PMC:4996403 / 13845-16908 JSONTXT

{"project":"2_test","denotations":[{"id":"27600234-25314065-69479983","span":{"begin":426,"end":429},"obj":"25314065"},{"id":"27600234-25213452-69479984","span":{"begin":1221,"end":1224},"obj":"25213452"},{"id":"27600234-19639168-69479985","span":{"begin":1375,"end":1378},"obj":"19639168"},{"id":"27600234-12679032-69479986","span":{"begin":1599,"end":1601},"obj":"12679032"},{"id":"27600234-19898900-69479987","span":{"begin":2021,"end":2024},"obj":"19898900"},{"id":"27600234-22127425-69479988","span":{"begin":2366,"end":2369},"obj":"22127425"},{"id":"27600234-24552139-69479989","span":{"begin":2726,"end":2729},"obj":"24552139"}],"text":"4.4. Selection of Comparison Samples\nIn general, microarrays are typically used to compare tumor tissue and corresponding normal tissue. However, when used to compare precancerous tissue with the corresponding normal tissue, it can identify alterations in gene expression and methylation events that lead to carcinogenesis, and thus may have the potential to evaluate the risk of carcinogenesis and recurrence.\nNomoto et al. [104] examined adjacent nonneoplastic liver tissue from a patient with hepatocellular carcinoma comparing with supernormal liver (SN) samples taken from metastatic secondary malignancies of the liver. The tissue of SN was actual normal liver. Therefore, it seemed that there was no molecule which showed fundamentally abnormal. However, it could not be denied that there was the individual feature. Then they thought that this individual projection was erased by mixing 11 SN samples. Expression profiling and methylation arrays revealed that expression of the thimet oligopeptidase (THOP1) gene in the background liver of HCC is likely to be a good biomarker for risk of HCC development.\nTo validate genome-wide DNA methylation profiles during multistage hepatocarcinogenesis, Ammerpohl et al. [105] revealed that the methylation status have changed gradually from normal to cirrhosis and further to HCC using a methylation array. Nagashiro et al. [106] established criteria for carcinogenetic risk estimation based on DNA methylation array profiling to compare samples of noncancerous liver tissue obtained from HCC patients with normal liver tissue samples. Arai et al. [85] performed bacterial artificial chromosome (BAC) array-based methylated CpG island amplification using a microarray of 4361 BAC clones in normal liver tissue obtained from patients without HCC, noncancerous liver tissue obtained from patients with HCC, and HCC samples. The DNA methylation status of the 41 BAC clones was correlated with the cancer-free and overall survival rates of patients with HCC.\nOkamoto et al. [107] classified patients with hepatitis C-positive HCC into two groups: the single nodular HCC group and multicentric (MC) HCC group. The authors compared gene expression patterns of the noncancerous liver tissue specimens using cDNA microarrays, and created a scoring system to estimate the risk for MC hepatocarcinogenesis. Utsunomiya et al. [108] performed miRNA microarrays to compare the miRNA expression patterns in the non-cancerous liver tissues between the MC recurrence group and no MC recurrence group to identify miRNAs related to MC recurrence. The authors detected 20 differently expressed miRNAs, 18 of which were downregulated in the MC group and 2 of which were upregulated.\nSato et al. [109] performed genome-wide DNA methylation array analysis in normal lung tissue obtained from patients without any primary lung tumor, non-cancerous lung tissue obtained from patients with lung adenocarcinomas, and tumorous tissue. DNA hypermethylation at precancerous tissues was strengthened during progression to lung adenocarcinomas."}