Hepatocellular carcinoma(HCC) is the fifth most common cancer and the third most common cause of cancer-related death worldwide. There have been great improvements in the diagnosis and treatment of HCC in recent years...Hepatocellular carcinoma(HCC) is the fifth most common cancer and the third most common cause of cancer-related death worldwide. There have been great improvements in the diagnosis and treatment of HCC in recent years, but the problems, including difficult diagnosis at early stage, quick progression, and poor prognosis remain unsolved. Surgical resection is the mainstay of the treatment for HCC. However, 70%-80% of HCC patients are diagnosed at an advanced stage when most are ineligible for potentially curative therapies such as surgical resection and liver transplantation. In recent years, non-surgical management for unrespectable HCC, such as percutaneous ethanol injection, percutaneous microwave coagulation therapy, percutaneous radiofrequency ablation, transcatheter arterial chemoembolization, radiotherapy, chemotherapy, biotherapy, and hormonal therapy have been developed. These therapeutic options, either alone or in combination, have been shown to control tumor growth, prolong survival time, and improve quality of life to some extent. This review covers the current status and progress of non-surgical management for HCC.展开更多
AIM To detect the mechanisms of Helicobacter pylori(H. pylori) infection in the invasion and metastasis of gastric cancer(GC).METHODS Specimens from 99 patients with GC were collected. The correlation among H. pylori ...AIM To detect the mechanisms of Helicobacter pylori(H. pylori) infection in the invasion and metastasis of gastric cancer(GC).METHODS Specimens from 99 patients with GC were collected. The correlation among H. pylori infection, heparanase(HPA) and mitogen-activated protein kinase(MAPK) expression, which was determined by immunohistochemistry, and the clinical features of GC was analysed using SPSS 22.0. Overall survival(OS) and relapse-free survival(RFS) of GC patients were estimated by the KaplanMeier method. Independent and multiple factors of HPA and MAPK with prognosis were determined with COX proportional hazards models. HPA and MAPK expression in MKN-45 cells infected with H. pylori was analysed using Western blot. RESULTS H. pylori infection was observed in 70 of 99 patients with GC(70.7%), which was significantly higher than that in healthy controls. H. pylori infection was related to lymph metastasis and expression of HPA and MAPK(P < 0.05); HPA expression was relevant to MAPK expression(P = 0.024). HPA and MAPK expression in MKN-45 cells was significantly upregulated following H. pylori infection and peaked at 24 h and 60 min, before decreasing(P < 0.05). SB203580, an inhibitor of MAPK, significantly decreased HPA expression. HPA was related to lymph metastasis and invasive depth. HPA positive GC cases and H. pylori positive GC cases showed poorer prognosis than HPA negative cases(P < 0.05). COX models showed that the prognosis of GC was connected with HPA expression, lymph metastasis, tissue differentiation, and invasive depth. CONCLUSION H. pylori may promote the invasion and metastasis of GC by increasing HPA expression that may associate with MAPK activation, thus causing a poorer prognosis of GC.展开更多
AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion...AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion,and migration of CBP-TE-1 cells,as well as the expression of Src were then determined and compared with those in normal TE-1 cells.RESULTS:The expression of Src was decreased by the overexpression of CBP in TE-1 cells.The growth,invasion,and migration of TE-1 cells were decreased by the overexpression of CBP.CONCLUSION:This study indicates that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src.CBP may be a potential tumor suppressor and targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.展开更多
AIM:To examine transforming growth factor-β1(TGF-β1)promoter methylation in gastric cancer and to determine if Helicobacter pylori(H.pylori)or interleukin(IL)-1β could induce TGF-β1 hypermethylation in vitro.METHO...AIM:To examine transforming growth factor-β1(TGF-β1)promoter methylation in gastric cancer and to determine if Helicobacter pylori(H.pylori)or interleukin(IL)-1β could induce TGF-β1 hypermethylation in vitro.METHODS:We examined the frequency and extent of TGF-β1 promoter methylation using methylationspecific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects.H.pylori infection was confirmed by a positive result from either a serological test,histological analysis or C13urea breath test.GES-1 and MKN-45 cells co-cultured with H.pylori or treated with IL-1β for 12,24 and 48 h in vitro tested the effects of H.pylori or IL-1β on TGF-1β.RESULTS:Twenty-four/forty-seven(51%)cases of gastric cancer(GC)tissues showed TGF-β1 promoter methylation,15/47(31.9%)cases of matched noncancerous gastric mucosa tissues from the GC patients,and 11/39(28%)case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation(51%vs 28%,P<0.05).Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients(0.24±0.06 vs 0.17±0.04,P<0.05)and normal gastric tissues from non-GC subjects(0.24±0.06 vs 0.15±0.03,P<0.05).TGF-β1 methylation was found in 48.3% of H.pylori-positive gastric mucosal tissues whereas only 23.1% of H.pylori-negative gastric mucosal tissues showed TGF-β1 methylation(48.3%vs 23.1%,P<0.05).IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h.Further studies showed that pre-treatment of GES-1 cells with 20ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation.Infection of GES-1cells by H.pylori was not found to induce significant TGF-β1 promoter methylation.CONCLUSION:Our data revealed that TGF-1 promoter is methylated in GC patients.IL-1β may be an important mediator for H.pylori induced gene methylation during GC development.展开更多
