Gene expression profile differences in gastric cancer, pencancerous epithelium and normal gastric mucosa by gene chip

AIM: To study the difference of gene expression in gastric cancer (T), pericancerous epithelium (P) and normal tissue of gastric mucosa (C), and to screen an associated novel gene in early gastric carcinogenesis by oligonudeotide microarray.METHODS: U133A (Affymetrix, Santa Clara, CA) gene chip was used to detect the gene expression profile difference in T, P and C, respectively. Bioinformatics was used to analyze the detected results.RESULTS: When gastric cancer was compared with normal gastric mucosa, 766 genes were found, with a difference of more than four times in expression levels. Of the 766 genes,530 were up-regulated (Signal Log Ratio [SLR]＞2), and 236 were down-regulated (SLR＜-2). When pericancerous epithelium was compared with normal gastric mucosa, 64genes were found, with a difference of more than four times in expression levels. Of the 64 genes, 50 were up-regulated (SLR＞2), and 14 were down-regulated (SLR＜-2). Compared with normal gastric mucosa, a total of 143 genes with a difference in expression levels (more than four times, either in cancer or in pericancerous epithelium) were found in gastric cancer (T) and pericancerous epithelium (P). Of the 143 genes, 108 were up-regulated (SLR＞2), and 35were down-regulated (SLR＜-2).CONCLUSION: To apply a gene chip could find 143 genes associated with the genes of gastric cancer in pericancerous epithelium, although there were no pathological changes in the tissue slices. More interesting, six genes of pericancerous epithelium were up-regulated in comparison with genes of gastric cancer and three genes were down-regulated in comparison with genes of gastric cancer. It is suggested that these genes may be related to the carcinogenesis and development of early gastric cancer.

Screening of the carcinogenesis associated gene in gastric mucosa by gene chip

Objective： To study the difference of gene expression and screen the carcinogenesis associated gene in gastric mucosa by oligonucleotide microarray. Methods： Using the U133A gene chip to detect the gene expression profile difference between pericancerous mucosa （mucosa inside nearly 2 cm by cancer） and normal section of gastric mucosa. Bioinformatics was used to analyze the detected result on their localization and function in chromosome. Results＂ （1） A total of 150 genes with a difference of more than 3 times in expression levels by comparing the pericancerous mucosa with normal gastric mucosa, of 130 genes were up-regulated （SLR〉I.5）, and 20 were down- regulated （SLR〈 -1.5）. From the gene expression difference was to do the function classification, among those 22 enzyme and 6 enzyme regular genes were most one （18.7%）. The next were 17 nucleic acid binding associated genes （11.3%）. The third were 15 signal transduction associated genes （10%）. Fourth, were 13 protein binding associated genes （8.7%）. Besides the 40 genes were unknown their function, above mentioned 4 groups were 48.7% of the gene total number; （2） The pericancerous mucosa （P） and gastric cancer （T） were simultaneously compared with normal gastric mucosa, which had 71 genes with the same expression difference, of 61 genes were up-regulated （pericancerous SLR〉I.5）, and other 10 genes were down-regulated （pericancerous SLR〈 -1.5）. From their localization on the chromosome, there was simultaneously 71 genes appearance both in the pericancerous mucosa and in gastric cancer. The most one was 11 abnormal genes on the No. 19 chromosome. The next was No. 1, 2, 16 and 17 chromosomes which had 6 genes, respectively. It was not finding an abnormal gene on the No. 5, 14, 22 and Y chromosome. Conclusion： It suggested those genes may be related to the promotion in early gastric carcinogenesis and their progress. Four main groups （enzyme and enzyme regular, nucleic acid binding, signal transduction, protein binding） that associated gene＇s abnormality be played an importance role in studying the carcinogenesis of gastric cancer. The No. 19 and No. 1, 2, 16, 17 chromosomes are important sites of the oncogene transformation.