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| 1 | History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer显示文摘Helicobacter pylori(H.pylori)infection underlies gastric ulcer disease,gastric cancer and duodenal ulcer disease.The disease expression reflects the pattern and extent of gastritis/gastric atrophy(i.e.,duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis).Gastric and duodenal ulcers and gastric cancer have been known for thousands of years.Ulcers are generally non-fatal and until the 20th century were difficult to diagnose.However,the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present.It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century.Here,we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern,as it proved to be when it could be examined directly in the late 19th century.The environment before the 20th century favored acquisition of H.pylori infection and atrophic gastritis(e.g.,poor sanitation and standards of living,seasonal diets poor in fresh fruits and vegetables,especially in winter,vitamin deficiencies,and frequent febrile infections in childhood).The latter part of the 19th century saw improvements in standards of living,sanitation,and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent.In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for'surgical disease'or for'Sippy'diets.We show that while H.pylori remained common and virulent in Europe and the United States,environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H.pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H.pylori-related diseases. | David Y Graham | 2014 | World Journal of Gastroenterology2014，20，18： | 52 |
| 2 | Immunotherapy in gastric cancer显示文摘Gastric cancer is the second most common of cancerrelated deaths worldwide.In the majority of cases gastric cancer is advanced at diagnosis and although medical and surgical treatments have improved,survival rates remain poor.Cancer immunotherapy has emerged as a powerful and promising clinical approach for treatment of cancer and has shown major success in breast cancer,prostate cancer and melanoma.Here,we provide an overview of concepts of modern cancer immunotherapy including the theory,current approaches,remaining hurdles to be overcome,and the future prospect of cancer immunotherapy in the treatment of gastric cancer.Adaptive cell therapies,cancer vaccines,gene therapies,monoclonal antibody therapies have all been used with some initial successes in gastric cancer.However,to date the results in gastric cancer have been disappointing as current approaches often do not stimulate immunity efficiently allowing tumors continue to grow despite the presence of a measurable immune response.Here,we discuss the identification of targets for immunotherapy and the role of biomarkers in prospectively identifying appropriate subjects or immunotherapy.We also discuss the molecular mechanisms by which tumor cells escape host immunosurveillance and produce an immunosuppressive tumor microenvironment.We show how advances have provided tools for overcoming the mechanisms of immunosuppression including the use of monoclonal antibodies to block negative regulators normally expressed on the surface of T cells which limit activation and proliferation of cytotoxic T cells.Immunotherapy has greatly improved and is becoming an important factor in such fields as medical care and welfare for human being.Progress has been rapid ensuring that the future of immunotherapy for gastric cancer is bright. | Satoko Matsueda David Y Graham | 2014 | World Journal of Gastroenterology2014，20，7： | 19 |
| 3 | Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment显示文摘AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer. | Massimo Rugge Matteo Fassan Marco Pizzi Fabio Farinati Giacomo Carlo Sturniolo Mario Plebani David Y Graham | 2011 | World Journal of Gastroenterology2011，17，41： | 19 |
