目的 探讨中性粒细胞计数与淋巴细胞计数比(NLR)对胰腺腺癌根治术后患者预后的评估价值.方法 回顾性分析郑州大学第一附属医院肝胆胰外科行胰腺癌根治术的77例患者的临床资料,通过术前的血常规结果计算出NLR值,取NLR中位数2.63为截点将患者分为高NLR和低NLR 2组.比较2组患者术后第1年、第3年的生存率,并分别对其影响因素进行分析.结果 低NLR组第1年、第3年的生存率分别为89.2％、40.5％,均高于高NLR组的65.7％、11.4％,差异有统计学意义(P<0.05);单因素及多因素分析提示NLR为胰腺癌根治术后患者预后的影响因素(P<0.05).结论 外周血高NLR是一个提示胰腺癌预后较差的指标.

目的 探究原发性肝癌术后复发行经皮射频消融(RFA)后的疗效、生存率及其影响因素.方法 回顾性分析2012年6月至2016年6月郑州大学第一附属医院行手术切除的原发性肝癌术后复发的67例患者临床资料,采用统计软件SPSS 21.0分析,生存曲线采用Kaplan-Meier法绘制,组间比较采用Log-Rank检验,Cox风险比例模型进行预后因素分析.结果 67例术后复发的肝癌患者经皮RFA治疗后1、3、5年总体生存率分别为94％、62％、50％,1、3、5年无瘤总体生存率分别为56％、39％、26％.根据肝癌切除术后复发的肿瘤直径分为小肝癌组(≤3 cm,n=47)和中肝癌组(>3 cm且≤5 cm,n=20),小肝癌组及中肝癌组行经皮RFA治疗后1、3、5年生存率分别为98％、67％、54％及86％、55％、40％,小肝癌组的生存率明显高于中肝癌组(P=0.007).通过Cox模型多因素分析,结果显示复发病灶直径、术后甲胎蛋白(AFP)水平是影响患者经皮RFA后生存时间的危险因素.结论 经皮RFA治疗术后复发性肝癌疗效确切,能以较小的创伤达到治疗的目的,小肝癌及术后AFP低行RFA预后更好.

Objective Analysis the date of patients with stage B Primary hepatocellular carcinoma in Barcelona Clinical Liver Classification (BCLC-B),and to explore the value of aspartate transaminase and platelet ratio index (APRI) combined with the indocyanine green retention rate at 15 mins (ICGR15)in evaluating the risk of the posthepatectomy liver failure (PHLF) for BCLC-B.Methods Analysis of clinical data of 216 patients with BCLC-B hepatocellular carcinoma undergoing hepatectomy.The best cut-off point of APRI value was obtained by receiver operating characteristic (ROC) curve.the logistic regression model was used to identify independent predictive indices for PHLF.According to whether Postopeatectomy Liver Failure (PHLF),they were divided into hepatic failure group and non-hepatic failure group.The differences in clinical biochemical parameters,ICGR15 and APRI between the two groups were recorded and analyzed.Results A total of 216 patients were enrolled in this study,among whom 30 (12.9％) had PHLF.he univariate and multivariate analyses showed that APRI and ICGR15 were significantly associated with the prognosis of PHLF patients (P ＜0.01).The ROC curve analysis shows that APRI has a strong ability to predict PHLF (The area under the curve is 0.831,the sensitivity is 93.3％,and the specificity is 65.6％),and the best cut-off point is 0.59.APRI-ICGR15 had a significantly higher area under the receiver operating characteristic curve (AUC)than APRI or ICGR15,and The AUC of APRI and ICGR15 are similar.For patients with BCLC-B stage hepatocellular carcinoma (HCC),when APRI ＜ 0.59 and ICGRI5 ＜ 10％,the incidence of liver failure after hepatectomy is low;when APRI≥0.59 and ICGR15 ＜ 10％,or APRI ＜ 0.59 and ICGR15 ≥ 10％ at that time,the incidence of PHLF is slightly higher.At this time,surgical treatment should be cautious.Liver function should be actively corrected before operation,and active supportive treatment should be given after surgery.When APRI≥0.59 and ICGR15≥10％,the incidence of PHLF is higher.Surgical treatment is not recommended for the time being.Conclusion ICGR15 and APRI are good indicators for evaluating liver reserve function.The combination of the two can better evaluate the risk of postoperative liver failure in patients with BCLC-B HCC.

目的 探讨胆囊癌的外科诊治经验.方法 回顾性分析郑州大学第一附属医院肝胆外科治疗的47例胆囊癌患者的临床资料.结果 早期胆囊癌(NevinⅠ ～ Ⅱ期)患者的5 a生存率为100％,随着胆囊癌Nevin分期的增加,5 a生存率降低(Ⅲ期为46.2％,Ⅳ ～ Ⅴ期为0).不同术式对非早期胆囊癌患者生存率影响较大,采用根治术患者1 a、3 a、5 a生存率分别为81.8％、54.5％和36.4％,均分别高于姑息术患者的23.1％、0和0,差异有统计学意义(P<0.05).采用扩大根治术患者1 a、3 a、5 a生存率分别为75.0％、37.5％和25.0％,姑息术患者分别为23.1％、0和0.1 a和3 a差异均有统计学意义(P<0.05),5a的差异无统计学意义(P>0.05).采用根治术和扩大根治术患者的生存率差异均无统计学意义(P>0.05).结论 早期诊断且合理的手术方案可增加胆囊癌患者的生存率.

