Gastric Cancer
Copyright ©The Author(s) 2004.
World J Gastroenterol. Dec 1, 2004; 10(23): 3394-3398
Published online Dec 1, 2004. doi: 10.3748/wjg.v10.i23.3394
Figure 1
Figure 1 mRNA expression of p16INK4A, c-myc, mbd2 and MeCP2 in cancerous (lanes 1, 4, 7 and 10), para-cancerous (lanes 2, 5, 8 and 11) and non-cancerous (lanes 3, 6, 9 and 12) tissues from patients with gastric cancer by using RT-PCR.
Figure 2
Figure 2 Density of bands from RT-PCR in each lane normalized to the total RNA as determined by the density of bands in RT-PCR for β -actin. Assuming β -actin was 4 562.39 units (pixels of brightness), the calculation [4 562.39/(density of actin)] × (density of each gene) equals each gene normalized to β -actin. Data shown are representative of three separate experiments. aP < 0.05.
Figure 3
Figure 3 Hypermethylation of p16INK4A promoter (A) and hypomethylation of proto-oncogene c-myc promoter (B) in gastric cancer tissue indicated by MSP. U: unmethylation-spe-cific PCR; M: methylation-specific PCR.
Figure 4
Figure 4 Methylation analysis of hMSH2 gene promoter by bisulfite sequencing. The arrows indicate the changes of CG to TG in promoters of non-cancerous and para-cancerous tissue, but CG remained in cancerous tissues.