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| 1 | 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 |
| 2 | Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma:An intricate pathway显示文摘The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma(HCC)are still ill-defined;however,there is increasing evidence that the gradual accumulation of mutations,genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci,nodules,and finally,overt HCC.As well as many other neoplasias,liver cancer is considered an'inflammatory cancer',arising from a context of inflammation,and characterized by inflammation-related mechanisms that favor tumor cell survival,proliferation,and invasion.Molecular mechanisms that link inflammation and neoplasia have been widely investigated,and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species.The latter,in turn,probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation,and ultimately leading to cancer.The relationship amongst chronic liver injury,free radical production,and development of HCC is explored in the present review,particularly in the light of the complex network that involves oxidative DNA damage,cytokine synthesis,telomere dysfunction,and microRNA regulation. | Romilda Cardin Marika Piciocchi Marina Bortolami Andromachi Kotsafti Luisa Barzon Enrico Lavezzo Alessandro Sinigaglia Kryssia Isabel Rodriguez-Castro Massimo Rugge Fabio Farinati | 2014 | World Journal of Gastroenterology2014，20，12： | 14 |
| 3 | Wilson disease:Histopathological correlations with treatment on follow-up liver biopsies显示文摘AIM:To investigate the progression of hepatic histopathology in serial liver biopsies from Wilson disease(WD)patients.METHODS:We report a group of 12 WD patients treated with zinc and/or penicillamine who underwent multiple follow-up liver biopsies.Demographic,clinical and laboratory data were gathered and all patients underwent an initial biopsy and at least one repeat biopsy.RESULTS:Time to repeat biopsy ranged from 2 to 12 years.Six patients(non-progressors)showed stable hepatic histology or improvement.In one case,we observed improvement of fibrosis from stage 2 to 0.Six patients(progressors)had worsening of fibrosis.There was no significant correlation between the histological findings and serum aminotransferases or copper me-tabolism parameters.The hepatic copper concentration reached normal levels in only two patients:one from the non-progressors and one from the progressors group.The estimated rate of progression of hepatic fibrosis in the entire group was 0 units per year in the time frame between the first and the second liver biopsy(4 years),and 0.25 between the second and the third(3 years).In the progressors group,the rate of progression of liver fibrosis was estimated at 0.11 fibrosis units per year between the first and second biopsy and,0.6 fibrosis units between the second and third biopsy.CONCLUSION:The inability of clinical tools to detect fibrosis progression in WD suggests that a liver biopsy with hepatic copper quantification every 3 years should be considered. | Sandy Cope-Yokoyama Milton J Finegold Giacomo Carlo Sturniolo Kyoungmi Kim Claudia Mescoli Massimo Rugge Valentina Medici | 2010 | World Journal of Gastroenterology2010，16，12： | 10 |
| 4 | Targeted therapies in metastatic gastric cancer: Current knowledge and future perspectives显示文摘Gastric cancer(GC)represents a leading cause of cancer related morbidity and mortality worldwide accounting for more than 1 million of newly diagnosed cases and thousands of deaths every year.In the last decade,the development of targeted therapies and the optimization of already available chemotherapeutic drugs has expanded the available treatment options for advanced GC and granted better survival expectations to the patients.At the same time,global efforts have been undertaken to investigate in detail the genomic and epigenomic heterogeneity of this disease,resulting in the identification of new specific and sensitive predictive and prognostic biomarkers and in innovative molecular classifications based on gene expression profiling.Nonetheless,several randomized studies aimed at exploring new innovative agents,such as immune checkpoint inhibitors,failed to demonstrate clinically meaningful survival