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学科主题基础医学
p16, cyclin D1, Ki-67, and AMACR as markers for dysplasia in Barrett esophagus
Shi, Xue Ying1,2; Bhagwandeen, Brahm1; Leong, Anthony S-Y1,2
关键词barrett esophagus dysplasia adenocarcinoma immunohistochemistry p16 (INK4A/CDKN2A) Ki-67 Cyclin DI (CCNDI) alpha-methylacyl-CoA racemase (AMACR)
刊名APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
2008-10-01
16期:5页:447-452
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Anatomy & Morphology ; Medical Laboratory Technology ; Pathology
研究领域[WOS]Anatomy & Morphology ; Medical Laboratory Technology ; Pathology
关键词[WOS]HIGH-GRADE DYSPLASIA ; METHYLACYL-COA RACEMASE/P504S ; COENZYME-A RACEMASE ; CARCINOMA-SEQUENCE ; PROTEIN EXPRESSION ; SUBCELLULAR-LOCALIZATION ; ADENOCARCINOMA ; EPITHELIUM ; DIAGNOSIS ; METAPLASIA
英文摘要

Barrett esophagus (BE) (BE) is in established precursor of esophageal adenocarcinoma (AdenoCa). One hundred and one cases of BE diagnosed by esophageal biopsy and resections were examined morphologically for dysplasia. These were categorized as BE without dysplasia (n = 25). indefinite for dysplasia (IND, n = 17). low-grade dysplasia (LGD, it 18)7 high-grade dysplasia (HGD. n=15). and AdenoCa (n= 26). Immunostaining for p16 (INK4A CDKN2A). Cyclin D1 (CCND1). Ki-67. and alpha-methylacyl-CoA racemase (AMACR) was employed to assess their potential as diagnostic discriminators. Abnormal p16 expression (negative. cytoplasmic. or combined cytoplasillic and nuclear staining) was present in all categories rising from 68% in BE without dysplasia to 100% in AdenoCa. with cytoplasmic staining, only showing a significant correlation with the severity of dysplasia. Cyclin DI expression was present in almost all cases. bill high expression ( > 50% cells positive) was displayed mostly in HGD and AdenoCa (46.7% and 42.1%, respectively). Ki-67 index increased with the severity of dysplasia and labeling extended from the lower third of the Crypts 10 file superficial epithelium. The frequency of AMACR-positivity was 12% in BE. 47.1% in IND 44.4% in LGD. 93.3% in HGD and 96.2% in AdenoCa. The intensity bind extent ol′A′NIACR staining also increased with the severity of dysplasia. Aberrant 1) 16 and high-cyclin DI expression may reflect early genetic events during the progression of Barrett-associated carcinogenesis. Cytoplasmic staining of p16 is specific. It may represent a different Pathway of p16 dysfunction. The pattern and extent of Ki-67 staining and AMACR overexpression are useful additional parameters for identifying dysplasia in BE.

语种英语
WOS记录号WOS:000259648200006
资助机构HAPS Research Fellowship
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被引频次:27[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57981
专题北京大学基础医学院_病理学系
作者单位1.Hunter Area Pathol Serv, Div Anat Pathol, Newcastle, NSW 2310, Australia
2.Peking Univ, Dept Pathol, Sch Basic Med Sci, Beijing 100871, Peoples R China
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Shi, Xue Ying,Bhagwandeen, Brahm,Leong, Anthony S-Y. p16, cyclin D1, Ki-67, and AMACR as markers for dysplasia in Barrett esophagus[J]. APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY,2008,16(5):447-452.
APA Shi, Xue Ying,Bhagwandeen, Brahm,&Leong, Anthony S-Y.(2008).p16, cyclin D1, Ki-67, and AMACR as markers for dysplasia in Barrett esophagus.APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY,16(5),447-452.
MLA Shi, Xue Ying,et al."p16, cyclin D1, Ki-67, and AMACR as markers for dysplasia in Barrett esophagus".APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY 16.5(2008):447-452.
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