Authors
Derek Y Chiang, Augusto Villanueva, Yujin Hoshida, Judit Peix, Philippa Newell, Beatriz Minguez, Amanda C LeBlanc, Diana J Donovan, Swan N Thung, Manel Sole, Victoria Tovar, Clara Alsinet, Alex H Ramos, Jordi Barretina, Sasan Roayaie, Myron Schwartz, Samuel Waxman, Jordi Bruix, Vincenzo Mazzaferro, Azra H Ligon, Vesna Najfeld, Scott L Friedman, William R Sellers, Matthew Meyerson, Josep M Llovet
Publication date
2008/8/15
Journal
Cancer research
Volume
68
Issue
16
Pages
6779-6788
Publisher
American Association for Cancer Research
Description
Hepatocellular carcinomas represent the third leading cause of cancer-related deaths worldwide. The vast majority of cases arise in the context of chronic liver injury due to hepatitis B virus or hepatitis C virus infection. To identify genetic mechanisms of hepatocarcinogenesis, we characterized copy number alterations and gene expression profiles from the same set of tumors associated with hepatitis C virus. Most tumors harbored 1q gain, 8q gain, or 8p loss, with occasional alterations in 13 additional chromosome arms. In addition to amplifications at 11q13 in 6 of 103 tumors, 4 tumors harbored focal gains at 6p21 incorporating vascular endothelial growth factor A (VEGFA). Fluorescence in situ hybridization on an independent validation set of 210 tumors found 6p21 high-level gains in 14 tumors, as well as 2 tumors with 6p21 amplifications. Strikingly, this locus overlapped with copy gains in 4 of 371 lung …
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Scholar articles
DY Chiang, A Villanueva, Y Hoshida, J Peix, P Newell… - Cancer research, 2008