| 4 | Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21^(st) century显示文摘Restitution of normal fat absorption in exocrine pancreatic insufficiency remains an elusive goal. Although many patients achieve satisfactory clinical results with enzyme therapy, few experience normalization of fat absorption, and many, if not most, will require individualized therapy. Increasing the quantity of lipase administered rarely eliminates steatorrhea but increases the cost of therapy. Enteric coated enzyme microbead formulations tend to separate from nutrients in the stomach precluding coordinated emptying of enzymes and nutrients. Unprotected enzymes mix well and empty with nutrients but are inactivated at pH 4 or below. We describe approaches for improving the results of enzyme therapy including changing to, or adding, a different product, adding non-enteric coated enzymes,(e.g., giving unprotected enzymes at the start of the mealand acid-protected formulations later), use of antisecretory drugs and/or antacids, and changing the timing of enzyme administration. Because considerable lipid is emptied in the first postprandial hour, it is prudent to start therapy with enteric coated microbead prior to the meal so that some enzymes are available during that first hour. Patients with hyperacidity may benefit from adjuvant antisecretory therapy to reduce the duodenal acid load and possibly also sodium bicarbonate to prevent duodenal acidity. Comparative studies of clinical effectiveness of different formulations as well as the characteristics of dispersion, emptying, and dissolution of enteric-coated microspheres of different diameter and density are needed; many such studies have been completed but not yet made public. We discuss the history of pancreatic enzyme therapy and describe current use of modern preparations, approaches to overcoming unsatisfactory clinical responses, as well as studies needed to be able to provide reliably effective therapy. | Tony Trang Johanna Chan David Y Graham | 2014 | World Journal of Gastroenterology2014，20，33： | 17 |
| 5 | Autoimmune gastritis:Pathologist's viewpoint显示文摘Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic(and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and(intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integratingendoscopy, serology, histology and molecular profiling. | Irene Coati Matteo Fassan Fabio Farinati David Y Graham Robert M Genta Massimo Rugge | 2015 | World Journal of Gastroenterology2015，21，42： | 8 |
| 6 | Hybrid therapy for Helicobacter pylori infection:A systemic review and meta-analysis显示文摘AIM: To compare the effectiveness of hybrid therapy with other recommended regimens using metaanalysis.METHODS: Bibliographical searches for randomized trials comparing hybrid and other therapies were performed in Pubmed, the Cochrane Library and relevant congresses up to February 2015 using the following keywords(all fields and/or me SH):('Helicobacter pylori ' or 'H. pylori') and('hybrid therapy' or 'sequential-concomitant therapy'). metaanalyses were performed with Cochrane Review manager 5.1. The random effect model proposed by Der Simonian and Laird and the mantel-Haenszel method were used to estimate the pooled relative risk and 95%CI of the efficacy outcomes between hybrid therapy and other eradication therapies. RESULTS: Eight studies(2516 subjects) met entry criteria. The antimicrobial resistance in the study groups ranged from 6.9% to 23.5%. The mean cure rates of hybrid therapy by intention-to-treat(ITT) and perprotocol analyses were 88.5%(n = 1207; range: 80.0% to 97.4%) and 93.3%(n = 1109; range: 85.7% to99.1%), respectively. meta-analysis showed there was no significant difference in ITT eradication rate between hybrid and sequential therapy(relative risk: 1.01; 95%CI: 0.92-1.11). Subgroup analysis revealed hybrid therapy was more effective than sequential therapy in the non-Italian populations(95%CI: 1.01-1.18) and was only less effective in one, Italian population(95%CI: 0.83-0.98). There was no significant difference in eradication rate between hybrid therapy and concomitant therapy(95%CI: 0.93-1.02). No head-tohead comparisons of hybrid therapy and standard triple therapy or bismuth quadruple therapy were found. However, a multicenter, randomized trial showed that reverse hybrid therapy was superior to standard triple therapy(95.5% vs 88.6% ITT; P = 0.011).CONCLUSION: Hybrid therapy appears to be an effective, safe, and well-tolerated treatment for H. pylori infection in the era of increasing antibiotic resistance. | Ping-I Hsu Pei-Chin Lin David Y Graham | 2015 | World Journal of Gastroenterology2015，21，45： | 8 |
