ObjectiveTo investigate the clinical features of drug-induced liver injury (DILI) caused by antitumor drugs during the treatment of malignant tumors. MethodsA retrospective analysis was performed for the clinical data of 56 patients who were diagnosed with malignant tumors in Henan Provincial People′s Hospital from January 2015 to December 2016 and experienced DILI during the treatment with antitumor drugs, including sex, age, type of primary tumor, hepatotropic virus infection, liver function, type of chemotherapeutics, onset time of liver injury, application of liver-protecting drugs, and outcome of liver injury. ResultsAmong the 56 patients with DILI caused by antitumor drugs, 30 (53.6%) had hepatocellular injury, and 45 (80.4%) had mild liver injury. FOLFOX, GP/DP, and CHOP were the most common regimens for DILI, and of all 56 patients, 50 (89.3%) had DILI caused by multiple drugs. Platinum-based drugs, anti-microtubule agents, and alkylating agents were the common drugs causing DILI. Of all 56 patients, 35 (62.5%) developed DILI within 1-2 weeks after medication. ConclusionDILI caused by antitumor drugs mainly has a mild degree and hepatocellular injury type is the most common clinical type. Platinum-based antitumor drugs and related chemotherapeutic regimens are the most common drugs for DILI. A combination of multiple antitumor drugs is more likely to cause DILI, and patients with such DILI often have a good prognosis.

Objective To explore the expression of scavenger receptor class type B 1 (SR-B1) in esophageal squamous cell carcinoma (ESCC) ,and its effects on proliferation and invasion of ESCC cells . Methods From May 2012 to August 2017 ,63 ESCC patients who underwent surgical resection in Henan Provincial People′s Hospital were enrolled and ESCC tissues and corresponding normal tissues were collected . The expression of SR-B1 protein in collected tissues and ESCC cells were detected by immunohistochemistry and Western blotting .ESCC EC1 cells and TE1 cells were transfected with SR-B1 small interfering RNA (siRNA) ,control siRNA ,pcDNA3 .1 and pcDNA3 .1-SR-B1 ,respectively .After transfection ,the expression of SR-B1 protein was examined by Western blotting .The cell proliferation , cell cycle and invasion ability of ESCC EC1 cells and TE1 cells after transfection were determined by cell counting kit-8 (CCK-8) assay ,flow cytometry and Transwell chamber .Chi-square test and t test were performed for statistical analysis .Results The positive rate of SR-B1 protein expression in ESCC tissues was 60 .3％ (38/63) ,which was higher than that of corresponding normal tissues (30 .2％ ,19/63) ,and the difference was statistically significant (χ2=11 .565 , P=0 .001) .The expression of SR-B1 protein in ESCC cells Eca109 ,EC9706 ,EC1 ,TE1 and KYSE70 were 0 .244 ± 0 .012 ,0 .285 ± 0 .018 ,0 .455 ± 0 .016 ,0 .479 ± 0 .019 and 0 .390 ± 0 .022 ,respectively ,which were all higher than that of normal esophageal epithelial cell Het-1A (0 .027 ± 0 .011) ,and the differences were statistically significant (t=23 .252 ,21 .633 ,39 .081 ,36 .010 and 25 .591 ;all P<0 .01) .The expression of SR-B1 protein in ESCC EC1 and TE1 was downregulated by SR-B1 siRNA . The downregulation of SR-B1 protein expression suppressed the proliferation of ESCC EC1 cells and TE1 cells ,increased the percentage of cells at G0/G1 phase of ESCC EC1 cells and TE1 cells ((64 .92 ± 1 .68)％ and (64 .34 ± 0 .94)％ ) ,and reduced the invasion abilities of EC1 and TE1 cells (33 .33 ± 7 .51 and 21 .67 ± 4 .04) .The upregulation of SR-B1 expression promoted the proliferation of ESCC EC1 cells and TE1 cells ,reduced the percentage of cells at G0/G1 phase ((31 .72 ± 1 .30)％ and (33 .12 ± 1 .04)％ ) ,and enhanced cell invasion abilities (285 .33 ± 28 .10 and 247 .33 ± 28 .29) .Conclusions The overexpression of SR-B1 in ESCC may be associated with the occurrence and development of ESCC .Treatment targeting SR-B1 may be a novel therapeutic strategy in ESCC .

Objective To construct the prokaryotic expression vector of human esophageal cancer related gene 4 (ECRG4), to purify the recombinant ECRG4 protein and to verify the biological function of the recombinant ECRG4 protein. Methods DNA recombination technology was utilized to construct the ECRG4 protein prokaryotic expression vector. The recombinant ECRG4 protein was purified with the transformation of escherichia coli. Then the purity of the recombinant ECRG4 protein was examined by using sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis. Furthermore, esophageal cancer EC-18 cell line was treated by recombinant ECRG4 protein (10 μg/ml) for phosphate buffer (PBS) 48 h respectively, and the tumor cell cycle change was examined by using flow cytometry. Results SDS-PAGE analysis showed that the high purity of recombinant ECRG4 protein was obtained and the ECRG4 protein prokaryotic expression vector was successfully constructed. The cell proportion of G1 phase in PBS control group was lower than that in the recombinant ECRG4 protein group [(60.4 ±2.1) ％ vs. (71.6 ±1.8) ％; t= 25.695, P= 0.002]. The cell proportion of S phase in PBS control group was higher than that in the recombinant ECRG4 protein group [(24.6±1.4) ％ vs. (16.5±1.0) ％; t= 36.905, P= 0.001]. The cell proportion of G2/M phase in PBS control group was higher than that in the recombinant ECRG4 protein group [(15.0 ±1.1) ％ vs. (11.9 ±0.8) ％; t=6.471, P=0.023], which indicated that the recombinant ECRG4 protein could induce the G1 phase arrest of EC-18 cells. Conclusion The ECRG4 protein prokaryotic expression vector is successfully constructed. And the recombinant ECRG4 protein has an active biological function in esophageal carcinoma.

OBJECTIVETo evaluate the prognosis and predictive values of preoperative Glasgow prognostic score (GPS) for adenocarcinoma of esophagogastric junction(AEG) patients.

METHODSA retrospective study of 322 AEG patients who received operation between January 2007 and March 2010 in Henan Provincial People's Hospital was performed. Clinical data, pathological characteristics, laboratory parameters and survival data were collected. The GPS was calculated based on C-reactive protein(CRP) and serum albumin(ALB) levels. Univariate and multivariate analysis were used to evaluate the prognostic value of GPS.

RESULTSAmong 322 patients, 0, 1, 2 of GPS were 192, 104 and 26 patients respectively. The median follow-up was 37 (4-73) months. In Kaplan-Meier analysis, median diseases-free survival (DFS) of GPS 0, 1, 2 was 47.0 (95% CI: 31.6-62.4), 15.0 (95% CI: 11.8-8.2) and 4.7 (95% CI: 3.8-5.6) months (P<0.01), and median overall survival (OS) was out of reach, 20.6 (95% CI: 15.8-25.4) and 7.0 (95% CI: 5.8-8.2) months (P<0.01). Univariate and multivariate analysis revealed that GPS was an independent predictor of DFS (P<0.01) and OS (P<0.01) of AEG.

CONCLUSIONGPS is an effective predictor of survival in AEG.

