Lin Lian-Jie, Asaoka Yoshinari, Tada Motohisa, Sanada Masashi, Nannya Yasuhito, Tanaka Yasuo, Tateishi Keisuke, Ohta Miki, Seto Motoko, Sasahira Naoki, Tada Minoru, Kawabe Takao, Zheng Chang-Qing, Kanai Fumihiko, Ogawa Seishi, Omata Masao
Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Oncology. 2008;75(1-2):102-12. doi: 10.1159/000155813. Epub 2008 Sep 12.
To chart molecular genetic events in pancreatic cancer.
We analyzed genome-wide copy number alterations and loss of heterozygosity (LOH) in 25 established pancreatic cancer cell lines using a high-density single nucleotide polymorphism (SNP) array. We verified the data using genomic PCR and applied them to clinical samples.
Twenty-six homozygous deletion regions were detected in at least 1 cell line and LOH was found at 9p, 18q, 17p, 8p, 13q, 6q, 3p, 6p, 22q, 9q and 12q with high frequency (>50%), consistent with a previous study. Moreover, we found 23 amplified regions in at least 2 cell lines, including 8 unreported loci. We then examined representative genes at the 8 amplified loci in matched pairs of pancreatic cancer and normal tissues. The amplification was detected in 1 (7.1%) to 5 (35.7%) of 14 microdissected tissue specimens.
Using high-resolution SNP arrays, we studied genome-wide copy number alterations and LOH simultaneously. We identified several novel and minute genomic amplifications, which contained candidate oncogenes in human pancreatic cancers.
绘制胰腺癌中的分子遗传事件图谱。
我们使用高密度单核苷酸多态性（SNP）阵列分析了25个已建立的胰腺癌细胞系中的全基因组拷贝数改变和杂合性缺失（LOH）。我们使用基因组PCR验证了数据并将其应用于临床样本。
在至少1个细胞系中检测到26个纯合缺失区域，并且在9p、18q、17p、8p、13q、6q、3p、6p、22q、9q和12q处高频（>50%）发现LOH，这与先前的研究一致。此外，我们在至少2个细胞系中发现了23个扩增区域，包括8个未报告的位点。然后，我们在胰腺癌和正常组织的配对样本中检查了8个扩增位点处的代表性基因。在14个显微切割组织样本中的1个（7.1%）至5个（35.7%）中检测到了扩增。
使用高分辨率SNP阵列，我们同时研究了全基因组拷贝数改变和LOH。我们鉴定了几种新的和微小的基因组扩增，其包含人类胰腺癌中的候选癌基因。
