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Transposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model.

Nature genetics (2013-12-10)
Emilie A Bard-Chapeau, Anh-Tuan Nguyen, Alistair G Rust, Ahmed Sayadi, Philip Lee, Belinda Q Chua, Lee-Sun New, Johann de Jong, Jerrold M Ward, Christopher Ky Chin, Valerie Chew, Han Chong Toh, Jean-Pierre Abastado, Touati Benoukraf, Richie Soong, Frederic A Bard, Adam J Dupuy, Randy L Johnson, George K Radda, Eric Cy Chan, Lodewyk Fa Wessels, David J Adams, Nancy A Jenkins, Neal G Copeland
RESUMEN

The most common risk factor for developing hepatocellular carcinoma (HCC) is chronic infection with hepatitis B virus (HBV). To better understand the evolutionary forces driving HCC, we performed a near-saturating transposon mutagenesis screen in a mouse HBV model of HCC. This screen identified 21 candidate early stage drivers and a very large number (2,860) of candidate later stage drivers that were enriched for genes that are mutated, deregulated or functioning in signaling pathways important for human HCC, with a striking 1,199 genes being linked to cellular metabolic processes. Our study provides a comprehensive overview of the genetic landscape of HCC.

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Sigma-Aldrich
Ácido pirúvico, 98%
Sigma-Aldrich
Ácido pirúvico, ≥97%, FG
Sigma-Aldrich
Ácido pirúvico, 95%
Sigma-Aldrich
Ácido pirúvico, natural, ≥95%, FG