AIM:To compare non-liquid and clear-liquid diets,and to assess whether the latter is the optimal treatment for mild acute pancreatitis.METHODS:The Cochrane Library,PUBMED,EMBASE,EBM review databases,Science Citation I...AIM:To compare non-liquid and clear-liquid diets,and to assess whether the latter is the optimal treatment for mild acute pancreatitis.METHODS:The Cochrane Library,PUBMED,EMBASE,EBM review databases,Science Citation Index Expanded,and several Chinese databases were searched up to March 2011.Randomized controlled trials(RCTs) that compared non-liquid with clear-liquid diets in patients with mild acute pancreatitis were included.A meta-analysis was performed using available evidence from RCTs.RESULTS:Three RCTs of adequate quality involving a total of 362 participants were included in the final analysis.Compared to liquid diet,non-liquid diet significantly decreased the length of hospitalization [mean difference(MD):1.18,95% CI:0.82-1.55;P﹤0.00001] and total length of hospitalization(MD:1.31,95% CI:0.45-2.17;P = 0.003).The subgroup analysis showed solid diet was more favorable than clear liquid diet in the length of hospitalization,with a pooled MD being-1.05(95% CI:-1.43 to-0.66;P﹤0.00001).However,compared with clear liquid diet,both soft and solid diets did not show any significant differences for recurrence of pain after re-feeding,either alone [relative risk(RR):0.95;95% CI:0.51-1.87;P = 0.88] and(RR:1.22;95% CI:0.69-2.16;P = 0.49),respectively,or analyzed together as non-liquid diet(RR:0.80;95% CI:0.47-1.36;P = 0.41).CONCLUSION:The non-liquid soft or solid diet did not increase pain recurrence after re-feeding,compared with the clear-liquid diet.The non-liquid diet reduced hospitalization.展开更多
Correction to"Liu LP,Sheng XP,Shuai TK,Zhao YX,Li B,Li YM.Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression.World J Gastroenterol 2018;24:4565-4577[PMID:303...Correction to"Liu LP,Sheng XP,Shuai TK,Zhao YX,Li B,Li YM.Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression.World J Gastroenterol 2018;24:4565-4577[PMID:30386106 DOI:10.3748/wjg.v24.i40.4565]."In this article,we have identified some of the images in Figure 2A,C,E,G,and I are identical to the images in Figures 1B,2A,3B,3E,and 3G of another paper entitled"Liu L,Zhao Y,Fan G,Shuai T,Li B,Li Y.Helicobacter pylori infection enhances heparanase leading to cell proliferation via mitogenactivated protein kinase signalling in human gastric cancer cells.",which was published by us in the Molecular Medicine Reports in December,2018[PMID:30320396 DOI:10.3892/mmr.2018.9558].The reason why we asked to replace the pictures was that when we were simultaneously preparing to submit our two different articles to the World Journal of Gastroenterology(WJG)and Molecular Medicine Reports,we uploaded the wrong pictures to the WJG,which were same as those submitted to the Molecular Medicine Reports.We apologize for this negligence and any inconvenience that this may cause.We would be grateful if you could replace the wrong pictures with the correct ones attached.展开更多
Solid pseudopapillary tumor (SPT) of the pancreas is a rare pancreatic disease. Generally, it is considered a benign or low-grade malignant tumor. SPT of the pancreas with liver metastasis or invasion to adjacent orga...Solid pseudopapillary tumor (SPT) of the pancreas is a rare pancreatic disease. Generally, it is considered a benign or low-grade malignant tumor. SPT of the pancreas with liver metastasis or invasion to adjacent organs is usually uncommon.展开更多
AIM: To investigate the effects of superoxide dismutase (SOD) polymorphisms (rs4998557 , rs4880), Helicobacter pylori (H. pylori ) infection and environmental factors in gastric cancer (GC) and malignant potential of ...AIM: To investigate the effects of superoxide dismutase (SOD) polymorphisms (rs4998557 , rs4880), Helicobacter pylori (H. pylori ) infection and environmental factors in gastric cancer (GC) and malignant potential of gastric precancerous lesions (GPL). METHODS: Copper-zinc superoxide dismutase (SOD1, CuZn-SOD)-G7958A (rs4998557 ) and manganese superoxide dismutase (SOD2, Mn-SOD)-Val16Ala (rs4880 ) polymorphisms were genotyped by SNaPshot multiplex polymerase chain reaction (PCR) in 145 patients with GPL (87 cases of gastric ulcer, 33 cases of gastric polyps and 25 cases of atrophic gastritis), 140 patients with GC and 147 healthy controls. H. pylori infection was detected by immunoblotting analysis. RESULTS: The SOD1-7958A allele was associated with a higher risk of gastric cancer [odds ratio (OR) = 3.01, 95% confidence intervals (95% CI): 1.83-4.95]. SOD216Ala/Val genotype was a risk factor for malignant potential of GPL (OR = 2.04, 95% CI: 1.19-3.49). SOD216Ala/genotype increased the risk of gastric cancer (OR = 2.85, 95% CI: 1.66-4.89). SOD1-7958A/genotype, SOD2-16Ala/genotype, alcohol drinking, positive family history and type Ⅰ H. pylori infection were associated with risk of gastric cancer, and there were additive interactions between the two genotypes and the other three risk factors. SOD2-16Ala/Val genotype and positive family history were associated with malignant potential of GPL and jointly contributed to a higher risk for malignant potential of GPL (OR = 7.71, 95% CI: 2.10-28.22). SOD1-7958A/genotype and SOD2-16Ala/genotype jointly contributed to a higher risk for gastric cancer (OR = 6.43, 95% CI: 3.20-12.91). CONCLUSION: SOD1-7958A/and SOD2-16Ala/-genotypes increase the risk of gastric cancer in Chinese Han population. SOD2-16Ala/-genotype is associated with malignant potential of GPL.展开更多
