Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1

Binaifer R. Balsara, Jianming Pei, Assunta De Rienzo, Daniela Simon, Alessandra Tosolini, You Yong Lu, Fu Min Shen, Xianglin Fan, Wen Yao Lin, Kenneth Buetow, W. Thomas London, Joseph R. Testa

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

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 Iq (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.

Original languageEnglish (US)
Pages (from-to)245-253
Number of pages9
JournalGenes Chromosomes and Cancer
Volume30
Issue number3
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Hepatocellular Carcinoma
Comparative Genomic Hybridization
Tumor Suppressor Genes
Chromosomes
Loss of Heterozygosity
Oncogenes
Microsatellite Repeats
Carcinogenesis

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

Cite this

Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1. / Balsara, Binaifer R.; Pei, Jianming; De Rienzo, Assunta; Simon, Daniela; Tosolini, Alessandra; Lu, You Yong; Shen, Fu Min; Fan, Xianglin; Lin, Wen Yao; Buetow, Kenneth; Thomas London, W.; Testa, Joseph R.

In: Genes Chromosomes and Cancer, Vol. 30, No. 3, 2001, p. 245-253.

Research output: Contribution to journalArticle

Balsara, Binaifer R. ; Pei, Jianming ; De Rienzo, Assunta ; Simon, Daniela ; Tosolini, Alessandra ; Lu, You Yong ; Shen, Fu Min ; Fan, Xianglin ; Lin, Wen Yao ; Buetow, Kenneth ; Thomas London, W. ; Testa, Joseph R. / Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1. In: Genes Chromosomes and Cancer. 2001 ; Vol. 30, No. 3. pp. 245-253.
@article{93ba8b212354453ab60aa22785aebac9,
title = "Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1",
abstract = "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 Iq (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.",
author = "Balsara, {Binaifer R.} and Jianming Pei and {De Rienzo}, Assunta and Daniela Simon and Alessandra Tosolini and Lu, {You Yong} and Shen, {Fu Min} and Xianglin Fan and Lin, {Wen Yao} and Kenneth Buetow and {Thomas London}, W. and Testa, {Joseph R.}",
year = "2001",
doi = "10.1002/1098-2264(2000)9999:9999<::AID-GCC1083>3.0.CO;2-M",
language = "English (US)",
volume = "30",
pages = "245--253",
journal = "Genes Chromosomes and Cancer",
issn = "1045-2257",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - Human hepatocellular carcinoma is characterized by a highly consistent pattern of genomic imbalances, including frequent loss of 16q23.1-24.1

AU - Balsara, Binaifer R.

AU - Pei, Jianming

AU - De Rienzo, Assunta

AU - Simon, Daniela

AU - Tosolini, Alessandra

AU - Lu, You Yong

AU - Shen, Fu Min

AU - Fan, Xianglin

AU - Lin, Wen Yao

AU - Buetow, Kenneth

AU - Thomas London, W.

AU - Testa, Joseph R.

PY - 2001

Y1 - 2001

N2 - 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 Iq (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.

AB - 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 Iq (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.

UR - http://www.scopus.com/inward/record.url?scp=0035150349&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035150349&partnerID=8YFLogxK

U2 - 10.1002/1098-2264(2000)9999:9999<::AID-GCC1083>3.0.CO;2-M

DO - 10.1002/1098-2264(2000)9999:9999<::AID-GCC1083>3.0.CO;2-M

M3 - Article

C2 - 11170281

AN - SCOPUS:0035150349

VL - 30

SP - 245

EP - 253

JO - Genes Chromosomes and Cancer

JF - Genes Chromosomes and Cancer

SN - 1045-2257

IS - 3

ER -