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世界胃肠病学杂志(英文版)
世界胃肠病学杂志(英文版)

潘伯荣

周刊

1007-9327

wjg@wjgnet.com

010-85381901-628

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北京市朝阳区东四环中路62号楼远洋国际中心D座903室

世界胃肠病学杂志(英文版)/Journal World Journal of GastroenterologyCSCDCSTPCDSCI
查看更多>>主要报道和刊登国内外、特别是我国消化病学者具有创造性的、有较高学术水平的基础和临床研究论文、研究快报等. 对具有中国特色的研究论文, 如食管癌、胃癌、肝癌、大肠癌、病毒性肝炎、幽门螺杆菌、中医中药、中西医结合和基于作者自己研究工作为主的综述性论文, 将优先发表. 读者对象为基础研究或临床研究的消化专业工作者。
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    Esophageal malignancy: A growing concern

    Jianyuan ChaiM Mazen Jamal
    6521-6526页
    查看更多>>摘要:Esophageal cancer is mainly found in Asia and east Africa and is one of the deadliest cancers in the world.However,it has not garnered much attention in the Western world due to its low incidence rate.An increasing amount of data indicate that esophageal cancer,particularly esophageal adenocarcinoma,has been rising by 6-fold annually and is now becoming the fastest growing cancer in the United States.This rise has been associated with the increase of the obese population,as abdominal fat puts extra pressure on the stomach and causes gastroesophageal reflux disease (GERD).Long standing GERD can induce esophagitis and metaplasia and,ultimately,leads to adenocarcinoma.Acid suppression has been the main strategy to treat GERD; however,it has not been proven to control esophageal malignancy effectively.In fact,its side effects have triggered multiple warnings from regulatory agencies.The high mortality and fast growth of esophageal cancer demand more vigorous efforts to look into its deeper mechanisms and come up with better therapeutic options.

    Does antecolic reconstruction decrease delayed gastric emptying after pancreatoduodenectomy?

    Nadia PepariniPiero Chirletti
    6527-6531页
    查看更多>>摘要:Delayed gastric emptying (DGE) is a frequent complication after pylorus-preserving pancreatoduodenectomy (PpPD).Kawai and colleagues proposed pylorus-resecting pancreatoduodenectomy (PrPD) with antecolic gastrojejunal anastomosis to obviate DGE occurring after PpPD.Here we debate the reported differences in the prevalence of DGE in antecolic and retrocolic gastro/duodeno-jejunostomies after PrPD and PpPD,respectively.We conduded that the route of the gastro/duodeno-jejunal anastomosis with respect to the transverse colon;i.e.,antecolic route or retrocolic route,is not responsible for the differences in prevalence of DGE after pancreatoduodenectomy (PD) and that the impact of the reconstructive method on DGE is related mostly to the angulation or torsion of the gastro/duodeno-jejunostomy.We report a prevalence of 8.9% grade A DGE and 1.1%grade C DGE in a series of 89 subtotal stomach-preserving PDs with Roux-en Y retrocolic reconstruction with anastomosis of the isolated Roux limb to the stomach and single Roux limb to both the pancreatic stump and hepatic duct.Retrocolic anastomosis of the isolated first jejunal loop to the gastric remnant allows outflow of the gastric contents by gravity through a "straight route".

    Tumor budding as a potential histopathological biomarker in colorectal cancer: Hype or hope?

    Fabio GrizziGiuseppe CelestiGianluca BassoLuigi Laghi...
    6532-6536页
    查看更多>>摘要:Colorectal cancer (CRC),the third most commonly diagnosed type of cancer in men and women worldwide is recognized as a complex multi-pathway disease,an observation sustained by the fact that histologically identical tumors may have different outcome,including various response to therapy.Therefore,particularly in early and intermediate stage (stages Ⅱ and Ⅲ,respectively) CRC,there is a compelling need for biomarkers helpful of selecting patients with aggressive disease that might benefit from adjuvant and targeted therapy.Histopathological examination shows that likely other solid tumors the development and progression of human CRC is not only determined by genetically abnormal cells,but also by intricate interactions between malignant cells and the surrounding microenvironment.This has led to reconsider the features of tumor microenvironment as potential predictive and prognostic biomarkers.Among the histopathological biomarkers,tumor budding (i.e.,the presence of individual cells and small clusters of tumor cells at the tumor invasive front)has received much recent attention,particularly in the setting of CRC.Although its acceptance as a reportable factor has been held back by a lack of uniformity with respect to qualitative and quantitative aspects,tumor budding is now considered as an independent adverse prognostic factor in CRC that may allow for stratification of patients into risk categories more meaningful than those defined by tumor-node-metastasis staging alone,and also potentially guide treatment decisions,especially in T2-T3 NO (stage Ⅱ) CRCs.