Objective To investigate the relationship between the expression of breast cancer resistance protein (BCRP) and the clinicopathological features in hepatocellular carcinoma (HCC) and the influence of the BCRP expression on the proliferation and apoptosis of HCC cells.Methods To detect the expression of BCRP in hepatocellular carcinoma tissues by reverse transcriptase-polymerase chain reaction (RT-PCR),and analyze the relationship with clinicopathological parameters;BCRP-small interfering RNA (siRNA) was transfected into human hepatoma SMMC-7721 cells by LipofectamineTM 2000 liposome mediated method;cell proliferation,apoptosis and BCRP,proliferation cell nuclear antigen (Ki-67),B cell lymphoma/leukemia-2 associated X protein (bax),Notch1 and Hes1 protein expression were detected by methyl thiazol tetrazolium (MTT) method,flow cytometry and Western blotting,respectively.Results The expression of BCRP in HCC was not related to the sex,age and tumor size of HCC patients,and it was related to pathological grade,clinical stage and metastasis of tumor;expression of BCRP in SMMC-7721 cells after BCRP-siRNA was transfected cells was inhibited in the level of transcription and translation;cell proliferation (0.287 ± 0.022) and expression of Ki-67 (0.142 ± 0.018),Notch1 (0.162 ± 0.021) and Hes1 (0.111 ± 0.015) protein in BCRP-siRNA group were significantly lower than Control group (0.411 ±0.026,0.258 ±0.026,0.462 ±0.032,0.241 ±0.023;Pproliferation =0.001,PKi-67=0.001,PNotch1 =0.000,PHesl =0.001),the apoptosis rate (14.63 ±0.88)％ and the expression of bax protein (0.324±0.034) was significantly higher than Control group ([1.32 ±0.15)％,0.106 ± 0.012;Papoptosis =0.000,Pbax =0.000].Conclusion The expression of BCRP is related to pathological grade,clinical stage and metastasis of HCC,inhibition of its expression can reduce the proliferation of hepatocellular carcinoma cells and induce cell apoptosis,the mechanism is related to the regulation of Ki-67,bax expression and Notch1 signaling pathway.

Objective: To explore the core mechanism of long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) in the regulation of multidrug resistance of pancreatic cancer cells. Methods: mRNA levels of GAS5, miR-181c-5p and Hippo pathway related genes were detected by quantitative real-time PCR (qRT-PCR). Protein levels of MDR-1, MST1, YAP and TAZ were measured by western blot. Cell viability was detected by MTT assay. The combination between GAS5 and miR-181c-5p was confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assay. We also established pancreatic cancer-bearing mice model and analyzed tumor volumes. Results: Our data showed GAS5 expression was significantly down-regulated, miR-181c-5p expression was significantly up-regulated in pancreatic cancer cells. Besides, Overexpresson of GAS5 obviously inhibited cell viability, while GAS5 knockdown showed the opposite outcome. Additionally, we also found that GAS5 negatively regulated miR-181c-5p, and miR-181c-5p dramatically promoted pancreatic cancer cell chemoresistance through inactivating the Hippo signaling. GAS5 regulated chemoresistance and Hippo pathway of pancreatic cancer cells via miR-181c-5p/Hippo. Finally, we confirmed that overexpression of GAS5 inhibited tumor growth in pancreatic cancer-bearing mice model. Conclusion: GAS5 regualtes Hippo signaling pathway via miR-181c-5p to antagonize the development of multidrug resistance in pancreatic cancer cells.

Objective To investigate the Expression of Girdin gene in hepatocellular carcinoma cells and inhibition of its expression on proliferation and apoptosis of cells.Methods The expression of Girdin protein in HL-7702 normal liver cells and liver cancer Huh7,HepG2,MHCC97H,HCCLM3 cells were detected by Western blotting;Girdin small interfering RNA (siRNA) were transfected into HCCLM3 cells by LipofectamineTM2000,and set the negative control group and blank control group,the expression of proliferation cell nuclear antigen (Ki-67),cysteinyl aspartate-specific protease (Caspase)-3,B cell lymphoma/leukemia-2 associated X protein (bax),phosphorylation of janus kinase 2 (JAK2) and signal transducer and activators of transcription 3 (STAT3) protein were detected by Western blotting;cells activity were detected by cell counting kit-8 (CCK-8) assay in transfected 24,48 and 72 h;cell apoptosis were detected by flow cytometry in transfected 48 h.Results The expression of Girdin in HepG2 (0.355 ± 0.043),HCCLM3 (0.599 ± 0.068),MHCC97H (0.462 ± 0.055),Huh7 (0.378 ± 0.049)HCC cells was significantly higher than that in normal liver cells HL-7702 (0.112 ± 0.013,PHepG2 =0.001;PHCCLM3 =0.000;PMHCC97H =0.000;PHuh7 =0.001);cell activity in Girdin-siRNA group in 24 h (0.247 ± 0.032),48 h (0.477 ± 0.043) and 72 h (0.666 ± 0.073) were significantly lower than the control group (0.385 ±0.045),(0.711 ±0.068),(0.936 ±0.096),the apoptosis rate (16.18 t± 1.38) ％ in 48 h was significantly higher than the blank control group (1.87 ± 0.39) ％,the expression of Ki-67 (0.162 ±0.019),p-JAK2 (0.096 ±0.011) and p-STAT3 (0.057 ±0.009) protein were significantly lower than the control group (0.626 ± 0.073),(0.170 ± 0.021),(0.145 ± 0.018),the expression of Caspase-3 (0.257 ±0.032) and bax (0.279 ±0.032) protein were significantly higher than the control group (0.120 ±0.013,0.135 ±0.015) (PKi-67 =0.000;Pp-J.AK2 =0.006;Pp-STAT3 =0.002;PCaspase-3 =0.002;Pbax =0.002).Conclusion Girdin gene is highly expressed in hepatocellular carcinoma cells and inhibiting of Girdin expression by RNA interference can reduce the proliferation and induce apoptosis of cancer cells by down regulating the JAK2/STAT3 signal.

