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| 1 | Signet-ring cell carcinoma of the stomach: Impact on prognosis and specific therapeutic challenge显示文摘While the incidence of gastric cancer has decreased worldwide in recent decades,the incidence of signetring cell carcinoma(SRCC) is rising. SRCC has a specific epidemiology and oncogenesis and has two forms: early gastric cancer,which can be resected endoscopically in some cases and which has a better outcome than non-SRCC,and advanced gastric cancer,which is generally thought to have a worse prognosis and lower chemosensitivity than non-SRCC. However,the prognosis of SRCC and its chemosensitivity with specific regimens are still controversial as SRCC is not specifically identified in most studies and its poor prognosis may be due to its more advanced stage. It therefore remains unclear if a specific therapeutic strategy is justified,as the benefit of perioperative chemotherapy and the value of taxanebased chemotherapy are unclear. In this review we analyze recent data on the epidemiology,oncogenesis,prognosis and specific therapeutic strategies in both early and advanced SRCC of the stomach and in hereditary diffuse gastric cancer. | Simon Pernot Thibault Voron Geraldine Perkins Christine Lagorce-Pages Anne Berger Julien Taieb | 2015 | World Journal of Gastroenterology2015，21，40： | 30 |
| 2 | Circulating micro RNAs and long non-coding RNAs in gastric cancer diagnosis:An update and review显示文摘Gastric cancer(GC) is the fourth most common cancer and the third leading cause of cancer mortality worldwide. Micro RNAs(mi RNAs) and long non-coding RNAs(lnc RNAs) are the most popular non-coding RNAs in cancer research. To date,the roles of mi RNAs and lnc RNAs have been extensively studied in GC,suggesting that mi RNAs and lnc RNAs represent a vital component of tumor biology. Furthermore,circulating mi RNAs and lnc RNAs are found to be dysregulated in patients with GC compared with healthy individuals. Circulating mi RNAs and lnc RNAs may function as promising biomarkers to improve the early detection of GC. Multiple possibilities for mi RNA secretion have been elucidated,including active secretion by microvesicles,exosomes,apoptotic bodies,highdensity lipoproteins and protein complexes as well as passive leakage from cells. However,the mechanism underlying lnc RNA secretion and the functions of circulating mi RNAs and lnc RNAs have not been fully illuminated. Concurrently,to standardize results of global investigations of circulating mi RNAs and lnc RNAs biomarker studies,several recommendations for preanalytic considerations are put forward. In this review,we summarize the known circulating mi RNAs and lnc RNAs for GC diagnosis. The possible mechanism of mi RNA and lnc RNA secretion as well as methodologies for identification of circulating mi RNAs and lnc RNAs are also discussed. The topics covered here highlight new insights into GC diagnosis and screening. | Ya-Kai Huang Jian-Chun Yu | 2015 | World Journal of Gastroenterology2015，21，34： | 22 |
| 3 | Second-line treatment of metastatic gastric cancer:Current options and future directions显示文摘Gastric cancer remains one among the leading causes of cancer-related deaths, regardless of its decreasing incidence and newly available treatment options. Most patients present at an advanced stage and are treated with upfront systemic chemotherapy. Those patients receiving first-line therapy may initially respond to treatment, but many of them relapse over time. In such condition, second-line treatment for disease progression remains the only available option. Although there exists no standard approach in the second-line setting, several phase Ⅲ trials have shown modest survival benefit in patients receiving irinotecan, taxane and ramucirumab over the best supportive care or active agents. This review analyzes the currently available treatment regimens and future directions of research in the second-line setting for metastatic gastric cancer with the best available evidence. Additionally, the prognostic factors that influence patient survival in those receiving second-line therapy are discussed. | Dheepak Kanagavel Mikhail Fedyanin Alexey Tryakin Sergei Tjulandin | 2015 | World Journal of Gastroenterology2015，21，41： | 16 |
| 4 | Targeted therapy for advanced gastric cancer: A review of current status and future prospects显示文摘In the West in particular, the vast majority of gastric cancer(GC) patients present with advanced-stage disease. Although combination chemotherapy is stillthe most important component of treatment for these patients, it confers a modest survival advantage. Recently, increased knowledge of the key molecular signaling pathways involved in gastric carcinogenesis has led to the discovery of specific molecular-targeted therapeutic agents. Some of these agents such as trastuzumab and ramucirumab have changed the treatment paradigm for this disease. In this paper, we will summarize the current clinical status of targeted drug therapy in the management of GC. | Ozkan Kanat Bert O'Neil Safi Shahda | 2015 | World Journal of Gastrointestinal Oncology2015，7，12： | 13 |
| 5 | Helicobacter pylori in gastric carcinogenesis显示文摘Gastric cancer still is a major concern as the third most common cancer worldwide, despite declining rates of incidence in many Western countries. Helicobacter pylori(H. pylori) is the major cause of gastric carcinogenesis, and its infection insults gastric mucosa leading to theoccurrence of atrophic gastritis which progress to intestinal metaplasia, dysplasia, early gastric cancer, and advanced gastric cancer consequently. This review focuses on multiple factors including microbial virulence factors, host genetic factors, and environmental factors, which can heighten the chance of occurrence of gastric adenocarcinoma due to H. pylori infection. Bacterial virulence factors are key components in controlling the immune response associated with the induction of carcinogenesis, and cag A and vac A are the most well-known pathogenic factors. Host genetic polymorphisms contribute to regulating the inflammatory response to H. pylori and will become increasingly important with advancing techniques. Environmental factors such as high salt and smoking may also play a role in gastric carcinogenesis. It is important to understand the virulence factors, host genetic factors, and environmental factors interacting in the multistep process of gastric carcinogenesis. To conclude, prevention via H. pylori eradication and controlling environmental factors such as diet, smoking, and alcohol is an important strategy to avoid H. pylori-associated gastric carcinogenesis. | Hyo Jun Ahn Dong Soo Lee | 2015 | World Journal of Gastrointestinal Oncology2015，7，12： | 10 |
| 6 | Perspectives in the treatment of pancreatic adenocarcinoma显示文摘Pancreatic ductal adenocarcinoma(PDAC) is an incurable lethal disease whose incidence rate is growing. There is no effective screening for detection of early stage tumors and,in most cases,PDAC is diagnosed at advanced disease stages,when radical pancreatic resection is not possible. The aggressive nature of pancreatic tumor cells lies in the complex genetic mechanisms behind their uncontrolled capability to grow and metastasize,which involve essential adaptive changes in cellular metabolism,signaling,adhesion and immunoediting. In addition,PDAC cells promote a dense functional stroma that facilitates tumor resistance to chemotherapy and radiation. During the last two decades,gemcitabine has been the reference for the systemic treatment of PDAC. However,recently,a regimen combining fluorouracil,irinotecan,oxaliplatin,and leucovorin(FOLFIRINOX) and another combining albumin-bound paclitaxel with gemcitabine have shown clear therapeutic advantage in advanced PDAC,with survival outcomes of 11.3 and 8.5 mo on phase Ⅲ trials,respectively,over singleagent gemcitabine. With the pending issue of their higher toxicities,these regimens set the reference for ongoing and future clinical studies in advanced PDAC. In addition,the efficacy of oral fluoropyrimidine(S-1) has been well documented in Asiatic PDAC patients. The development of therapeutic approaches other than cytotoxic drugs has proven difficult in the past,with only one drug(erlotinib) approved to date. Besides,a number of agents targeting signaling pathways in tumor or stroma cells are being investigated. Likewise,immunotherapies that target PDAC in various ways are the subject of a number of clinical trials. The search for reliable biomarkers with diagnostic and prognostic value using genomics and mass spectrometry methods may facilitate monitoring and refinement of therapies. This review focuses on current understanding of the pathogenesis of PDAC and the latest developments in the treatment of advanced PDAC. | Angel Cid-Arregui Victoria Juarez | 2015 | World Journal of Gastroenterology2015，21，31： | 8 |