AIM:To investigate the correlation between the Helicobacter pylori(H.pylori)infection and host genetic background of healthy populations in Indonesia.METHODS:In March 2007,epidemiological studies were undertaken on th...AIM:To investigate the correlation between the Helicobacter pylori(H.pylori)infection and host genetic background of healthy populations in Indonesia.METHODS:In March 2007,epidemiological studies were undertaken on the general population of a city in Indonesia(Mataram,Lombok).The participants included 107 men and 187 women,whose ages ranged from6 to 74 years old,with an average age of 34.0(±14.4)(±SD).The H.pylori of subject by UBT method determination,and through the polymerase chain reaction with confronting two-pair primers(PCR-CTPP)method parsing the single nucleotide polymorphism of interleukin(IL)-8,IL-4,IL-1β,CD14,tumor necrosis factor(TNF-a)and tyrosine-protein phosphates non-receptor type 11(PTPN11)genotypes.The experimental data were analyzed by the statistical software SAS.RESULTS:The H.pylori infection rates in the healthy Indonesian population studied were 8.4%for men and12.8%for women;no obvious differences were noted for H.pylori infection rates by sex or age.TC genotypes of IL-4,TC and CC genotypes of TNF-a,and GA genotypes of PTPN11,were higher in frequency.Both CC and TC genotype of TNF-a T-1031C loci featured higher expressions in the healthy Indonesian population Indonesia studied of(OR=1.99;95%CI:0.67-5.89)and(OR=1.66;95%CI:0.73-3.76),respectively.C allele of IL-1βT-31C gene locus was at a higher risk(OR=1.11;95%CI:0.70-1.73)of H.pylori infection,but no statistical significance was found in our study.CONCLUSION:We reveal that the association between the TNF-a and IL-1βgenotypes may be the susceptibility of H.pylori in the studied population.展开更多
AIM：To clarify the role of activated Notch2 in the invasiveness of gastric cancer.METHODS：To investigate the invasiveness of silencing Notch2 gene expression,we established a Notch2small interfering RNA（siRNA） tra...AIM：To clarify the role of activated Notch2 in the invasiveness of gastric cancer.METHODS：To investigate the invasiveness of silencing Notch2 gene expression,we established a Notch2small interfering RNA（siRNA） transfected cell line using the MKN-45 gastric cancer cell line.After the successful transfection confirmed by real-time reverse transcription-polymerase chain reaction（RT-PCR） and Western blotting,migration and invasion assays were employed to evaluate the aggressiveness of the gastric cancer.RT-PCR and Western blottings were employed to confirm the down-regulation of Notch2 and to evaluate the expression of epithelial mesenchymal transition-related gene matrix metallopeptidase 9（MMP9）,Akt,p-Akt.To confirm the relationship between PI3KAkt and MMP9,the PI3K inhibitor LY294002 was used to treat MKN-45 cells.RESULTS：Notch2 expression was dramatically decreased after Notch2 siRNA transfection（100.00% ± 9.74% vs 11.61% ± 3.85%,P 〈 0.01 by qRT-PCR）.There was also a marked reduction of Notch target gene Hes1（100.00% ± 4.74% vs 61.61% ± 3.58%,P 〈 0.05） at the mRNA,indicating an inhibition of Notch signaling.Inhibition of Notch signaling was also confirmed by the marked reduction of Notch2 intracellular domain at the protein levels（100.00% ± 9.74% vs 65.61% ± 7.58%,P 〈 0.05）.Down-regulation of Notch2 by siRNA enhanced tumor cell invasion（100.00% ± 21.64% vs 162.22% ± 16.84%,P 〈 0.05） and expression of MMP9（1.56 fold,P 〈 0.05）,and activated the pro-MMP9 protein to its active form（1.48 fold,P 〈 0.05）.There was no significant difference in the protein levels of Akt between the two groups（100.00% ± 10.87% vs 96.61% ± 7.33%,P 〉 0.05）,while down-regulation of Notch2 elevated p-Akt expression（100.00% ± 9.87% vs 154.61% ± 13.10%,P 〈 0.05）.Furthermore,p-Akt and MMP9 was down-regulated in response to the inhibitor LY294002（p-Akt 100.00% ± 8.87% vs 58.27% ± 5.01%,P 〈 0.05;MMP9 100.00% ± 9.17% vs 50.03% ± 4.88%,P 〈 0.05）.CONCLUSION：Notch2 may negatively regulate cell invasion by inhibiting the PI3K-Akt signaling pathway展开更多
Background Acute severe biliary pancreatitis （ASBP） is a severe and fatal disease, and the expenditure is huge and therapeutic effects are still not satisfactory. This study aimed to improve the therapeutic effects ...Background Acute severe biliary pancreatitis （ASBP） is a severe and fatal disease, and the expenditure is huge and therapeutic effects are still not satisfactory. This study aimed to improve the therapeutic effects and reduce the expenditure of ASBP treatment.Methods One hundred and five patients diagnosed with ASBP were referred to our department from January 2004 to July 2009. Diagnosis was based on the 2007 criteria of the Chinese Society of Surgery. Patients were divided into two groups; the E group： 50 patients who underwent endoscopic retrograde choledochopancreatography （ERCP） ＋ endoscopic sphincterotomy （EST） ＋ endoscopic lithotripsy basket （ESR） ＋endoscopic retrograde biliary drainage （ERBD）and enteral nutrition （EN）, and the R group： 55 patients who underwent traditional treatment without ERCP. Subsequently,subjective symptoms, signs, biochemical analysis, serum endotoxin, tumor necrosis factor a, grades by computed tomography （CT）, cost of hospitalization and length of stay were compared between the two groups.Results All enrolled patients complied well with all therapeutic regimens. Endoscopic therapy that combined EN could significantly improve symptoms, clinical signs, laboratory values, tumor necrosis factor a and endotoxin while significantly reducing hospital expenditure and length of hospital stay. The experimental findings revealed that there were obvious advantages in the E group compared with the R group.Conclusions Endoscopic therapy combined with EN is an effective, safe and economic therapeutic regimen of ASBP.展开更多
