to quantify the ER α (ESR1) expression levels, and the Sequenom EpiTYPER assay was used to delineate the methylation patterns in the ESR1 promoter. We found that ESR1 expression was significantly reduced in tumor tissues (P < 0.001) compared to adjacent non-cancerous tissues. The CpG sites around the transcription start site were significantly hypermethylated in the tumor (P < 0.0001). This methylation pattern also correlated with the gene expression (P < 0.0001). Additionally, we found that the hypermethylation of ESR1 was associated with the presence of fibrous capsules (P = 1.2 × 10−4), the absence of microvascular invasions (P = 8.0 × 10−4), thin trabecular pattern (P = 0.025), and lower histologic gradings (P = 5.2 × 10−3). Thus, ESR1 expression is a candidate tumor suppressor gene in HCC. Further, promoter hypermethylation may be a mechanism by which expression of ESR1 is repressed, and the extent of hypermethylation of ESR1 may be a marker for HCC status and progression.

Overexpression of miR-218 inhibits hepatocellular carcinoma cell growth through RET

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world with poor prognosis. Here, we investigated the role of microRNA 218 (miR-218) in regulating human HCC development. Quantitative PCR (qPCR) was used to compare the expression levels of miR-218 between eight HCC and a normal liver cell lines, as well as nine primary HCC tissues and adjacent non-carcinoma tissues. HCC cell lines MHCC97L and Huh7 were transfected with lentiviral vector of miR-218 mimics. The effect of miR-218 overexpression on cancer cell growth, both in vitro and in vivo, as well as cancer cell invasion was examined. A bioinformatic method was used to predict the binding of miR-218 to RET proto-oncogene (RET). Small interfering RNA (SiRNA)-mediated genetic knock-down of RET was performed in MHCC97L and Huh7 cells, and its modulatory effect on miR-218-mediated HCC development was examined. miR-218 was found to be downregulated in HCC cell lines and primary HCC tissues. Overexpression of miR-218 in MHCC97L or Huh7 cells resulted in significant decrease in cell proliferation and invasion capability. Overexpression of miR-218 also reduced the tumor growth of xenografted Huh7 cells in vivo. The expression of endogenous RET was found to be upregulated by miR-218, and siRNA-induced RET downregulation resulted in phosphatase and tensin homolog deleted on chromosome 10 (PTEN) upregulation and reversal of the inhibitory effect of miR-218 upregulation on HCC proliferation. Our results indicate that miR-218 modulates HCC development, and this effect may be through RET and PTEN.