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Exosomal glypican-1 is elevated in pancreatic cancer precursors and can signal genetic predisposition in the absence of endoscopic ultrasound abnormalities

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World Journal of Gastroenterology 2022年第31期28卷 4310-4327页

作者： Pedro Moutinho-Ribeiro Ines A Batista Sofia T Quintas Bárbara Adem Marco Silva Rui Morais Armando Peixoto Rosa Coelho Pedro Costa-Moreira Renato Medas Susana Lopes Filipe Vilas-Boas Manuela Baptista Diogo Dias-Silva Ana L Esteves Filipa Martins Joanne Lopes Helena Barroca Fátima Carneiro Guilherme Macedo Sonia A Melo Serviço de Gastrenterologia Centro Hospitalar Universitário de Sao JoaoPorto 4200Portugal Faculty of Medicine University of PortoPorto 4200Portugal Instituto de Investigacao e Inovacao em Saúde(i3S) Universidade do PortoPorto 4200Portugal IPATIMUP-Institute of Molecular Pathology and Immunology University of PortoPorto 4200Portugal Instituto de Ciencias Biomédicas Abel Salazar(ICBAS) University of PortoPorto 4050Portugal Servico de Cirurgia Geral Centro Hospitalar Universitário de Sao JoaoPorto 4200Portugal Unidade de Saúde Familiar Serpa Pinto ACeS Porto OcidentalPorto 4250Portugal Serviço de Anatomia Patológica Centro Hospitalar Universitário de Sao JoaoPorto 4200Portugal

BACKGROUND Individuals within specific risk groups for pancreatic ductal adenocarcinoma(PDAC)[mucinous cystic lesions(MCLs),hereditary risk(HR),and new-late onset diabetes mellitus(NLOD)]represent an opportunity for early cancer *** ultrasound(EUS)is a premium image modality for PDAC screening and precursor lesion *** no specific biomarker is currently clinically available for this purpose,glypican-1(GPC1)is overexpressed in the circulating exosomes(crExos)of patients with PDAC compared with healthy subjects or those harboring benign pancreatic *** To evaluate the capacity of GPC1+crExos to identify individuals at higher risk within these specific groups,all characterized by *** This cross-sectional study with a prospective unicentric cohort included 88 subjects:40 patients with MCL,20 individuals with HR,and 20 patients with NLOD.A control group(CG)was submitted to EUS for other reasons than pancreatic pathology,with normal pancreas and absence of hereditary risk factors(n=8).The inclusion period was between October 2016 and January 2019,and the study was approved by the Ethics Committee of Centro Hospitalar Universitário de São João,Porto,*** patients provided written informed *** and blood tests for quantification of GPC1+crExos by flow cytometry and carbohydrate antigen 19-9(CA 19-9)levels by ELISA were performed in all ***-guided tissue acquisition was done whenever *** statistical analysis,SPSS®27.0(IBM Corp.,Armonk,NY,United States)version was *** graphs were created using GraphPad Prism 7.00(GraphPad Software,San Diego,CA,United States).RESULTS Half of MCLs harbored worrisome features(WF)or high-risk stigmata(HRS).Pancreatic abnormalities were detected by EUS in 10.0%and 35.0%in HR and NLOD individuals,respectively,all considered non-malignant and“harmless.”Median levels of GPC1+crExos were statistically different:MCL[99.4%,interquartile range(IQR):94.9%-99.8%],HR(8

关键词： Glypican-1 Circulating exosomes Endoscopic ultrasound Pancreatic cancer risk groups Pancreatic cancer precursor lesions genetic predisposition

Younger age of onset and multiple primary lesions associated with esophageal squamous cell carcinoma cases with a positive family history of the cancer suggests genetic predisposition

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Chinese Medical Journal 2014年第15期127卷 2779-2783页