Accumulating evidence has suggested that the gap junction plays an important role in the determination of cerebral ischemia, but the underlying mechanisms remain to be elucidated. In this study, we assessed the effect...Accumulating evidence has suggested that the gap junction plays an important role in the determination of cerebral ischemia, but the underlying mechanisms remain to be elucidated. In this study, we assessed the effect of a gap-junction blocker, carbenoxolone （CBX）, on ischemia/reperfusion-induced brain injury and the possible mechanisms. By using the transient cerebral ischemia model induced by occlusion of the middle cerebral artery for 30 min followed by reperfusion for 24 h, we found that pre-administration of CBX （25 mg/kg, intracerebroventricular injection, 30 min before cerebral ischemic surgery） diminished the infarction size in rats. And this was associated with a decrease of reactive oxygen species generation and inhibition of the activation of astrocytes and microglia. In PC12 cells, H202 treatment induced more coupling and apoptosis, while CBX partly inhibited the opening of gap junctions and improved the cell viability. These results suggest that cerebral ischemia enhances the opening of gap junctions. Blocking the gap junction with CBX may attenuate the brain injury after cerebral ischemia/reperfusion by partially contributing to amelioration of the oxidative stress and apoptosis.展开更多
Background Hepatitis B virus infection is closely related to hepatocellular carcinoma （HCC）. Cyclooxygenase-2 （COX-2） is overexpressed in HCC and considered to play a role in hepatic carcinogenesis. In this study,...Background Hepatitis B virus infection is closely related to hepatocellular carcinoma （HCC）. Cyclooxygenase-2 （COX-2） is overexpressed in HCC and considered to play a role in hepatic carcinogenesis. In this study, we analyzed the polymorphism of COX-2 promoter -899G/C in healthy controls, chronic hepatitis B （CHB） patients, liver cirrhosis patients, and hepatocellular carcinoma （HCC） patients, to investigate the relationship between COX-2 -899G/C polymorphism and the risk for hepatitis B-related liver cancer in a Chinese population from Gansu province. Methods Patients were divided into four groups： 300 patients with CHB, 300 patients with liver cirrhosis, 300 patients with HCC, and 300 healthy controls. The polymorphism of COX-2 -899G/C was detected by PCR-TaqMan probes. The results were analyzed by SPSS 17.0. Results The COX-2 -899G/C genotypes were GG, GC, and CC. Frequencies in CHB were 87.00%, 12.67%, 0.33%; in liver cirrhosis were 85.33%, 14.00%, 0.67%; in HCC were 77.00%, 21.67%, 1.33%; and in healthy controls were 90.67%, 9.00%, 0.33%, respectively. COX-2 -899C carriers may have an increased risk for hepatitis B-related liver cancer. Compared with the frequency of GG genotype, there were significant differences in the frequency of GC genotype between HCC and healthy control groups （0R=2.835, 95%C/： 1.751-4.589）; HCC and CHB groups （OR=1.933, 95%C/： 1.248-2.994）; and HCC and liver cirrhosis groups （OR=1. 175, 95%C/： 1.119-2.628）. Stratification analyses showed that COX-2 -899C allele carriers with a drinking history are more susceptible to develop HCC. Conclusion COX-2 -899C genotype may increase the susceptibility of individuals to hepatitis B-related liver cancer in Gansu province, China.展开更多
Background:Wilson's disease is an autosomal recessive disorder characterized by liver disease and/or neurologic deficits due to copper accumulation and is caused by pathogenic mutations in the ATP7B gene.Methods:T...Background:Wilson's disease is an autosomal recessive disorder characterized by liver disease and/or neurologic deficits due to copper accumulation and is caused by pathogenic mutations in the ATP7B gene.Methods:Two unrelated Chinese patients born to nonconsanguineous parents who were diagnosed with earlyonset Wiison's disease.DNA sequencing and bioinformation analysis were conducted.Results:We have identified four mutations in two family trios,of which two were novel,namely,c.3028A>G(p.K1010E) and c3992T>G (p.Y1331X),in each patient.Conclusions:Gene testing is playing an important role in diagnosis of Wilson's disease.The early-onset of Wilson's disease is apparently not associated with P-ATPase domain in the ATP7B protein.Our findings further widen the spectrum of mutations involving the ATP7B gene.展开更多
Hepatocellular carcinoma(HCC)is one of the malignant tumors with higher incidence and mortality worldwide.Recently,significant progress has been made in uncovering immunotherapy in HCC,for instance programmed death-1,...Hepatocellular carcinoma(HCC)is one of the malignant tumors with higher incidence and mortality worldwide.Recently,significant progress has been made in uncovering immunotherapy in HCC,for instance programmed death-1,cytotoxic T-lymphocyte antigen 4,chimeric antigen receptor T-cell therapy,T cell receptor T cell therapy,dendritic cell vaccine,and cytokine-induced killer cells.This paper reviews the advances in immunotherapy and focuses on the results of many of preclinical studies and clinical trials in the field,as well as some of the promising therapeutic strategies for HCC in the future.展开更多
文摘Hepatocellular carcinoma(HCC) is the fifth most common cancer and the third most common cause of cancer-related death worldwide. There have been great improvements in the diagnosis and treatment of HCC in recent years, but the problems, including difficult diagnosis at early stage, quick progression, and poor prognosis remain unsolved. Surgical resection is the mainstay of the treatment for HCC. However, 70%-80% of HCC patients are diagnosed at an advanced stage when most are ineligible for potentially curative therapies such as surgical resection and liver transplantation. In recent years, non-surgical management for unrespectable HCC, such as percutaneous ethanol injection, percutaneous microwave coagulation therapy, percutaneous radiofrequency ablation, transcatheter arterial chemoembolization, radiotherapy, chemotherapy, biotherapy, and hormonal therapy have been developed. These therapeutic options, either alone or in combination, have been shown to control tumor growth, prolong survival time, and improve quality of life to some extent. This review covers the current status and progress of non-surgical management for HCC.