| 7 | Metachronous gastric cancer after successful Helicobacter pylori eradication显示文摘The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori(H. pylori) eradication was approved coupled with endoscopy to assess for the presence of chronic gastritis. Current data support the notion that cure of the infection in those with non-atrophic gastritis will prevent development of gastric cancer. However, while progression to more severe damage is halted in those who have already developed, atrophic gastritis/gastric atrophy remain at risk for subsequent development of gastric cancer. That risk is directly related to the extent and severity of atrophic gastritis. Methods to stratify cancer risk include those based on endoscopic assessment of the atrophic border, histologic grading, and non-invasive methods based on serologic testing of pepsinogen levels. Continued surveillance is required because those with atrophic gastritis/gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. Those who have already experienced a resectable early gastric cancer are among those at highest risk as metachronous lesions are frequent even after H. pylorieradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer. Studies to refine risk markers to stratify for risk, surveillance methods, intervals, and duration after successful H. pylori eradication, and whether adjuvant therapy would change risk are needed. | Akiko Shiotani Ken Haruma David Y Graham | 2014 | World Journal of Gastroenterology2014，20，33： | 5 |
| 8 | 治疗 幽门螺杆菌根治后应用质子泵抑制剂可能增加胃癌发病风险显示文摘背景 幽门螺杆菌感染是胃癌发生最常见的诱因。幽门螺杆菌根治是否能降低或消除胃癌发病风险取决于根治时的风险。对于有黏膜损害和胃酸过少者,幽门螺杆菌根治可恢复泌酸。幽门螺杆菌根治后应用质子泵抑制剂(PPI)可极度减少胃酸分泌。然而,幽门螺杆菌根治后应用PPI对于胃癌发生风险的影响仍不清楚。 | Mimi Chang Tan David Y Graham 霍永丰(译) | 2018 | 英国医学杂志中文版2018，21，11： | 3 |
| 9 | Topographic patterns of intestinal metaplasia and gastric cancer显示文摘 | Mauro Cassaro Massimo Rugge Oscar Gutierrez Gioacchino Leandro David Y Graham Robert M Genta | 2000 | The American Journal of Gastroenterology2000，，： | 2 |
| 10 | Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes 显示文摘 | Qin Y Timothy E Graham N M | 2005 | Nature2005，436，： | 1 |
| 11 | Long-distance growth and connec- tivity of neural stem cells after severe spinal cord injury 显示文摘 | Lu P Wang Y Graham L | 2012 | Cell2012，150，6： | 1 |
| 12 | Coulson Rotavirus spike protein VP5 * binds a2bl integrin on the cell surface and competes with virus for cell binding and infectivity显示文摘 | Graham K L Takada Y Barbara S | 2006 | J GEN Virology2006，87，5： | 1 |
| 13 | New concepts of resistance in the treatment of Helicobacter pylori infections 显示文摘 | GRAHAM D Y SHIOTANI A | 2008 | Nat Clin Pract Gastr2008，5，： | 1 |
| 14 | Helicobacter pylori virulence and cancer pathogenesis显示文摘 | Yamaoka Y Graham DY | 2014 | Future Oncol2014，10，8： | 1 |
| 15 | A report card to grade Helicobaeter pylori therapy显示文摘 | Graham DY Lu H Yamaoka Y | 2007 | Helicobacter2007，12，4： | 1 |
| 16 | Determi- nants of the specificity of rotavirus interactions with the a2131 integrin显示文摘 | Fleming F E Graham K L Takada Y | 2011 | Biol Chem2011，286，8： | 1 |
| 17 | Helicobacter pylori virulence factors: facts and fantasies显示文摘 | Hong Lu Yoshio Yamaoka David Y Graham | 2005 | Current Opinion in Gastroenterology2005，，6： | 1 |
| 18 | Junggar basin, northwest China:Trapped late Paleozoic ocean 显示文摘 | Carroll A R Liang Y Graham S A | 1990 | Tectonophysics1990，181，： | 1 |
| 19 | Survival from early,intermediate,and late stages of HIV infection显示文摘 | Nger C Graham N Peng Y | 1996 | JAMA1996，275，17： | 1 |
| 20 | From helical jump to chain diffusion: solid-state NMR study of chain dynam- ics in semi-crystalline polymers显示文摘 | Yao Y F Chen Q Graham A W | 2010 | Annual Reports on NMR Spectroscopy2010，69，： | 1 |
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