Background: Long non-coding RNA growth arrest-specific transcript 5 (lncRNA GAS5) is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. The precise role of GAS5 in pancreatic cancer (PC) progression is currently unknown, so the aim of this study was to explore the functional participation of GAS5 in PC metastasis. Methods: The expression changes of GAS5, miR-32-5p and PTEN in human PC specimens and cell lines were compared by means of molecular biology methods. Transfection of the recombinant plasmid was applied to modulate the expression levels of the target genes. RIP and RNA pull-down assays were designed to investigate the interaction between GAS5 and miR-32-5p. The effect of GAS5 and miR-32-5p on PC progression was assessed with cell proliferation, migration, invasion and apoptosis in vitro. Results: GAS5 and PTEN protein were decreased in human PC tissues and cells, but miR-32-5p was increased. GAS5 induction greatly inhibited the proliferation, migration and invasion of PC cells PANC-1 and BxPC-3 in vitro and simultaneously induced cell apoptosis. Moreover, GAS5 positively regulated the expression of PTEN through miR-32-5p. Furthermore, GAS5 suppressed the proliferation, migration and invasion of PC cells through regulating miR-32-5p/PTEN axis. Additionally, this finding was further supported by the results of in vivo experiments. Conclusion: GAS5 could positively regulate PTEN-induced tumor-suppressor pathway via miR-32-5p, thereby suppressing PC metastasis.

Objective To investigate the effect of B cell lymphoma/leukemia-2-associated athanogene-1 gene (BAG-1) gene expression by RNA interference on the proliferation,apoptosis and Wnt/β-catenin signaling pathway in hepatocellular carcinoma cells.Methods Human normal fiver cells L02 as control cells,reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the expression of BAG-1 in human hepatocellular carcinoma cell lines HepG2,Huh7,MHCC97L,MHCC97H and HCCLM3;the negative small interfering RNA (siRNA) and BAG-1-siRNA transfected HCCLM3 cells,and not transfected cells for the blank control group,transfection effect was detected after cells transfected for 48 h;the proliferation of the cells was detected by cell counting kit-8 (CCK-8) after cells were transfected at 24,48 and 72 h;the cells apoptosis after cells were transfected for 48 h was detected by flow cytometry;β-catenin,Survivin,c-Myc protein expression were detected by Western blotting.Results The expression of BAG-1 in hepatocellular carcinoma cells were significantly higher than those of control cells L02 ((mRNA:PHepG2 =0.000,PHuh7 =0.000,PMHCC97L =0.000,PMHCC97H =0.000,PHCCLM3 =0.000;protein:PHepG2 =0.030,PHuh7 =0.001,PMHCC97L =0.000,PMHCC97H =0.000,PHCCLM3 =0.000);the expression of BAG-1 protein (0.097 ± 0.010) after BAG-1-siRNA were transfected into HCCLM3 cells was significantly lower than the control Group (0.489 ±0.039)(P =0.000);the cells proliferation after BAG-1-siRNA transfected HCCLM3 cells for 48 h (0.312 ±0.024) and 72 h (0.673 ± 0.051) were significantly lower than the control group (0.448 ± 0.032),(0.673 ± 0.051) (P48h =0.004,P72 h =0.002);compared with the control group (2.13 ± 0.11) ％,(0.512±0.048),(0.349 ±0.032),(0.166 ±0.015),the apoptosis rate (13.47 ± 1.05)％ in BAG-1-siRNA group increased significantly,β-catenin (0.247 ± 0.028),Survivin (0.153 ±0.017),e-Myc (0.089 ± 0.009),protein expression was down regulated (Pβ in =0.001,Psurvisin =0.001,Pc-Myc =0.002).Conclusion Inhibiting of BAG-1 expression can reduce the proliferation of hepatoma cells and promote apoptosis by inhibiting the Wnt/β-catenin signaling pathway.