Author/Authors :
Tsuji، نويسنده , , Kazuhiro and Yasui، نويسنده , , Kohichiroh and Gen، نويسنده , , Yasuyuki and Endo، نويسنده , , Mio and Dohi، نويسنده , , Osamu and Zen، نويسنده , , Keika and Mitsuyoshi، نويسنده , , Hironori and Minami، نويسنده , , Masahito and Itoh، نويسنده , , Yoshito and Taniwaki، نويسنده , , Masafumi and Tanaka، نويسنده , , Shinji and Arii، نويسنده , , Shigeki and Okanoue، نويسنده , , Takeshi and Yoshi، نويسنده ,
Abstract :
DNA copy number aberrations in human hepatocellular carcinoma (HCC) cell lines were investigated using a high-density oligonucleotide microarray, and a novel amplification at the chromosomal region 7q21 was detected. Molecular definition of the amplicon indicated that PEG10 (paternally expressed gene 10), a paternally expressed imprinted gene, was amplified together with CDK14 (cyclin-dependent kinase 14; previously PFTAIRE protein kinase 1, PFTK1) and CDK6 (cyclin-dependent kinase 6). An increase in PEG10 copy number was detected in 14 of 34 primary HCC tumors (41%). PEG10, but not CDK14 or CDK6, was significantly overexpressed in 30 of 41 tumors (73%) from HCC patients, compared with their nontumorous counterparts. These results suggest that PEG10 is a probable target, acting as a driving force for amplification of the 7q21 region, and may therefore be involved in the development or progression of HCCs.
