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Journal of Biomedicine and Biotechnology
Volume 2011, Article ID 780836, 10 pages
http://dx.doi.org/10.1155/2011/780836
Research Article

Diagnosis and Prognostication of Ductal Adenocarcinomas of the Pancreas Based on Genome-Wide DNA Methylation Profiling by Bacterial Artificial Chromosome Array-Based Methylated CpG Island Amplification

1Pathology Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
2Hepatobiliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo 104-0045, Japan
3Cancer Genomics Project, National Cancer Center Research Institute, Tokyo 104-0045, Japan
4Proteome Bioinformatics Project, National Cancer Center Research Institute, Tokyo 104-0045, Japan
5Department of Molecular Cytogenetics, Medical Research Institute and School of Biomedical Science, Tokyo Medical and Dental University, Tokyo 113-8510, Japan
6Cancer Genome Center, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan

Received 22 July 2010; Accepted 12 November 2010

Academic Editor: Alain Filloux

Copyright © 2011 Masahiro Gotoh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Wilcoxon test (P < .01) revealed that the average signal ratios of the 331 BAC clones in samples of cancerous tissue (T) differed significantly from those in both samples of normal pancreatic tissue obtained from patients without ductal adenocarcinomas (C) and samples of noncancerous pancreatic tissue obtained from patients with ductal adenocarcinomas (N) in the learning cohort. Such 331 BAC clones are listed and their chromosomal loci based on the UCSC Genome Browser (http://genome.ucsc.edu/cgi-bin/hgGateway) are summarized in Supplementary Table SI.

In 12 BAC clones, using cutoff values of the signal ratios shown in Table 2, samples of cancerous tissue were discriminated from both samples of normal pancreatic tissue obtained from patients without ductal adenocarcinomas and samples of noncancerous pancreatic tissue obtained from patients with ductal adenocarcinomas in the learning cohort with 100% specificity. Genes located on the 12 BAC clones are summarized in Supplementary Table SII (a). In 11 BAC clones, using cutoff values of the signal ratios shown in Table 3, samples of cancerous tissue from patients belonging to the early-relapse group were discriminated from those belonging to the no-relapse group in the learning cohort with 100% specificity. Genes located on the 11 BAC clones are summarized in Supplementary Table SII (b).

  1. Supplementary Material