| 7 | Tight junction disruption: Helicobacter pylori and dysregulation of the gastric mucosal barrier显示文摘Long-term chronic infection with Helicobacter pylori(H. pylori) is a risk factor for gastric cancer development. In the multi-step process that leads to gastric cancer,tight junction dysfunction is thought to occur and serve as a risk factor by permitting the permeation of luminal contents across an otherwise tight mucosa. Mechanisms that regulate tight junction function and structure in the normal stomach,or dysfunction in the infected stomach,however,are largely unknown. Although conventional tight junction components are expressed in gastric epithelial cells,claudins regulate paracellular permeability and are likely the target of inflammation or H. pylori itself. There are 27 different claudin molecules,each with unique properties that render the mucosa an intact barrier that is permselective in a way that is consistent with cell physiology. Understanding the architecture of tight junctions in the normal stomach and then changes that occur during infection is important but challenging,because most of the reports that catalog claudin expression in gastric cancer pathogenesis are contradictory. Furthermore,the role of H. pylori virulence factors,such as cytotoxin-associated gene A and vacoulating cytotoxin,in regulating tight junction dysfunction during infection is inconsistent in different gastric cell lines and in vivo,likely because non-gastric epithelial cell cultures were initially used to unravel the details of their effects on the stomach. Hampering further study,as well,is the relative lack of cultured cell models that have tight junction claudins that are consistent with native tissues. This summary will review the current state of knowledge about gastric tight junctions,normally and in H. pylori infection,and make predictions about the consequences of claudin reorganization during H. pylori infection. | Tyler J Caron Kathleen E Scott James G Fox Susan J Hagen | 2015 | World Journal of Gastroenterology2015，21，40： | 7 |
| 8 | Polymorphisms in mucin genes in the development of gastric cancer显示文摘Gastric cancer(GC) is the third leading cause of cancerrelated death worldwide.In areas of high prevalence,such as Japan,South Korea and China,most cases of GC are related to Helicobacter pylori(H.pylori),which involves well-characterized sequential stages,including infection,atrophic gastritis,intestinal metaplasia,dysplasia,and GC.Mucins are the most abundant highmolecular-weight glycoproteins in mucus,which is the first line of defense and plays a major role in blocking pathogenic factors.Normal gastric mucosa shows expression of MUC1,MUC5 AC and MUC6 that is specific to cell type.However,the specific pattern of MUC1,MUC5 AC and MUC6 expression is changed in gastric carcinogenesis,accompanied by de novo expression of secreted MUC2.Recent studies have provided evidence that variations in these mucin genes affect many steps of GC development,such as H.pylori infection,and gastric precancerous lesions.In this review,we focus on studies of the association between polymorphisms in mucin genes and development of GC.This information should be helpful for the early detection,surveillance,and treatment of GC. | Rong Wen Fang Gao Cheng-Jiang Zhou Yan-Bin Jia | 2015 | World Journal of Gastrointestinal Oncology2015，7，11： | 5 |
| 9 | Contactin 1: A potential therapeutic target and biomarker in gastric cancer显示文摘Despite advances in diagnosis and treatment,gastric cancer remains one of the most common malignant tumors worldwide,and early diagnosis remains a challenge.The lack of effective methods to detect these tumors early is a major factor contributing to the high mortality in patients with gastric cancer,who are typically diagnosed at an advanced stage.Additionally,the early detection of metastases and the curative treatment of gastric cancer are difficult to achieve,and the detailed mechanisms remain to be fully elucidated.Thus,the identification of valuable predictive biomarkers and therapeutic targets to improve the prognosis of patients with gastric cancer is becoming increasingly important.Contactin 1(CNTN1),a cell adhesion molecule,is a glycosylphosphatidylinositolanchored neuronal membrane protein that plays an important role in cancer progression.The expression of CNTN1 is upregulated in primary lesions,and its expression level correlates with tumor metastasis in cancer patients.The current evidence reveals that the functions of CNTN1 in the development and progression of cancer likely promote the invasion and metastasis of cancer cells via the VEGFC/FLT4 axis,the RHOAdependent pathway,the Notch signaling pathway and the epithelial-mesenchymal transition progression.Therefore,CNTN1 may be a novel biomarker and a possible therapeutic target in cancer treatment in the near future. | De-Hu Chen Ji-Wei Yu Bo-Jian Jiang | 2015 | World Journal of Gastroenterology2015，21，33： | 5 |
| 10 | 应用MSN模型估计中国大陆地区2012年肝癌死亡情况显示文摘目的利用'中国疾病预防控制信息系统'全国监测点数据估计中国大陆地区2012年肝癌死亡情况。方法按照国家统计局分类方法将全国分为东、中、西三层,应用非均质表面估计模型(MSN)估计全国、分地区和分省的肝癌死亡率和死亡数。结果 2012年全国肝癌死亡率为26.12/10万,死亡人数为350 886.5人,中部地区肝癌死亡率最高30.14/10万,东部和西部地区分别为24.55/10万和24.07/10万;死亡人数东部最高136 190.02人,中部次之127 977.40人,西部最低87 626.74人。从分省的结果来看,肝癌死亡率估计值最高的5个省份是广西、重庆、黑龙江、吉林和上海,死亡率(1/10万)分别为46.23、41.49、41.38、40.96和37.82。肝癌死亡数最高的5个省份是广东、山东、河南、四川和广西,其值分别为28 639.7、25 293.93、24 692.93、24 561.92和21 289.84。结论应用MSN模型能够充分利用监测点的数据,相对准确地估算全国肝癌死亡情况,更好地为公共卫生决策服务。 | 李日健 郭莹 冯国双 徐成东 胡茂桂 王劲峰 胡跃华 于石成 马家奇 | 2015 | 慢性病学杂志2015，15，4： | 2 |
| 11 | Transposon mouse models to elucidate the genetic mechanisms of hepatitis B viral induced hepatocellular carcinoma显示文摘The major type of human liver cancer is hepatocellular carcinoma(HCC), and there are currently many risk factors that contribute to this deadly disease. The majority of HCC occurrences are associated with chronic hepatitis viral infection, and hepatitis B viral(HBV) infection is currently a major health problem in Eastern Asia. Elucidating the genetic mechanisms associated with HBV-induced HCC has been difficult due to the heterogeneity and genetic complexity associated with this disease. A repertoire of animal models has been broadly used to study the pathophysiology and to develop potential treatment regimens for HBVassociated HCC. The use of these animal models has provided valuable genetic information and has been an important contributor to uncovering the factors involved in liver malignant transformation, invasion and metastasis. Recently, transposon-based mouse models are becoming more widely used in liver cancer research to interrogate the genome by forward genetics and also used to validate genes rapidly in a reverse genetic manner. Importantly, these transposon-based rapid reverse genetic mouse models could become crucial in testing potential therapeutic agents before proceeding to clinical trials in human. Therefore, this review will cover the use of transposon-based mouse models toaddress the problems of liver cancer, especially HBVassociated HCC occurrences in Asia. | Amy P Chiu Barbara R Tschida Lilian H Lo Branden S Moriarity Dewi K Rowlands David A Largaespada Vincent W Keng | 2015 | World Journal of Gastroenterology2015，21，42： | 2 |
| 12 | Genomic alterations in pancreatic cancer and their relevance to therapy显示文摘Pancreatic cancer is a highly lethal cancer type, for which there are few viable therapeutic options. But, with the advance of sequencing technologies for global genomic analysis, the landscape of genomic alterations in pancreatic cancer is becoming increasingly well understood. In this review, we summarize current knowledge of genomic alterations in 12 core signaling pathways or cellular processes in pancreatic ductal adenocarcinoma, which is the most common type of malignancy in the pancreas, including four commonly mutated genes and many other genes that are mutated at low frequencies. We also describe the potential implications of these genomic alterations for development of novel therapeutic approaches in the context of personalized medicine. | Erina Takai Shinichi Yachida | 2015 | World Journal of Gastrointestinal Oncology2015，7，10： | 2 |
| 13 | Towards curative therapy in gastric cancer:Faraway, so close!显示文摘Although recent diagnostic and therapeutic advances have substantially improved the survival of patients with gastric cancer(GC), the overall prognosis is still poor. Surgery is the only curative treatment and should be performed in experienced centers. Due to high relapse following surgery, complementary and systemic treatment aimed at eradicating micrometastasis should be performed in most cases. Cytotoxic treatments are effective in downstaging locally advanced cancer, but different sensitivities and toxicities probably exist in different GC subtypes. Current treatment protocols are based primarily on clinical data and histological features, but molecular biomarkers that would allow for the prediction of treatment responses are urgently needed. Understanding how host factors are responsible for inter-individual variability of drug response or toxicity will also contribute to the development of more effective and less toxic treatments. | Marília Cravo Catarina Fidalgo Rita Garrido Tania Rodrigues Gon?alo Luz Carolina Palmela Marta Santos Fábio Lopes Rui Maio | 2015 | World Journal of Gastroenterology2015，21，41： | 2 |
