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Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1–24.1
Author(s) -
Balsara Binaifer R.,
Pei Jianming,
De Rienzo Assunta,
Simon Daniela,
Tosolini Alessandra,
Lu You Yong,
Shen FuMin,
Fan Xianglin,
Lin WenYao,
Buetow Kenneth H.,
London W. Thomas,
Testa Joseph R.
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1083>3.0.co;2-m
Subject(s) - loss of heterozygosity , hccs , comparative genomic hybridization , biology , carcinogenesis , hepatocellular carcinoma , genetics , chromosome , suppressor , microsatellite , gene , tumor suppressor gene , cancer research , allele
Comparative genomic hybridization (CGH) analysis was used to identify chromosomal imbalances in 52 human primary hepatocellular carcinomas (HCCs). The most prominent changes were gains of part or all of chromosome arms 8q (83% of cases) and 1q (73%) and loss of 16q (63%). Other commonly overrepresented sites were 5p, 7q, and Xq. Recurrent sites of DNA sequence amplification included 8q23–24 (five cases) and 11q13–14 (four cases). Other frequently underrepresented sites were 4q, 8p, 16p, and 17p. Taken collectively, these findings and data from other CGH studies of HCCs define a subset of chromosome segments that are consistently over‐ or underrepresented and highlight sites of putative oncogenes and tumor suppressor genes, respectively, involved in hepatocellular oncogenesis. Loss of heterozygosity analysis with a panel of polymorphic microsatellite markers distributed along 16q defined a minimal region of chromosomal loss at 16q23.1–24.1, suggesting that this region harbors a tumor suppressor gene whose loss/inactivation may contribute to the pathogenesis of many HCCs. © 2000 Wiley‐Liss, Inc.