    Anti-tumor immunity, autophagy and chemotherapy

    Gy(o)rgyi MüzesFerenc Sipos
    6537-6540页
    查看更多>>摘要:Autophagy or self-digestion of cells is activated upon various stressful stimuli and has been found to be a survival and drug resistance pathway in cancer.However,genetic studies support that autophagy can act as a tumor suppressor.Furthermore,defective autophagy is implicated in tumorigenesis,as well.The precise impact of autophagy on malignant transformation has not yet been clarified,but recent data suggest that this complex process is mainly directed by cell types,phases,genetic background and microenvironment.Relation of autophagy to anticancer immune responses may indicate a novel aspect in cancer chemotherapy.

    Solitary rectal ulcer syndrome in children: A literature review

    Seyed Mohsen DehghaniAbdorrasoul MalekpourMahmood Haghighat
    6541-6545页
    查看更多>>摘要:Solitary rectal ulcer syndrome (SRUS) is a benign and chronic disorder well known in young adults and less in children.It is often related to prolonged excessive straining or abnormal defecation and clinically presents as rectal bleeding,copious mucus discharge,feeling of incomplete defecation,and rarely rectal prolapse.SRUS is diagnosed based on clinical symptoms and endoscopic and histological findings.The current treatments are suboptimal,and despite correct diagnosis,outcomes can be unsatisfactory.Some treatment protocols for SRUS include conservative management such as family reassurance,regulation of toilet habits,avoidance of straining,encouragement of a high-fiber diet,topical treatments with salicylate,sulfasalazine,steroids and sucralfate,and surgery.In children,SRUS is relatively uncommon but troublesome and easily misdiagnosed with other common diseases,however,it is being reported more than in the past.This condition in children is benign; however,morbidity is an important problem as reflected by persistence of symptoms,especially rectal bleeding.In this review,we discuss current diagnosis and treatment for SRUS.

    Genetic and epigenetic variants influencing the development of nonalcoholic fatty liver disease

    Yu-Yuan Li
    6546-6551页
    查看更多>>摘要:Nonalcoholic fatty liver disease (NAFLD) is common worldwide.The importance of genetic and epigenetic changes in etiology and pathogenesis of NAFLD has been increasingly recognized.However,the exact mechanism is largely unknown.A large number of single nucleotide polymorphisms (SNPs) related to NAFLD has been documented by candidate gene studies (CGSs).Among these genes,peroxisome proliferatoractivated receptor-y,adiponectin,leptin and tumor necrosis factor-α were frequently reported.Since the introduction of genome-wide association studies (GWASs),there have been significant advances in our understanding of genomic variations of NAFLD.Patatinlike phospholipase domain containing family member A3 (PNPLA3,SNP rs738409,encoding I148M),also termed adiponutrin,has caught most attention.The evidence that PNPLA3 is associated with increased hepatic fat levels and hepatic inflammation has been validated by a series of studies.Epigenetic modification refers to phenotypic changes caused by an adaptive mechanism unrelated to alteration of primary DNA sequences.Epigenetic regulation mainly includes microRNAs (miRs),DNA methylation,histone modifications and ubiquitination,among which miRs are studied most extensively.miRs are small natural single stranded RNA molecules regulating mRNA degradation or translation inhibition,subsequently altering protein expression of target genes.The miR-122,a highly abundant miR accounting for nearly 70% of all miRs in the liver,is significantly under-expressed in NAFLD subjects.Inhibition of miR-122 with an antisense oligonucleotide results in decreased mRNA expression of lipogenic genes and improvement of liver steatosis.The investigation into epigenetic involvement in NAFLD pathogenesis is just at the beginning and needs to be refined.This review summarizes the roles of genetics and epigenetics in the development of NAFLD.The progress made in this field may provide novel diagnostic biomarkers and therapeutic targets for NAFLD management.