基金Supported by the Natural Science Foundation of Gansu Province,No.1506RJZA255the National Natural Science Foundation of China,No.81572437+1 种基金the Open Topics of the Key Laboratory of Biological Treatment and Regenerative Medicine in Gansu Province,No.zdsyskfkt-201702the Fund of Donggang Branch,The First Hospital of Lanzhou University,No.ldyydgyn-201705
文摘AIM To detect the mechanisms of Helicobacter pylori(H. pylori) infection in the invasion and metastasis of gastric cancer(GC).METHODS Specimens from 99 patients with GC were collected. The correlation among H. pylori infection, heparanase(HPA) and mitogen-activated protein kinase(MAPK) expression, which was determined by immunohistochemistry, and the clinical features of GC was analysed using SPSS 22.0. Overall survival(OS) and relapse-free survival(RFS) of GC patients were estimated by the KaplanMeier method. Independent and multiple factors of HPA and MAPK with prognosis were determined with COX proportional hazards models. HPA and MAPK expression in MKN-45 cells infected with H. pylori was analysed using Western blot. RESULTS H. pylori infection was observed in 70 of 99 patients with GC(70.7%), which was significantly higher than that in healthy controls. H. pylori infection was related to lymph metastasis and expression of HPA and MAPK(P < 0.05); HPA expression was relevant to MAPK expression(P = 0.024). HPA and MAPK expression in MKN-45 cells was significantly upregulated following H. pylori infection and peaked at 24 h and 60 min, before decreasing(P < 0.05). SB203580, an inhibitor of MAPK, significantly decreased HPA expression. HPA was related to lymph metastasis and invasive depth. HPA positive GC cases and H. pylori positive GC cases showed poorer prognosis than HPA negative cases(P < 0.05). COX models showed that the prognosis of GC was connected with HPA expression, lymph metastasis, tissue differentiation, and invasive depth. CONCLUSION H. pylori may promote the invasion and metastasis of GC by increasing HPA expression that may associate with MAPK activation, thus causing a poorer prognosis of GC.
基金Supported by Gansu Provincial Natural Science Foundation,No.1308RJZA188the Fundamental Research Funds for the Central Universities,No.lzujbky-2011-T03-16
文摘AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion,and migration of CBP-TE-1 cells,as well as the expression of Src were then determined and compared with those in normal TE-1 cells.RESULTS:The expression of Src was decreased by the overexpression of CBP in TE-1 cells.The growth,invasion,and migration of TE-1 cells were decreased by the overexpression of CBP.CONCLUSION:This study indicates that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src.CBP may be a potential tumor suppressor and targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.
基金Supported by The National Natural Science Foundation of ChinaNo.31270532+2 种基金the Foundation of Key Laboratory of Digestive System Tumors of Gansu Provincethe Fundamental Research Funds for the Central UniversitiesNo.lzujbky2011-t03-03
文摘AIM:To examine transforming growth factor-β1(TGF-β1)promoter methylation in gastric cancer and to determine if Helicobacter pylori(H.pylori)or interleukin(IL)-1β could induce TGF-β1 hypermethylation in vitro.METHODS:We examined the frequency and extent of TGF-β1 promoter methylation using methylationspecific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects.H.pylori infection was confirmed by a positive result from either a serological test,histological analysis or C13urea breath test.GES-1 and MKN-45 cells co-cultured with H.pylori or treated with IL-1β for 12,24 and 48 h in vitro tested the effects of H.pylori or IL-1β on TGF-1β.RESULTS:Twenty-four/forty-seven(51%)cases of gastric cancer(GC)tissues showed TGF-β1 promoter methylation,15/47(31.9%)cases of matched noncancerous gastric mucosa tissues from the GC patients,and 11/39(28%)case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation(51%vs 28%,P<0.05).Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients(0.24±0.06 vs 0.17±0.04,P<0.05)and normal gastric tissues from non-GC subjects(0.24±0.06 vs 0.15±0.03,P<0.05).TGF-β1 methylation was found in 48.3% of H.pylori-positive gastric mucosal tissues whereas only 23.1% of H.pylori-negative gastric mucosal tissues showed TGF-β1 methylation(48.3%vs 23.1%,P<0.05).IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h.Further studies showed that pre-treatment of GES-1 cells with 20ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation.Infection of GES-1cells by H.pylori was not found to induce significant TGF-β1 promoter methylation.CONCLUSION:Our data revealed that TGF-1 promoter is methylated in GC patients.IL-1β may be an important mediator for H.pylori induced gene methylation during GC development.
文摘AIM:To compare non-liquid and clear-liquid diets,and to assess whether the latter is the optimal treatment for mild acute pancreatitis.METHODS:The Cochrane Library,PUBMED,EMBASE,EBM review databases,Science Citation Index Expanded,and several Chinese databases were searched up to March 2011.Randomized controlled trials(RCTs) that compared non-liquid with clear-liquid diets in patients with mild acute pancreatitis were included.A meta-analysis was performed using available evidence from RCTs.RESULTS:Three RCTs of adequate quality involving a total of 362 participants were included in the final analysis.Compared to liquid diet,non-liquid diet significantly decreased the length of hospitalization [mean difference(MD):1.18,95% CI:0.82-1.55;P﹤0.00001] and total length of hospitalization(MD:1.31,95% CI:0.45-2.17;P = 0.003).The subgroup analysis showed solid diet was more favorable than clear liquid diet in the length of hospitalization,with a pooled MD being-1.05(95% CI:-1.43 to-0.66;P﹤0.00001).However,compared with clear liquid diet,both soft and solid diets did not show any significant differences for recurrence of pain after re-feeding,either alone [relative risk(RR):0.95;95% CI:0.51-1.87;P = 0.88] and(RR:1.22;95% CI:0.69-2.16;P = 0.49),respectively,or analyzed together as non-liquid diet(RR:0.80;95% CI:0.47-1.36;P = 0.41).CONCLUSION:The non-liquid soft or solid diet did not increase pain recurrence after re-feeding,compared with the clear-liquid diet.The non-liquid diet reduced hospitalization.
文摘Correction to"Liu LP,Sheng XP,Shuai TK,Zhao YX,Li B,Li YM.Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression.World J Gastroenterol 2018;24:4565-4577[PMID:30386106 DOI:10.3748/wjg.v24.i40.4565]."In this article,we have identified some of the images in Figure 2A,C,E,G,and I are identical to the images in Figures 1B,2A,3B,3E,and 3G of another paper entitled"Liu L,Zhao Y,Fan G,Shuai T,Li B,Li Y.Helicobacter pylori infection enhances heparanase leading to cell proliferation via mitogenactivated protein kinase signalling in human gastric cancer cells.",which was published by us in the Molecular Medicine Reports in December,2018[PMID:30320396 DOI:10.3892/mmr.2018.9558].The reason why we asked to replace the pictures was that when we were simultaneously preparing to submit our two different articles to the World Journal of Gastroenterology(WJG)and Molecular Medicine Reports,we uploaded the wrong pictures to the WJG,which were same as those submitted to the Molecular Medicine Reports.We apologize for this negligence and any inconvenience that this may cause.We would be grateful if you could replace the wrong pictures with the correct ones attached.
基金supported by a grant from International Cooperation Project of Ministry of Science and Technology of China(2015DFA31650)
文摘Solid pseudopapillary tumor (SPT) of the pancreas is a rare pancreatic disease. Generally, it is considered a benign or low-grade malignant tumor. SPT of the pancreas with liver metastasis or invasion to adjacent organs is usually uncommon.
基金Supported by National Natural Science Foundation of China,No. 30870364
文摘AIM: To investigate the effects of superoxide dismutase (SOD) polymorphisms (rs4998557 , rs4880), Helicobacter pylori (H. pylori ) infection and environmental factors in gastric cancer (GC) and malignant potential of gastric precancerous lesions (GPL). METHODS: Copper-zinc superoxide dismutase (SOD1, CuZn-SOD)-G7958A (rs4998557 ) and manganese superoxide dismutase (SOD2, Mn-SOD)-Val16Ala (rs4880 ) polymorphisms were genotyped by SNaPshot multiplex polymerase chain reaction (PCR) in 145 patients with GPL (87 cases of gastric ulcer, 33 cases of gastric polyps and 25 cases of atrophic gastritis), 140 patients with GC and 147 healthy controls. H. pylori infection was detected by immunoblotting analysis. RESULTS: The SOD1-7958A allele was associated with a higher risk of gastric cancer [odds ratio (OR) = 3.01, 95% confidence intervals (95% CI): 1.83-4.95]. SOD216Ala/Val genotype was a risk factor for malignant potential of GPL (OR = 2.04, 95% CI: 1.19-3.49). SOD216Ala/genotype increased the risk of gastric cancer (OR = 2.85, 95% CI: 1.66-4.89). SOD1-7958A/genotype, SOD2-16Ala/genotype, alcohol drinking, positive family history and type Ⅰ H. pylori infection were associated with risk of gastric cancer, and there were additive interactions between the two genotypes and the other three risk factors. SOD2-16Ala/Val genotype and positive family history were associated with malignant potential of GPL and jointly contributed to a higher risk for malignant potential of GPL (OR = 7.71, 95% CI: 2.10-28.22). SOD1-7958A/genotype and SOD2-16Ala/genotype jointly contributed to a higher risk for gastric cancer (OR = 6.43, 95% CI: 3.20-12.91). CONCLUSION: SOD1-7958A/and SOD2-16Ala/-genotypes increase the risk of gastric cancer in Chinese Han population. SOD2-16Ala/-genotype is associated with malignant potential of GPL.
文摘AIM:To investigate the correlation between the Helicobacter pylori(H.pylori)infection and host genetic background of healthy populations in Indonesia.METHODS:In March 2007,epidemiological studies were undertaken on the general population of a city in Indonesia(Mataram,Lombok).The participants included 107 men and 187 women,whose ages ranged from6 to 74 years old,with an average age of 34.0(±14.4)(±SD).The H.pylori of subject by UBT method determination,and through the polymerase chain reaction with confronting two-pair primers(PCR-CTPP)method parsing the single nucleotide polymorphism of interleukin(IL)-8,IL-4,IL-1β,CD14,tumor necrosis factor(TNF-a)and tyrosine-protein phosphates non-receptor type 11(PTPN11)genotypes.The experimental data were analyzed by the statistical software SAS.RESULTS:The H.pylori infection rates in the healthy Indonesian population studied were 8.4%for men and12.8%for women;no obvious differences were noted for H.pylori infection rates by sex or age.TC genotypes of IL-4,TC and CC genotypes of TNF-a,and GA genotypes of PTPN11,were higher in frequency.Both CC and TC genotype of TNF-a T-1031C loci featured higher expressions in the healthy Indonesian population Indonesia studied of(OR=1.99;95%CI:0.67-5.89)and(OR=1.66;95%CI:0.73-3.76),respectively.C allele of IL-1βT-31C gene locus was at a higher risk(OR=1.11;95%CI:0.70-1.73)of H.pylori infection,but no statistical significance was found in our study.CONCLUSION:We reveal that the association between the TNF-a and IL-1βgenotypes may be the susceptibility of H.pylori in the studied population.
基金Supported by The National Natural Science Foundation of China,No. 30870364Fund for Key Laboratory of Digestive System Tumors,Gansu Province,No. lzujbky-2011-t03
文摘AIM：To clarify the role of activated Notch2 in the invasiveness of gastric cancer.METHODS：To investigate the invasiveness of silencing Notch2 gene expression,we established a Notch2small interfering RNA（siRNA） transfected cell line using the MKN-45 gastric cancer cell line.After the successful transfection confirmed by real-time reverse transcription-polymerase chain reaction（RT-PCR） and Western blotting,migration and invasion assays were employed to evaluate the aggressiveness of the gastric cancer.RT-PCR and Western blottings were employed to confirm the down-regulation of Notch2 and to evaluate the expression of epithelial mesenchymal transition-related gene matrix metallopeptidase 9（MMP9）,Akt,p-Akt.To confirm the relationship between PI3KAkt and MMP9,the PI3K inhibitor LY294002 was used to treat MKN-45 cells.RESULTS：Notch2 expression was dramatically decreased after Notch2 siRNA transfection（100.00% ± 9.74% vs 11.61% ± 3.85%,P 〈 0.01 by qRT-PCR）.There was also a marked reduction of Notch target gene Hes1（100.00% ± 4.74% vs 61.61% ± 3.58%,P 〈 0.05） at the mRNA,indicating an inhibition of Notch signaling.Inhibition of Notch signaling was also confirmed by the marked reduction of Notch2 intracellular domain at the protein levels（100.00% ± 9.74% vs 65.61% ± 7.58%,P 〈 0.05）.Down-regulation of Notch2 by siRNA enhanced tumor cell invasion（100.00% ± 21.64% vs 162.22% ± 16.84%,P 〈 0.05） and expression of MMP9（1.56 fold,P 〈 0.05）,and activated the pro-MMP9 protein to its active form（1.48 fold,P 〈 0.05）.There was no significant difference in the protein levels of Akt between the two groups（100.00% ± 10.87% vs 96.61% ± 7.33%,P 〉 0.05）,while down-regulation of Notch2 elevated p-Akt expression（100.00% ± 9.87% vs 154.61% ± 13.10%,P 〈 0.05）.Furthermore,p-Akt and MMP9 was down-regulated in response to the inhibitor LY294002（p-Akt 100.00% ± 8.87% vs 58.27% ± 5.01%,P 〈 0.05;MMP9 100.00% ± 9.17% vs 50.03% ± 4.88%,P 〈 0.05）.CONCLUSION：Notch2 may negatively regulate cell invasion by inhibiting the PI3K-Akt signaling pathway
文摘Background Acute severe biliary pancreatitis （ASBP） is a severe and fatal disease, and the expenditure is huge and therapeutic effects are still not satisfactory. This study aimed to improve the therapeutic effects and reduce the expenditure of ASBP treatment.Methods One hundred and five patients diagnosed with ASBP were referred to our department from January 2004 to July 2009. Diagnosis was based on the 2007 criteria of the Chinese Society of Surgery. Patients were divided into two groups; the E group： 50 patients who underwent endoscopic retrograde choledochopancreatography （ERCP） ＋ endoscopic sphincterotomy （EST） ＋ endoscopic lithotripsy basket （ESR） ＋endoscopic retrograde biliary drainage （ERBD）and enteral nutrition （EN）, and the R group： 55 patients who underwent traditional treatment without ERCP. Subsequently,subjective symptoms, signs, biochemical analysis, serum endotoxin, tumor necrosis factor a, grades by computed tomography （CT）, cost of hospitalization and length of stay were compared between the two groups.Results All enrolled patients complied well with all therapeutic regimens. Endoscopic therapy that combined EN could significantly improve symptoms, clinical signs, laboratory values, tumor necrosis factor a and endotoxin while significantly reducing hospital expenditure and length of hospital stay. The experimental findings revealed that there were obvious advantages in the E group compared with the R group.Conclusions Endoscopic therapy combined with EN is an effective, safe and economic therapeutic regimen of ASBP.