advantages.Therefore,it is essential to further improve the molecular characterization of GC subgroups in order to provide researchers and medical oncologists with new tools for patients’selection and stratification in future clinical development programs and subsequent trials.The aim of the present manuscript is to provide a global overview of the recent molecular classifications from The Cancer Genome Atlas and the Asian Cancer Research Group and to present key promising developments in the field of immunotherapy and targeted therapies in metastatic GC. | Antonio Pellino Erika Riello Floriana Nappo Stefano Brignola Sabina Murgioni Selma Ahcene Djaballah Sara Lonardi Vittorina Zagonel Massimo Rugge Fotios Loupakis Matteo Fassan | 2019 | World Journal of Gastroenterology2019，25，38： | 9 |
| 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 | miRNAs in precancerous lesions of the gastrointestinal tract显示文摘In spite of the well-established understanding of the phenotypic lesions occurring in the shift from native epithelia to invasive (adeno) carcinoma, the molecular typing of the precancerous changes in the gastrointestinal tract remains unreliable. In recent years, no biomarkers have aroused as much interest as the miRNAs,a class of non-coding RNA molecules that function as endogenous silencers of numerous target genes. Aberrant miRNA expression is a hallmark of human disease,including cancer. Unlike most mRNAs, miRNAs are both long-living in vivo and very stable in vitro . Such characteristics allow their testing in paraffin-embedded tissue samples, which is essential in the biological profiling of small (phenotypically characterized) preneoplastic lesions of the gastrointestinal tract (as well as in other fields of human pathology). The upcoming challenge lies in the reliable identification of disease-specific targets of dysregulated miRNAs, to enable miRNA testing in the clinical management of the secondary prevention of gastrointestinal cancer. | Matteo Fassan Carlo M Croce Massimo Rugge | 2011 | World Journal of Gastroenterology2011，17，48： | 7 |
| 7 | Does Helicobacter pylori infection eradication modify peptic ulcer prevalence? A 10 years' endoscopical survey显示文摘瞄准:为了在病人比较消化性溃疡流行,在根除治疗的进步散开以后在 pre-Helicobacter 时代和十年在二所意大利的医院里为上面的胃肠的内视镜检查法参考了。方法:我们检查了连续地在 1992 和 2002 期间在 1986-1987 和 1995-1996 期间在 Padova 的肠胃病学单位,并且在 Parma 的肠胃病学单位执行的所有内视镜的考试。迟平方测试被用于统计分析。结果:从两个的数据内视镜的中心在溃疡的流行显示出统计上重要的减少:从 12.7% ~ 6.3%(P<0.001 ) 在 Padova 并且从 15.6% ~ 12%(P<0.001 ) 在 Parma。减少两个都是重要的为十二指肠(从 8.8% ~ 4.8% , P<0.001 ) 并且胃溃疡(3.9% ~ 1.5% , P<0.001 ) 在 Padova,并且仅仅为在 Parma 的十二指肠溃疡(9.2% ~ 6.1% , P<0.001;胃溃疡:6.3% ~ 5.8% , NS ) 。结论:在征兆的病人的根除在消化性溃疡流行导致了重要减小的广泛的 Helicobacter pylori (H pylori ) 的十年。这减小在 Padova 是特别地明显的,在为在一般 practioners 之中的 H pylori 根除的致敏的一个工程在 1990 和 1992 之间被执行的地方。假如我们的假设应该是真的, H pylori 根除可能在未来导致是的消化性溃疡一稀罕内视镜的发现。 | Giorgio Nervi Stefania Liatopoulou Lucas Giovanni Cavallaro Alessandro Gnocchi Nadia Dal Bò Massimo Rugge Veronica Iori Giulia Martina Cavestro Marta Maino Giancarlo Colla Angelo Franzè Francesco Di Mario | 2006 | World Journal of Gastroenterology2006，12，15： | 5 |
| 8 | Oxidative damage,pro-inflammatory cytokines,TGF-αand c-myc in chronic HCV-related hepatitis and cirrhosis显示文摘AIM: To assess whether a correlation exists between oxidative DNA damage occurring in chronic HCV-related hepatitis and expression levels of pro-inflammatory cytokines, TGF-αand c-myc. METHODS: The series included 37 patients with chronic active HCV-related hepatitis and 11 with HCV-related compensated cirrhosis. Eight-hydroxydeoxyguanosine in liver biopsies was quantified using an electrochemical detector. The mRNA expression of TIMF-α, IL-1β, TGF-αand c-myc in liver specimens was detected by semi-quantitative comparative RT-PCR. RESULTS: TNF-αlevels were significantly higher in hepatitis patients than in cirrhosis patients (P=0.05). IL-1βwas higher in cirrhosis patients (P=0.05). A significant correlation was found between TNF-αand staging (P=0.05) and between IL-1βlevels and grading (P=0.04). c-myc showed a significantly higher expression in cirrhosis patients (P=0.001). Eight-hydroxydeoxyguanosine levels were significantly higher in cirrhosis patients (P=0.05) and in HCV genotype 1 (P=0.03). Considering all patients, 8-hydroxydeoxyguanosine