title: Chromosome 8p deletion is associated with metastasis of human hepatocellular carcinoma when high and low metastatic models are compared.
abstract: Recently, we found that chromosome 8p deletion might be associated with hepatocellular carcinoma (HCC) metastasis by analyzing the differences in chromosomal alterations between primary tumors and their matched metastatic lesions of HCC with comparative genomic hybridization (CGH) (Qin et al. 1999). To further confirm this interesting finding, the genomic changes of two models bearing human HCC with different metastatic potentials (LCI-D20 and LCI-D35), and the new human HCC cell line with high metastatic potential (MHCC97) were analyzed by CGH. Gains on 1q, 6q, 7p, and 8q, and losses on 13p, 14p, 19p, 21, and 22 were detected in both LCI-D20 and LCI-D35 models. However, high copy number amplification of a minimum region at 1q12-q22 and 12q, and deletions on 1p32-pter, 3p21-pter, 8p, 9p, 10q, 14q, and 15p were detected only in the LCI-D20 model. Gains on 1p21-p32, 2p13-p21, 6p12-pter, 9p, 15q, and 16q11-q21, and losses on 2p23-pter, 4q24-qter, 7q31-qter, 12q, 17p, and 18 were detected only in the LCI-D35 model. The chromosomal aberration patterns in the MHCC97 cell line were similar to its parent LCI-D20 model, except that gains on 19q and losses on 4, 5, 10q, and 13q were found only in the cell line. These results provide some indirect clues to the metastasis-related chromosomal aberrations of HCC and further support the finding that 8p deletion is associated with HCC metastasis. 1q12-22 and 12q might harbor a novel oncogene(s) that contributes to the development and progression of HCC. Amplification on 8q and deletions on 4q and 17p may be not necessary for HCC metastasis.
authors.affiliation: Liver Cancer Institute and Zhongshan Hospital, Medical Center of Fudan University, Shanghai, China.
authors.forename: L X
authors.initials: LX
authors.lastname: Qin
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Tang
authors.forename: S L
authors.initials: SL
authors.lastname: Ye
authors.forename: Y K
authors.initials: YK
authors.lastname: Liu
authors.forename: Z C
authors.initials: ZC
authors.lastname: Ma
authors.forename: X D
authors.initials: XD
authors.lastname: Zhou
authors.forename: Z Q
authors.initials: ZQ
authors.lastname: Wu
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Lin
authors.forename: F X
authors.initials: FX
authors.lastname: Sun
authors.forename: J
authors.initials: J
authors.lastname: Tian
authors.forename: X Y
authors.initials: XY
authors.lastname: Guan
authors.forename: S D
authors.initials: SD
authors.lastname: Pack
authors.forename: Z P
authors.initials: ZP
authors.lastname: Zhuang
mesh_terms: D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000556:secondary*; D002872:Chromosome Deletion; D002878:Chromosomes, Human, Pair 1 / Q000235:genetics; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics; D002896:Chromosomes, Human, Pair 6 / Q000235:genetics; D002898:Chromosomes, Human, Pair 8 / Q000235:genetics*; D004195:Disease Models, Animal; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D007399:Interphase; D008113:Liver Neoplasms / Q000235:genetics* / Q000473:pathology*; D051379:Mice; D008819:Mice, Nude