200例胃底腺息肉临床病理特征分析

《200例胃底腺息肉临床病理特征分析》由会员上传分享，免费在线阅读，更多相关内容在学术论文-天天文库。

1、授予单位代码10089学号或申请号13519HebeiMedicalUniversity硕士学位论文在职科学学位200例胃底腺息肉临床病理特征分析学位申请人：阮联英导师：张杰英教授专业：病理学与病理生理学二级学院：基础医学院2015年3月河北医科大学学位论文使用授权及知识产权归属承诺本学位论文在导师(或指导小组)的指导下，由本人独立完成。本学位论文研究所获得的研究成果，其知识产权归河北医科大学所有。河北医科大学有权对本学位论文进行交流、公开和使用。凡发表与学位论文主要内容相关的论文，第一署名为单位河北医科

2、大学，试验材料、原始数据、申报的专利等知识产权均归河北医科大学所有。否则，承担相应法律责任。研究生签名：导师签章。^级学院领导盖章：：乂年T月巧曰河北医科大学研究生学位论文独创性声明本论文是在导师指导下进行的研究工作及取得的研究成果,除了文中特别加以标注和致谢等内容外,文中不包含其他人已经发表或撰写的研究成果,指导教师对此进行了审定。本论文由本人独立撰写，文责自负。研究生签名：目录中文摘要···························································

3、··················1英文摘要·············································································4研究论文200例胃底腺息肉临床病理特征分析前言·············································································8材料与方法················································

4、····················8结果·············································································11附图·············································································13附表······································································

5、·······18讨论·············································································20结论·············································································22参考文献·······································································23综述胃底腺息肉

6、的研究进展··················································26致谢···················································································38个人简历·············································································39中文摘要200例胃底腺息肉临床病理特征分析摘要胃底腺息肉

7、是指胃底胃体黏膜形成的单发或多发性广基息肉样隆起，现已是胃息肉的常见组织学类型。WHO推出的消化系统肿瘤分类最新版本中，将胃息肉从广义上分为肿瘤性息肉和非肿瘤性息肉两大类。胃内肿瘤性息肉病变包括呈息肉样外观的癌、神经内分泌肿瘤、腺瘤性息肉（肠型）、胃型腺瘤（幽门腺腺瘤和小凹型腺瘤）以及胃底腺息肉(fundicglandpolyps，FGPs)。其他息肉病变如增生性息肉、错构瘤性息肉以及其它具有息肉样生长方式的病变等均归类为非肿瘤性病变。胃底腺息肉虽归类于肿瘤性息肉，但一般被认为是良性病变，临床常多发。目前

8、胃底腺息肉发病机制不清，临床缺乏规范诊治指南。既往认为家族性腺瘤性息肉病(familialadenomatouspolyposis，FAP)常合并FGPs，其癌变风险很高。但近年报道无FAP的患者亦发生FGPs。FAP患者多合并腺瘤息肉病杆菌(APC)及其下游目标靶向基因β-连接素基因的突变。β-连接素是Wnt信号转导通路中致癌的关键分子，可激活下游靶基因CyclinD1的转录，引起细胞增殖和分化失控，导致肿瘤发生。国内关于非