作者： Jia Nan Wen Xiaoduo Zhang Nan YangYi Zhang Liwei Wang Xiaoling Wang Na Wen Denggui Department of Surgery Hebei Tumor Hospital and theFourth Hospital of Hebei Medical University Shijiazhuang Hebei050011 China Department of Tumor Image Hebei Tumor Hospital and theFourth Hospital of Hebei Medical University Shijiazhuang Hebei050011 China Department of Medical Information Hebei Tumor Hospital and theFourth Hospital of Hebei Medical University Shijiazhuang Hebei050011 China Department of Pathology Hebei Tumor Hospital and theFourth Hospital of Hebei Medical University Shijiazhuang Hebei050011 China Department of Oncology Hebei Tumor Hospital and theFourth Hospital of Hebei Medical University Shijiazhuang Hebei050011 China

Background Previous epidemiological studies have consistently found a positive family history of esophageal cancer is associated with a significantly increased risk of the ***,whether the elevated risk could be attributed to common household exposure or inherited susceptibility is *** study aimed to highlight the effect of genetic predisposition by noting the significant differences in onset age and multiple primary cancers between esophageal squamous cell carcinoma （ESCC） cases with or without a positive family history of the *** Age at onset and the percentage of multiple primary cancers were compared between ESCCs with （n=766） or without （n=1 776） a positive family history of the cancer in a consecutive surgery cohort at the Department of Thoracic Surgery of Hebei Tumor Hospital and the Fourth Hospital of Hebei Medical *** Overall,ESCCs with a positive family history of the cancer featured both a significantly younger age of onset and significantly more multiple primary cancers than those with a negative family history （onset age 51.83 vs.53.49 years old,P 〈0.01; percent of multiple primary cancers 5.50% vs.1.70%,x2=25.42,P 〈0.01）.Both the differences were evident in subgroup analyses,but did not *** age at onset differed significantly by family history among the male,smoking,and drinking groups,the difference of multiple primary cancers was significant among the otherwise nonsmoking,nondrinking,and younger onset age *** Younger age of onset and multiple primary cancers associated with ESCCs with a positive,as opposed to a negative family history of the cancer,suggest a genetic *** results of subgroup analyses indicate a younger age of ESCC development results from the interaction of environmental and genetic risk factors,but multiple primary cancers may be related only to genetic predisposition.

关键词： esophageal squamous cell carcinoma gastric cardia adenocarcinoma a positive family history of cancer genetic predisposition onset age multiple primary cancer

Replication of interleukin 23 receptor and autophagy-related 16-like 1 association in adult-and pediatric-onset inflammatory bowel disease in Italy

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World Journal of Gastroenterology 2008年第29期14卷 4643-4651页

作者： Anna Latiano Orazio Palmieri Maria Rosa Valvano Renata D'Incà Salvatore Cucchiara Gabriele Riegler Anna Maria Staiano Sandro Ardizzone Salvatore Accomando Gian Luigi de Angelis Giuseppe Corritore Fabrizio Bossa Vito Annese U.U. O.O. di Gastroenterologia ed Endoscopia Ospedale IRCCS-CSSSan Giovanni Rotondo (Fg) 71013 Italy Cattedra di Gastroenterologia Università di PadovaPadova 35122 Italy Clinica Pediatrica Università "La Sapienza" Roma 00185 Italy Cattedra di Gastroenterologia Università di NapoliNapoli 80131 Italy Clinica Pediatrica Università di Napoli Napoli 80131 Italy Unità di Gastroenterologia Ospedale "Sacco" Milano 20157 Italy Clinica Pediatrica Università di Palermo Palermo 90128 Italy Clinica Pediatrica Università di Parma Parma 43100 Italy

AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD genes. METHODS: Total of 763 patients with Crohn's disease (CD, 189 diagnosed at age < 19 years), 843 with ulcerative colitis (UC, 179 diagnosed <19 years), 749 healthy controls, and 546 healthy parents (273 trios) were included in the study. The rs2241880 [autophagy-related 16-like 1 (ATG16L1)], rs11209026 and rs7517847 [interleukin 23 receptor (IL23R)], rs2066844, rs2066845, rs2066847 (CARD15), rs1050152 (OCTN1), and rs2631367 (OCTN2) gene variants were genotyped. RESULTS: The frequency of G allele of ATG16L1 SNP (Ala197Thr) was increased in patients with CD compared with controls (59% vs 54% respectively) (OR = 1.25, CI = 1.08-1.45, P = 0.003), but not in UC (55%). The frequency of A and G (minor) alleles of Arg381Gln, rs11209026 and rs7517847 variants of IL23R were reduced significantly in CD (4%, OR = 0.62, CI = 0.45-0.87, P = 0.005; 28%, OR = 0.64, CI = 0.55-0.75, P < 0.01), compared with controls (6% and 38%, respectively). The A allele (but not G) was also reduced signifi cantly in UC (4%, OR = 0.69, CI = 0.5-0.94, P = 0.019). No association was demonstrated with sub-phenotypes and interaction with CARD15 , and OCTN1/2 genes, although both gene variants were associated with pediatric-onset disease. CONCLUSION: The present study confirms the association of IL23R polymorphisms with IBD, and ATG16L1 with CD, in both adult- and pediatric-onset subsets in our study population.

关键词： Inflammatory bowel disease Crohn'sdisease Ulcerative colitis genetic predisposition Autophagy-related 16-like 1 Interleukin 23 receptor Genome-wide association study Pediatric inflammatorybowel disease

Autoimmmune hepatitis

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Cellular & Molecular Immunology 2022年第2期19卷 158-176页

作者： Benedetta Terziroli Beretta-Piccoli Giorgina Mieli-Vergani Diego Vergani Epatocentro Ticino&Facoltàdi Scienze Biomediche Universitàdella Svizzera ItalianaLuganoSwitzerland Institute for Research in Biomedicine BellinzonaSwitzerland. King’s College London Faculty of Life Sciences&Medicine at King’s College Hospital LondonUK. Paediatric Liver GI and Nutrition CentreMowatLabsKing’s College HospitalLondonUK. Institute of Liver Studies MowatLabsKing’s College HospitalLondonUK.

Autoimmune hepatitis(AIH)is a T-cell mediated,inflammatory liver disease affecting all ages and characterized by female preponderance,elevated serum transaminase and immunoglobulin G levels,positive circulating autoantibodies,and presence of interface hepatitis at liver *** type 1,affecting both adults and children,is defined by positive anti-nuclear and/or antismooth muscle antibodies,while type 2 AIH,affecting mostly children,is defined by positive anti-liver-kidney microsomal type 1 and/or anti-liver cytosol type 1 *** the autoantigens of type 2 AIH are well defined,being the cytochrome P4502D6(CYP2D6)and the formiminotransferase cyclodeaminase(FTCD),in type 1 AIH they remain to be ***-1 predisposition is conferred by possession of the MHC class II HLA DRB1*03 at all ages,while DRB1*04 predisposes to late onset disease;AIH-2 is associated with possession of DRB1*07 and DRB1**** majority of patients responds well to standard immunosuppressive treatment,based on steroid and azathioprine;second-and third-line drugs should be considered in case of intolerance or insufficient *** review offers a comprehensive overview of pathophysiological and clinical aspects of AIH.

关键词： Autoimmune Hepatitis Immunopathophysiology Treatment genetic predisposition

HLA-DQ:Celiac disease vs inflammatory bowel disease

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World Journal of Gastroenterology 2018年第1期24卷 96-103页

作者： Marta Maia Bosca-Watts Miguel Minguez Dolores Planelles Samuel Navarro Alejandro Rodriguez Jesus Santiago Joan Tosca Francisco Mora Disease Department of the University Clinic Hospital of Valencia University of ValenciaValencia 46017Spain Histocompatibility Department of the Transfusion Center of the Valencian Community Valencia 46014Spain Pathology Department of the University Clinic Hospital of Valencia University of ValenciaValencia 46017Spain Digestive Disease Department of the Hospital Virgen del Castillo of Yecla Yecla 30510Spain Digestive Disease Department of the Hospital de Manises Valencia 46940Spain Digestive Disease Department of the University Clinic Hospital of Valencia University of ValenciaValencia 46017Spain

