1. Volume 122, Issue 4, Pages 1113-1121 (April 2002)
p16 Inactivation by methylation of the CDKN2A promoter occurs early during neoplastic progression in Barrett's esophagus 
Yan–Song Bian, Maria–Chiara Osterheld, Charlotte Fontolliet, Fred T. Bosman, Jean Benhattar 
Gastroenterology 
Volume 122, Issue 4, Pages (April 2002)
DOI: /gast
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2. Fig. 1
CDKN2A promoter hypermethylation and LOH of CDKN2A in a case with premalignant lesions and adenocarcinoma in Barrett's esophagus (Table 1, case 6). (A)Methylation analysis by MS-SSCA. Unmethylated mobilities observed in LG dysplasia (LG) differed from those completely methylated in adenocarcinoma (T) and HG dysplasia (HG). A mixture of methylated and unmethylated pattern was detected in metaplasia (M). No methylation was found in normal tissues (N). DNA from placenta (no methylation of CDKN2A promoter) and a colon cancer-derived cell line SW620 (complete methylation of CDKN2A promoter) was used as a positive control. Arrows indicate the methylated bands. (B) The detection of LOH in theCDKN2A gene locus (hMp16α-I1). LOH was noted in all premalignant lesions (M, LG, HG) and adenocarcinoma (T). DNA from normal tissues (N) of the same patient was used as a negative control.
Gastroenterology  , DOI: ( /gast )
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3. Fig. 2
IHC analysis of p16 expression in premalignant lesions and adenocarcinoma in Barrett's esophagus using G mAb. (A) Metaplasia, (B) dysplasia, and (C) adenocarcinoma without CDKN2A promoter hypermethylation showing nuclear immunostaining for p16. (D–F) Similar lesions with promoter methylation showing absence of immunostaining for p16, in contrast to background stromal and inflammatory cells, which were positive. Original magnification 100×.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions