Rapid Communication
Copyright ©2006 Baishideng Publishing Group Co.
World J Gastroenterol. Oct 7, 2006; 12(37): 6041-6045
Published online Oct 7, 2006. doi: 10.3748/wjg.v12.i37.6041
Figure 1
Figure 1 Immunohistochemical analysis of DAB2 in esophageal squamous cell carcinogenesis. A: Cytoplasmic expression of DAB2 in non-malignant normal esophageal mucosa; B: Hyperplastic esophageal mucosa showing no detectable expression of DAB2 protein; C: Dysplastic esophageal mucosa showing loss of DAB2 protein expression; D: ESCC section showing loss of DAB2 protein expression; and E: ESCC showing faint cytoplasmic DAB2 protein expression (A-D: Original magnification x 100; and E: Original magnification x 200).
Figure 2
Figure 2 DAB2 exon-1 promoter hypermethylation. Methylation-specific PCR was done to determine the possibility of promoter methylation-mediated gene silencing of DAB2. Eight of 10 ESCCs showed signal (PCR amplicon) for the unmethylated DAB2 alleles (samples 1, 4-10), while 2 cases showed the presence of both unmethylated and methylated PCR amplicon (samples 2 and 3). Burkitt’s lymphoma cell line Raji was used as a positive control for hypermethylation of DAB2 gene (sample 11). In each sample, lane U represents the unmethylated product, while M represents the methylated product, lane NTC refers to the no template control.