levels were found to be correlated with genotype (P=0.04) and grading (P=0.007). Also multiple logistic regression analysis demonstrated a significant correlation among the number of DNA adducts, TNF-αexpression and HCV genotype (P=0.02). CONCLUSION: In chronic HCV-related liver damage, oxidative DNA damage correlates with HCV genotype, grading and TNF-αlevels. As HCV-related liver damage progresses, TNF-αlevels drop while IL-1βand c-myc levels increase, which may be relevant to liver carcinogenesis. | Fabio Farinati Romilda Cardin Marina Bortolami Maria Guido Massimo Rugge | 2006 | World Journal of Gastroenterology2006，12，13： | 5 |
| 9 | Precancerous lesions in the stomach: From biology to clinical patient management显示文摘 | Massimo Rugge Lisette G. Capelle Rocco Cappellesso Donato Nitti Ernst J. Kuipers | 2013 | Best Practice & Research Clinical Gastroenterology2013，，2： | 4 |
| 10 | 钛合金保载疲劳失效特征及敏感性判定方法显示文摘钛合金在航空发动机上使用时存在保载疲劳失效现象。钛合金保载疲劳寿命显著低于普通疲劳寿命且其断裂特征有别于普通疲劳。本文通过系统的实验研究,从疲劳断口、二次裂纹以及应变积累等方面总结了保载疲劳的失效特征。研究对象涵盖了保载敏感性强、弱以及无的钛合金类型。利用上述总结的特征,给出了判定钛合金保载疲劳失效及敏感性强弱的方法。 | 邱建科 席国强 马英杰 吉海宾 雷家峰 黄爱军 Rugg David 杨锐 | 2017 | 稀有金属材料与工程2017，46，S1： | 4 |
| 11 | 第二相对Ti-25V-15Cr-2Al-0.2C-x(x=0,2%Mo,2%Nb,02%Si)合金拉伸断裂行为的影响显示文摘研究了第二相对Ti 2 5V 15Cr 2Al 0 .2C x (x=0 ,2 %Mo,2 %Nb ,0 .2 %Si)阻燃β钛合金拉伸断裂行为的影响。结果表明 ,β晶界上析出的α相增加了合金发生沿晶断裂的趋势 ,特别是热暴露后形成的连续晶界α膜是导致合金脆性沿晶断裂的主要原因。虽然粗大的碳化物颗粒是合金中的裂纹源之一 ,但细小、弥散分布的碳化物却能显著降低合金发生脆性沿晶断裂的趋势 。 | 雷力明 黄旭 吴学仁 曹春晓 Rugg D Voice W | 2004 | 稀有金属2004，28，1： | 3 |
| 12 | PDCD4/miR-21 dysregulation in inflammatory bowel disease-associated carcinogenesis显示文摘 | Kathrin Ludwig Matteo Fassan Claudia Mescoli Marco Pizzi Mariangela Balistreri Laura Albertoni Salvatore Pucciarelli Marco Scarpa Giacomo Carlo Sturniolo Imerio Angriman Massimo Rugge | 2013 | Virchows Archiv2013，，1： | 3 |
| 13 | Staging and grading of chronic gastritis显示文摘 | Massimo Rugge Robert M. Genta | 2005 | Human Pathology2005，，3： | 3 |
| 14 | 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 |
| 15 | OLGA staging for gastritis: A tutorial显示文摘 | M. Rugge P. Correa F. Di Mario E. El-Omar R. Fiocca K. Geboes R.M. Genta D.Y. Graham T. Hattori P. Malfertheiner S. Nakajima P. Sipponen J. Sung W. Weinstein M. Vieth | 2008 | Digestive and Liver Disease2008，，8： | 2 |
| 16 | Assessing risks for gastric cancer: New tools for pathologists显示文摘Although the Sydney Systems (original and updated) for the classification of gastritis have contributed substantially to the uniformity of the reporting of gastric conditions, they lack immediacy in conveying to the user information about gastric cancer risk. In this review, we summarize the current understanding of the gastric lesions associated with an increased risk for cancer, and present the rationale for a proposal for new ways of reporting gastritis. In addition to the traditional histopathological data gathered and evaluated according to the Sydney System rules, pathologists could add an assessment expressed as grading and staging of the gastric inflammatory and atrophic lesions and integrate these findings with pertinent laboratory information on pepsinogens and gastrin levels. Such an integrated report could facilitate clinicians’ approach to the management of patients with gastric conditions. | Robert M Genta Massimo Rugge | 2006 | World Journal of Gastroenterology2006，12，35： | 2 |
| 17 | HP-NAP inhibits the growth of bladder cancer in mice by activating a cytotoxic Th1 response显示文摘 | Gaia Codolo Matteo Fassan Fabio Munari Andrea Volpe Piefrancesco Bassi Massimo Rugge Francesco Pagano Mario Milco D’Elios Marina Bernard | 2012 | Cancer Immunology Immunotherapy2012，，1： | 2 |
| 18 | Management of Gastric Polyps: An Endoscopy-Based Approach显示文摘 | Yasser H. Shaib Massimo Rugge David Y. Graham Robert M. Genta | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 2 |
| 19 | Clinical,virologic and histologic outcome following seroconversion from HBeAg to anti-HBe in chronic hepatitis type B显示文摘 | Fattovich G Rugge M Brollo L Pontisso P Noventa F Guido M Alberti A Realdi G | 1986 | Hepatology1986，6，2： | 1 |
| 20 | The choice of journey destination: A theoretical and empirical analysis显示文摘 | Rugg D | 1973 | The Review of Economics and Statistics1973，55，1： | 1 |
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