| 14 | Management of asymptomatic primary tumours in stage Ⅳ colorectal cancer: Review of outcomes显示文摘AIM: To compare outcomes for patients presenting withstage IV colorectal cancer and an asymptomatic primary tumour, undergoing primary tumour resection(PTR) plus palliative chemotherapy vs primary chemotherapy up-front.METHODS: A literature search was conducted using MEDLINE and EMBASE. The primary outcome was overall survival. Secondary outcomes included perioperative mortality, morbidity and delayed surgical intervention rates in patients undergoing PTR and subsequent complication rates in patients with an un-resected primary tumour. Tertiary outcomes included impact on systemic treatment and identification of prognostic factors relevant for survival in this cohort. RESULTS: Twenty non-randomised studies met the inclusion criteria. Eleven studies included comparative overall survival data. Three studies showed an overall survival advantage for PTR, 7 studies showed no statistically significant advantage, and 1 study showed a significant worsening in survival in the surgical group. The perioperative mortality rate ranged from 0% to 8.5%, and post-operative morbidity rate from 10% to 35%, mainly minor complications that did not preclude subsequent chemotherapy. The rate of delayed primarytumour related symptoms, most commonly obstruction, in patients with an un-resected primary tumour ranged from 3% to 46%. The strongest independent poor prognostic factor was extensive hepatic metastases, in addition to poor performance status, M1 b stage and non-use of modern chemotherapy agents.CONCLUSION: Based on the current literature, both PTR and up front chemotherapy appear appropriate initial management strategies, with a trend towards an overall survival advantage with PTR. The procedure has a low post-operative mortality, and most complications are transient and minor. The results of recruiting randomised trials are eagerly anticipated. | Kate Jessica Wilkinson Wei Chua Weng Ng Aflah Roohullah | 2015 | World Journal of Gastrointestinal Oncology2015，7，12： | 1 |
| 15 | Influence of CD133^+ expression on patients' survival and resistance of CD133^+ cells to anti-tumor reagents in gastric cancer显示文摘Objective:To investigate the influence of CD133+expression on patients'survival and resistance of CD133+cells to anti-tumor agents in gastric cancer(GC).Methods:Influence of CD133 expression on prognosis was analyzed employing samples from patients with GC.GC cell lines were utilized to separate CD133+and CD133-subpopulations by immunomagnetic separation and to analyze the biological features of two subpopulations in vitro and in vivo,especially in resistant to anti-tumor reagents and its apoptotic mechanism.Results:The lower CD133+group showed a significantly better survival compared with the higher CD133+group.The highest content of CD133+subpopulations for KATO-III cells had stronger proliferative ability than CD133-subpopulations.A single CD133+cell was capable of generating new cell colony and the tumorigenicity rate in nude mice was100%for CD133+clonal spheres or for CD133+cells,but 0%for CD133-cells.Furthermore,the higher expression levels of Oct-4,Sox-2,Musashi-1 and ABCG2 in CD133+clonal spheres were identified compared with CD133+cells or CD133-cells.Under the treatment of anti-tumor reagents,CD133+cells had lower suppression rates compared with CD133-cells while lower level of Bcl-2 and higher level of Bax were found in CD133+cells compared with CD133-cells.Conclusions:The patients with lower CD133+expression had a better survival.Enriched CD133+cells in clonal sphere shared the ability to be self-renewable,proliferative,tumorigenic and resistant to anti-tumor agents as probably regulated by Bcl-2 and Bax. | De-Hu Chen Rui-Qi Lu Xiao-Chun Ni Ju-Gang Wu Shou-Lian Wang Bo-Jian Jiang Ji-Wei Yu | 2015 | Asian Pacific Journal of Tropical Biomedicine2015，5，12： | 0 |
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