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Genomic profiling of gastric carcinoma in situ and adenomas by array‐based comparative genomic hybridization
Authors:Masahiro Uchida  Yoshiyuki Tsukamoto  Tomohisa Uchida  Yuta Ishikawa  Takayuki Nagai  Naoki Hijiya  Lam Tung Nguyen  Chisato Nakada  Akiko Kuroda  Tadayoshi Okimoto  Masaaki Kodama  Kazunari Murakami  Tsuyoshi Noguchi  Keiko Matsuura  Masato Tanigawa  Masao Seto  Hisao Ito  Toshio Fujioka  Ichiro Takeuchi  Masatsugu Moriyama
Affiliation:1. Department of Molecular Pathology, Oita University, Oita, Japan;2. Department of Gastroenterology, Oita University, Oita, Japan;3. Department of Scientific and Engineering Simulation, Nagoya Institute of Technology, Nagoya, Japan;4. Department of Gastroenterology, Oita Kouseiren Tsurumi Hospital, Oita, Japan;5. Department of Gastrointestinal Surgery, Faculty of Medicine, Oita University, Oita, Japan;6. Division of Biomolecular Medicine and Medical Imaging, Oita University, Oita, Japan;7. Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya, Japan;8. Department of Microbiology and Pathology, Division of Organ Pathology, Tottori University, Faculty of Medicine, Yonago, Japan;9. Department of Computer Science, Nagoya Institute of Technology, Nagoya, Japan
Abstract:
Although genomic copy number aberrations (CNAs) of gastric carcinoma at the advanced stage have already been extensively characterized by array comparative genomic hybridization (array CGH) analysis, those of gastric carcinoma in situ (CIS) are still poorly understood. Furthermore, no reports have demonstrated correlations between CNAs and histopathological features of gastric adenoma. In this study, we investigated CNAs of 20 gastric CISs (Vienna category 4.2) and 20 adenomas including seven low‐grade adenomas (LGA; Vienna category 3) and 13 high‐grade adenomas (HGA; Vienna category 4.1), using oligonucleotide‐based array CGH. The most frequent aberrations in CIS were gains at 8q (85%) and 20q (50%), and losses at 5q (50%) and 17p (50%), suggesting that these CNAs are involved in the development of CIS. We found that the pattern of CNAs in HGA was quite different from that in LGA. The most frequent CNAs in HGA were gains at 8q (62%) and 7pq (54%), whereas those in LGA were gain at 7q21.3‐q22.1 (57%) and loss at 5q (43%). Interestingly, gains at 8q and 7pq, both of which occurred most frequently in HGA, were not detected in any cases of LGA. Of note, 8q gain was detected most frequently in both HGA and CIS but was undetected in LGA. Since HGA is believed to have a higher risk of progression to invasive carcinoma than LGA, these data suggest that 8q gain is important for the malignant transformation of gastric adenoma. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Keywords:gastric carcinoma in situ  gastric adenoma  array CGH  Vienna classification
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