基金supported by the National Natural Science Foundation of China (30872731)Natural Science Foundation of Gansu Province, China (2008GS01435 and 1010RJZA114)
文摘Accumulating evidence has suggested that the gap junction plays an important role in the determination of cerebral ischemia, but the underlying mechanisms remain to be elucidated. In this study, we assessed the effect of a gap-junction blocker, carbenoxolone （CBX）, on ischemia/reperfusion-induced brain injury and the possible mechanisms. By using the transient cerebral ischemia model induced by occlusion of the middle cerebral artery for 30 min followed by reperfusion for 24 h, we found that pre-administration of CBX （25 mg/kg, intracerebroventricular injection, 30 min before cerebral ischemic surgery） diminished the infarction size in rats. And this was associated with a decrease of reactive oxygen species generation and inhibition of the activation of astrocytes and microglia. In PC12 cells, H202 treatment induced more coupling and apoptosis, while CBX partly inhibited the opening of gap junctions and improved the cell viability. These results suggest that cerebral ischemia enhances the opening of gap junctions. Blocking the gap junction with CBX may attenuate the brain injury after cerebral ischemia/reperfusion by partially contributing to amelioration of the oxidative stress and apoptosis.
文摘Background Hepatitis B virus infection is closely related to hepatocellular carcinoma （HCC）. Cyclooxygenase-2 （COX-2） is overexpressed in HCC and considered to play a role in hepatic carcinogenesis. In this study, we analyzed the polymorphism of COX-2 promoter -899G/C in healthy controls, chronic hepatitis B （CHB） patients, liver cirrhosis patients, and hepatocellular carcinoma （HCC） patients, to investigate the relationship between COX-2 -899G/C polymorphism and the risk for hepatitis B-related liver cancer in a Chinese population from Gansu province. Methods Patients were divided into four groups： 300 patients with CHB, 300 patients with liver cirrhosis, 300 patients with HCC, and 300 healthy controls. The polymorphism of COX-2 -899G/C was detected by PCR-TaqMan probes. The results were analyzed by SPSS 17.0. Results The COX-2 -899G/C genotypes were GG, GC, and CC. Frequencies in CHB were 87.00%, 12.67%, 0.33%; in liver cirrhosis were 85.33%, 14.00%, 0.67%; in HCC were 77.00%, 21.67%, 1.33%; and in healthy controls were 90.67%, 9.00%, 0.33%, respectively. COX-2 -899C carriers may have an increased risk for hepatitis B-related liver cancer. Compared with the frequency of GG genotype, there were significant differences in the frequency of GC genotype between HCC and healthy control groups （0R=2.835, 95%C/： 1.751-4.589）; HCC and CHB groups （OR=1.933, 95%C/： 1.248-2.994）; and HCC and liver cirrhosis groups （OR=1. 175, 95%C/： 1.119-2.628）. Stratification analyses showed that COX-2 -899C allele carriers with a drinking history are more susceptible to develop HCC. Conclusion COX-2 -899C genotype may increase the susceptibility of individuals to hepatitis B-related liver cancer in Gansu province, China.
基金This study was supported by grants from the Natural Science Foundation of China(30700845)the Fundamental Research Funds for the Central Universities(lzujbky-2012-173,lzujbky-2013-m04).
文摘Background:Wilson's disease is an autosomal recessive disorder characterized by liver disease and/or neurologic deficits due to copper accumulation and is caused by pathogenic mutations in the ATP7B gene.Methods:Two unrelated Chinese patients born to nonconsanguineous parents who were diagnosed with earlyonset Wiison's disease.DNA sequencing and bioinformation analysis were conducted.Results:We have identified four mutations in two family trios,of which two were novel,namely,c.3028A>G(p.K1010E) and c3992T>G (p.Y1331X),in each patient.Conclusions:Gene testing is playing an important role in diagnosis of Wilson's disease.The early-onset of Wilson's disease is apparently not associated with P-ATPase domain in the ATP7B protein.Our findings further widen the spectrum of mutations involving the ATP7B gene.
基金supported by the National Natural Science Foundation of China(31770537)International S&T Cooperation Program of China(ISTCP)(2015DFA31650)International S&T Cooperation Program of Gansu Province(18YF1WA113).
文摘Hepatocellular carcinoma(HCC)is one of the malignant tumors with higher incidence and mortality worldwide.Recently,significant progress has been made in uncovering immunotherapy in HCC,for instance programmed death-1,cytotoxic T-lymphocyte antigen 4,chimeric antigen receptor T-cell therapy,T cell receptor T cell therapy,dendritic cell vaccine,and cytokine-induced killer cells.This paper reviews the advances in immunotherapy and focuses on the results of many of preclinical studies and clinical trials in the field,as well as some of the promising therapeutic strategies for HCC in the future.