    Way back for fructose and liver metabolism: Bench side to molecular insights

    Alba RebolloNúria RoglansMarta AlegretJuan C Laguna...
    6552-6559页
    查看更多>>摘要:The World Health Organization recommends that the daily intake of added sugars should make up no more than 10% of total energy.The consumption of sugarsweetened beverages is the main source of added sugars.Fructose,together with glucose,as a component of high fructose corn syrups or as a component of the sucrose molecule,is one of the main sweeteners present in this kind of beverages.Data from prospective and intervention studies clearly point to high fructose consumption,mainly in the form of sweetened beverages,as a risk factor for several metabolic diseases in humans.The incidence of hypertension,nonalcoholic fatty liver disease (NAFLD),dyslipidemia (mainly hypertriglyceridemia),insulin resistance,type 2 diabetes mellitus,obesity,and the cluster of many of these pathologies in the form of metabolic syndrome is higher in human population segments that show high intake of fructose.Adolescent and young adults from lowincome families are especially at risk.We recently reviewed evidence from experimental animals and human data that confirms the deleterious effect of fructose on lipid and glucose metabolism.In this present review we update the information generated in the past 2 years about high consumption of fructose-enriched beverages and the occurrence of metabolic disturbances,especially NAFLD,type 2 diabetes mellitus,and metabolic syndrome.We have explored recent data from observational and experimental human studies,as well as experimental data from animal and cell models.Finally,using information generated in our laboratory and others,we provide a view of the molecular mechanisms that may be specifically involved in the development of liver lipid and glucose metabolic alterations after fructose consumption in liquid form.

    Role of gastrin-peptides in Barrett's and colorectal carcinogenesis

    Eduardo ChuecaAngel LanasElena Piazuelo
    6560-6570页
    查看更多>>摘要:Gastrin is the main hormone responsible for the stimulation of gastric acid secretion; in addition,gastrin and its derivatives exert proliferative and antiapoptotic effects on several cell types.Gastrin synthesis and secretion are increased in certain situations,for example,when proton pump inhibitors are used.The impact of sustained hypergastrinemia is currently being investigated.In vitro experiments and animal models have shown that prolonged hypergastrinemia may be related with higher cancer rates; although,this relationship is less clear in human beings.Higher gastrin levels have been shown to cause hyperplasia of several cell types; yet,the risk for developing cancer seems to be the same in normo-and hypergastrinemic patients.Some tumors also produce their own gastrin,which can act in an autocrine manner promoting tumor growth.Certain cancers are extremely dependent on gastrin to proliferate.Initial research focused only on the effects of amidated gastrins,but there has been an interest in intermediates of gastrin in the last few decades.These intermediates aren't biologically inactive;in fact,they may exert greater effects on proliferation and apoptosis than the completely processed forms.In certain gastrin overproduction states,they are the most abundant gastrin peptides secreted.The purpose of this review is to examine the gastrin biosynthesis process and to summarize the results from different studies evaluating the production,levels,and effects of the main forms of gastrin in different overexpression states and their possible relationship with Barrett's and colorectal carcinogenesis.

    Relatedness of Helicobacter pylori populations to gastric carcinogenesis

    Quan-Jiang DongShu-Hui ZhanLi-Li WangYong-Ning Xin...
    6571-6576页
    查看更多>>摘要:Helicobacter pylori (H.pylori) is a Gram-negative bacterium that infects half of the human population.The infection is associated with chronic inflammation of the gastric mucosa and peptic ulcers.It is also a major risk factor for gastric cancer.Phylogenetic analysis of global strains reveals there are seven populations of H.pylori,including hpAfrica1,hpAfrica2,hpEastAsia,hpEurope,hpNEAfrica,hpAsia2 and hpSahul.These populations are consistent with their geographical origins,and possibly result from geographical separation of the bacterium leading to reduced bacterial recombination in some populations.For each population,H.pylori has evolved to possess genomic contents distinguishable from others.The hpEurope population is distinct in that it has the largest genome of 1.65 mbp on average,and the highest number of coding sequences.This confers its competitive advantage over other populations but at the cost of a lower infection rate.The large genomic size could be a cause of the frequent occurrence of the deletion of the cag pathogenicity island in H.pylori strains from hpEurope.The incidence of gastric cancer varies among different geographical regions.This can be attributed in part to different rates of infection of H.pylori.Recent studies found that different populations of H.pylori vary in their carcinogenic potential and contribute to the variation in incidence of gastric cancer among geographical regions.This could be related to the ancestral origin of H.pylori.Further studies are indicated to investigate the bacterial factors contributing to differential virulence and their influence on the dinical features in infected individuals.

