title: Genomic profiling of gastric carcinoma in situ and adenomas by array-based comparative genomic hybridization.
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.
authors.affiliation: Department of Molecular Pathology, Oita University, Oita, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Uchida
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Tsukamoto
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Uchida
authors.forename: Yuta
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Takayuki
authors.initials: T
authors.lastname: Nagai
authors.forename: Naoki
authors.initials: N
authors.lastname: Hijiya
authors.forename: Lam Tung
authors.initials: LT
authors.lastname: Nguyen
authors.forename: Chisato
authors.initials: C
authors.lastname: Nakada
authors.forename: Akiko
authors.initials: A
authors.lastname: Kuroda
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Okimoto
authors.forename: Masaaki
authors.initials: M
authors.lastname: Kodama
authors.forename: Kazunari
authors.initials: K
authors.lastname: Murakami
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Noguchi
authors.forename: Keiko
authors.initials: K
authors.lastname: Matsuura
authors.forename: Masato
authors.initials: M
authors.lastname: Tanigawa
authors.forename: Masao
authors.initials: M
authors.lastname: Seto
authors.forename: Hisao
authors.initials: H
authors.lastname: Ito
authors.forename: Toshio
authors.initials: T
authors.lastname: Fujioka
authors.forename: Ichiro
authors.initials: I
authors.lastname: Takeuchi
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Moriyama
mesh_terms: D000236:Adenoma / Q000235:genetics* / Q000473:pathology; D000368:Aged; D000369:Aged, 80 and over; D002278:Carcinoma in Situ / Q000235:genetics* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002869:Chromosome Aberrations; D055028:Comparative Genomic Hybridization; D018450:Disease Progression; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology