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学科主题: 基础医学
题名:
p16, cyclin D1, Ki-67, and AMACR as markers for dysplasia in Barrett esophagus
作者: 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
发表日期: 2008-10-01
卷: 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
项目资助者: HAPS Research Fellowship
WOS记录号: WOS:000259648200006
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57981
Appears in Collections:基础医学院_病理学系_期刊论文

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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

Recommended Citation:
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.
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