AIM To determine the genetic predisposition to celiacdisease(Ce D) in inflammatory bowel disease(IBD) patients by quantifying the frequency of Ce D-related human leucocyte antigen(HLA)(HLA-Ce D: HLA-DQ2 and-DQ8) in IBD patients globally, by type of IBD and gender, and by calculating the protective/risk contribution of these haplotypes in the development of the IBD *** We conducted a prospective study with IBD patients from our Unit. Clinical information was gathered and blood was tested for HLA-CeD. The control group was made up of unrelated Valencian organ ***1034 subjects were analyzed: 457 IBD [207 ulcerative coliti(UC) and 250 Crohn's disease(CD)] patients and 577 healthy controls. 39% of the controls and 34% of the patients had HLA-Ce D(P = 0.0852). HLA-DQ2 was less frequent in UC patients(P = 0.0287), and HLA-DQ8 in CD(P = 0.0217). In women with UC, the frequency of DQ2.5 cis(DQB1*02:01-DQA1*05:01) was reduced ≥ 50% [P = 0.0344; preventive fraction(PF) = 13%]. PFs(7%-14%) were obtained with all HLACe D haplotypes. HLA DQB1*02:02-DQA1*02:01(HLADQ2.2) was more frequent in CD patients with respect to controls(P = 0.001) and UC patients(etiological fraction = 15%).CONCLUSION HLA-CeD is not more frequent in IBD patients, with an even lower frequency of HLA-DQ2 and-DQ8 in UC and CD respectively. HLA-DQ2.5 confers protection from the development of UC, especially in women, and HLADQ8 does so for the appearance of CD. HLA-DQ2.2 is present in 34% of the CD patients and may constitute a genetic risk factor for CD development.

关键词： genetic predisposition Celiac disease Inflammatory bowel disease Crohn's disease Human leucocyte antigen Ulcerative colitis

Interaction of major genes predisposing to hepatocellular carcinoma with genes encoding signal transduction pathways influences tumor phenotype and prognosis

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World Journal of Gastroenterology 2008年第43期14卷 6601-6615页

作者： Francesco Feo Maddalena Frau Rosa Maria Pascale Department of Biomedical Sciences Division of Experimental Pathology and OntologyUniversity of SassariSassari 07100Italy

Studies on rodents and humans demonstrate an inherited predisposition to hepatocellular carcinoma （HCC）. Analysis of the molecular alterations involved in the acquisition of a phenotype resistant or susceptible to hepatocarcinogenesis showed a deregulation of G1 and S phases in HCC of genetically susceptible F344 rats and a G1-S block in lesions of resistant Brown norway （BN） rats. Unrestrained extracellular signal-regulated kinase （ERK） activity linked to proteasomal degradation of dual-specificity phosphatase 1 （DUSP1）, a specific ERK inhibitor, by the CKS1-SKP2 ubiquitin ligase complex occurs in more aggressive HCC of F344 rats and humans. This mechanism is less active in HCC of BN rats and human HCC with better prognosis. Upregulation of iNos cross-talk with IKK/NF-KB and RAS/ERK pathways occurs in rodent liver lesions at higher levels in the most aggressive models represented by HCC of F344 rats and c-Myc-TGF-α transgenic mice. iNOS, IKK/NF-κB, and RAS/ERK upregulation is highest in human HCC with a poorer prognosis and positively correlates with tumor proliferation, genomic instability and microvascularization, and negatively with apoptosis. Thus, cell cycle regulation and the activity of signal transduction pathways seem to be modulated by HCC modifier genes, and differences in their efficiency influence the susceptibility to hepatocarcinogenesis and probably the prognosis of human HCC.

关键词： Hepatocarcinogenesis genetic predisposition Polygenic disease, Redifferentiation Signal transduction pathways Cell cycle Cell proliferation Apoptosis Proteasomal degradation

Evaluation of the colorectal cancer risk conferred by rare UNC5C alleles

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World Journal of Gastroenterology 2014年第1期20卷 204-213页

作者： Sébastien Küry Céline Garrec Fabrice Airaud Flora Breheret Virginie Guibert Cécile Frenard Shuo Jiao Dominique Bonneau Pascaline Berthet Céline Bossard Olivier Ingster Estelle Cauchin Stéphane Bezieau CHU Nantes Service de Génétique Médicale44093 Nantes CEDEX 1France Public Health Sciences Division Fred Hutchinson Cancer Research CenterSeattleWA 98109United States CHU Angers Service de Génétique Médicale4 rue Larrey49933 AngersFrance Centre de Lutte contre le Cancer Fran?ois Baclesse 3 avenue du Général Harris14076 Caen Cedex 5France Université de Nantes Faculté de Médecine de NantesEA 4273 NantesFrance CHU Nantes Institut des Maladies de l’Appareil Digestif et Service d’Hépato-Gastroentérologie44093 Nantes Cedex 1France

AIM: To evaluate the risk associated with variants of the UNC5C gene recently suspected to predispose to familial colorectal cancer (CRC).

关键词： Colorectal cancer UNC5C genetic predisposition Familial study Association study Low risk

Changing trends of cardiovascular risk factors among Indians:a review of emerging risks

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Asian Pacific Journal of Tropical Biomedicine 2014年第12期4卷 1001-1008页

作者： Arun Kumar Department of Biochemistry Manipal College of Medical Sciences

The global burden of disease due to cardiovascular diseases(CVDs) is escalating,and the changing trends of CVD risk factors are identified among Indians experiencing rapid health *** causes include:growing population with demographic shifts and altered age profile,socio-economic factors,lifestyle changes due to *** are also having genetic predisposition to cardiovascular diseases and adult are susceptible to vascular disease linking possible gene-environment interactions influencing ethnic *** diets with more of junk foods along with diminished physical activity are additive factors contributing to the acceleration of CVD epidemics,along with all form of tobacco *** pace of health transition,however,varies across geographical regions from urban to rural population with consequent variations in the relative burdens of the dominant CVDs.A comprehensive public health response must be looked to plan over all strategies to integrate policies and programs that effectively impact on the multiple determinants of CVDs to provide protection over the life span through primordial,primary and secondary *** as well as individuals at risk must be protected through initiatives,enable nutritionbased preventive strategies to protect and promote cardiovascular health.

关键词： Cardiovascular risk factors genetic predisposition Modifiable risk Non-modifiable risk Indians

Molecular mechanisms of liver carcinogenesis related to metabolic syndrome

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Hepatoma Research 2022年第1期8卷 22-34页

作者： Claudia Campani Jean-Charles Nault Team of Functional Genomics of Solid Tumors Centre de Recherche des CordeliersSorbonne UniversitéInsermUniversitéde ParisParis F-75006France Equipe labellisée Ligue Nationale Contre le Cancer Labex OncoImmunologyParis F-75006France Department of Experimental and Clinical Medicine University of FlorenceFlorence 50139Italy Service d’hépatologie Hôpital AvicenneHôpitaux Universitaires Paris-Seine-Saint-DenisAssistance-Publique Hôpitaux de ParisBobigny 93000France Unitéde Formation et de Recherche SantéMédecine et Biologie Humaine UniversitéParis 13Communautéd’Universités et Etablissements Sorbonne Paris CitéBobigny 93000France

Global prevalence of non-alcoholic fatty liver disease(NAFLD)and of NAFLD-hepatocellular carcinoma(HCC)is estimated to grow in the next *** burden of NAFLD and the evidence that NAFLD-HCC arises also in noncirrhotic patients,explain the urgent need of a better characterization of the molecular mechanisms involved in NAFLD *** and diabetes cause a chronic inflammatory state which favors changes in serum cytokines and adipokines,an increase in oxidative stress,DNA damage,and the activation of multiple signaling pathways involved in cell ***,a role in promoting NAFLD-HCC has been highlighted in the innate and adaptive immune system,dysbiosis,and alterations in bile acids *** dietary,genetic,or combined mouse models have been used to study nonalcoholic steatohepatitis(NASH)development and its progression to HCC,but models that fully recapitulate the biological and prognostic features of human NASH are still *** humans,four single nucleotide polymorphisms(PNPLA3,TM6SF2,GCKR,and MBOAT7)have been linked to the development of both NASH and HCC in cirrhotic and non-cirrhotic patients,whereas HSD17B13 polymorphism has a protective *** addition,higher rates of somatic ACVR2A mutations and a novel mutational signature have been recently discovered in NASH-HCC *** knowledge of the molecular pathogenesis of NAFLD-HCC will be helpful to personalized screening programs and allow for primary and secondary chemopreventive treatments for NAFLD patients who are more likely to progress to HCC.

关键词： Hepatocellular carcinoma mouse model genetic predisposition cirrhosis non-alcoholic fatty liver disease immune system