Adenocarcinoma ; C-Reactive Protein ; Disease-Free Survival ; Esophageal Neoplasms ; Esophagogastric Junction ; Humans ; Kaplan-Meier Estimate ; Prognosis ; Retrospective Studies ; Stomach Neoplasms

Objective: To study the predictive and prognostic significance of high-sensitivity modified Glasgow Prognostic Score (HS-mGPS) on the effect of neoadjuvant chemotherapy for advanced gastric cancer. Methods: 117 patients with advanced gastric cancer received neoadjuvant chemotherapy with SOX (oxaliplatin+ S1) or mFOLFOX 6(oxaliplatin+ CF+ 5-FU) regimen. HS-mGPS was calculated according to blood C-reactive protein (CRP) concentration and serum albumin (ALB) level. The correlation between HS-mGPS and clinicopathological characteristics was determined and the predictors of survival were analyzed. Results: 117 patients with stage ⅡB (43 cases), stage Ⅲ (60), and stage Ⅳ (14) received preoperative neoadjuvant chemotherapy. The overall response rate of neoadjuvant chemotherapy was 61.5%(72/117), and the tumor control rate was 88.0% (103/117), with a pathological response rate of 91.5% (107/117). The R0 resection rate was 81.2% (95/117). The median disease-free survival (DFS) was 21.0 (95% CI 6.4-35.6) months. The median overall survival (OS) was 39.0 (95% CI 21.4-56.6) months. Higher HS-mGPS was associated with higher T stage, local lymph-node metastasis, distant metastasis, lower chemotherapy overall response rate and lower pathological response rate (all P<0.05). The univariate analysis and multivariate analysis showed that higher HS-mGPS, presence of local lymph-node metastasis and non R0 resection were associated with poorer DFS and OS (P<0.05). Conclusion HS-mGPS can be used to predict the benefits of neoadjuvant chemotherapy and as an independent prognostic factor for survival in patients with advanced gastric cancer.

Objective: To investigate the expression of microRNA-133b (miR-133b) in esophageal squamous cell carcinoma (ESCC), and explore its effect and the underlying molecular mechanisms on cell proliferation and invasion. Methods: Real-time quantitative PCR (qPCR) was used to examine miR-133b expression in 63 ESCC tissues and paired adjacent non-cancerous tissues, several ESCC cells (Eca109, EC9706, EC1, TE1, KYSE70) and normal esophageal epithelial cell Het-1A. MiR-133b mimic, inhibitor and negative control (NC) were transfected into TE1 cells. The effect of miR-133b on cell proliferation and invasion were determined by CCK-8 and Transwell assays, respectively. Subsequently, the target gene of miR-133b was predicted by online tools TargetScan and miRDB, which was verified by dual luciferase reporter assays. Finally, Western blot was utilized to detect the effects of miR-133b overexpression on expression of target gene TAGLN2 as well as EMT-related proteins E-cadherin, N-cadherin, Snail, Slug and Vimentin. Results: Relative levels of miR-133b in ESCC tissues (0.295±0.040) were significantly lower than those in adjacent non-cancerous tissues (1.002±0.011, P<0.001). The expression of miR-133b was tightly associated with clinical staging, lymph node metastasis and prognosis. Moreover, relative levels of miR-133b in ESCC cells Eca109, EC9706, EC1, TE1 and KYSE70 (0.679±0.031, 0.391±0.008, 0.236±0.016, 0.031±0.005 and 0.099±0.020) were evidently lower than that in normal esophageal epithelial cell Het-1A (1.005±0.016, all P<0.001). In TE1 cells, miR-133b mimic significantly increased the level of miR-133b to 6.199±0.627, and suppressed cell proliferation and invasion, whereas miR-133b inhibitor obviously decreased its expression to 0.182±0.023, and promoted cell proliferation and invasion. Most notably, the relative luciferase activities of miR-133b-mimic group (0.320±0.018) in TE1 cells transfected with TAGLN-3′UTR-WT were markedly lower than that in NC group (1.010±0.036, P<0.001), whereas those in TAGLN-3′UTR-MUT transfection cells were 1.019±0.056 and 1.008±0.021, respectively, showing no significantly statistical difference (P>0.05). Furthermore, miR-133b overexpression markedly downregulated TAGLN2, N-cadherin, Snail, Slug and Vimentin levels, and increased E-cadherin expression. Conclusion MiR-133b plays an important role in the proliferation and invasion of ESCC cells by regulating TAGLN2 expression, and it may be a potential therapeutic target for ESCC patients.