    Alterations in the human epidermal growth factor receptor 2-phosphatidylinositol 3-kinase-v-Akt pathway in gastric cancer

    Yasutaka SukawaHiroyuki YamamotoKatsuhiko NoshoHiroaki Kunimoto...
    6577-6586页
    查看更多>>摘要:AIM:To investigate human epidermal growth factor receptor 2 (HER2)-phosphatidylinositol 3-kinase (PI3K)-v-Akt murine thymoma viral oncogene homolog signaling pathway.METHODS:We analyzed 231 formalin-fixed,paraffinembedded gastric cancer tissue specimens from Japanese patients who had undergone surgical treatment.The patients' age,sex,tumor location,depth of invasion,pathological type,lymph node metastasis,and pathological stage were determined by a review of the medical records.Expression of HER2 was analyzed by immunohistochemistry (IHC) using the HercepTestTM kit.Standard criteria for HER2 positivity (0,1+,2+,and 3+) were used.Tumors that scored 3+ were considered HER2-positive.Expression of phospho Akt (pAkt)was also analyzed by IHC.Tumors were considered pAkt-positive when the percentage of positive tumor cells was 10% or more.PI3K,catalytic,alpha polypeptide (PIK3CA) mutations in exons 1,9 and 20 were analyzed by pyrosequencing.Epstein-Barr virus (EBV)infection was analyzed by in situ hybridization targeting EBV-encoded small RNA (EBER) with an EBER-RNA probe.Microsatellite instability (MSI) was analyzed by polymerase chain reaction using the mononucleotide markers BAT25 and BAT26.RESULTS:HER2 expression levels of 0,1+,2+ and 3+ were found in 167 (72%),32 (14%),12 (5%) and 20 (8.7%) samples,respectively.HER2 overexpression (IHC 3+) significantly correlated with intestinal histological type (15/20 vs 98/205,P =0.05).PIK3CA mutations were present in 20 cases (8.7%) and significantly correlated with MSI (10/20 vs 9/211,P < 0.01).The mutation frequency was high (21%) in T4 cancers and very low (6%) in T2 cancers.Mutations in exons 1,9 and 20 were detected in 5 (2%),9 (4%) and 7(3%) cases,respectively.Two new types of PIK3CA mutation,R88Q and R108H,were found in exon1.All PIK3CA mutations were heterozygous missense singlebase substitutions,the most common being H1047R (6/20,30%) in exon20.Eighteen cancers (8%) were EBV-positive and this positivity significantly correlated with a diffuse histological type (13/18 vs 93/198,P =0.04).There were 7 cases of lymphoepithelioma-like carcinomas (LELC) and 6 of those cases were EBV-positive (percent/EBV:6/18,33%; percent/all LELC:6/7,86%).pAkt expression was positive in 119 (53%) cases but showed no correlation with clinicopathological characteristics.pAkt expression was significantly correlated with HER2 overexpression (16/20 vs 103/211,P < 0.01) but not with PIK3CA mutations (12/20 vs 107/211,P =0.37) or EBV infection (8/18 vs 103/211,P =0.69).The frequency of pAkt expression was higher in cancers with exon20 mutations (100%) than in those with exon1 (40%) or exon9 (56%) mutations.One case showed both HER2 overexpression and EBV infection and 3 cases showed both PIK3CA mutations and EBV infection.However,no cases showed both PIK3CA mutations and HER2 overexpression.One EBVpositive cancer with PIK3CA mutation (H1047R) was MSI-positive.Three of these 4 cases were positive for pAkt expression.In survival analysis,pAkt expression significantly correlated with a poor prognosis (hazard ratio 1.75; 95%CI:1.12-2.80,P =0.02).CONCLUJSION:HER2 expression,PIK3CA mutations and EBV infection in gastric cancer were characterized.pAkt expression significantly correlates with HER2 expression and with a poor prognosis.