Karyotypic characterization of an established human hepatoma cell line HA22T/VGH

Wuu, Kuang-Dong; Kang, Lily; Su, Yuh-mey; Wang-Wuu, Sheng; Hu, Cheng-Po; Chang, Chung-Ming

doi:10.1016/0165-4608(87)90062-8

Cited by 6 publications

(2 citation statements)

References 8 publications

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“…Several at-tempts have been undertaken to characterize chromosomal abnormalities in HCC, most of them analysing transformed HCC cell lines by conventional cytogenetics [6,[18][19][20]30]. Consistent findings of these studies and of the few successful direct cytogenetic preparations of HCC [4,22,23,28] are polysomy and structural aberrations of chromosome 1 maintaining the centromeric region.…”

Section: Introductionmentioning

confidence: 94%

Trisomy 1 and 8 occur frequently in hepatocellular carcinoma but not in liver cell adenoma and focal nodular hyperplasia. A fluorescence in situ hybridization study

Nasarek

Werner

Nolte

et al. 1995

Vichows Archiv A Pathol Anat

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Conventional cytogenetic studies revealed gains and structural aberrations of chromosome 1 to be the most consistent chromosomal aberrations in hepatocellular carcinoma (HCC). We investigated touch preparations of eight HCC, five cholangiocellular carcinomas (CCC), five liver cell adenomas (LCA), four focal nodular hyperplasias (FNH) as well as nine specimens of normal liver tissue using fluorescence in situ hybridization (FISH) with centromere specific probes for chromosomes 1 and 8. Polysomies of chromosome 1, especially trisomy 1, were found in five of eight HCC and four of five CCC but in no normal liver tissue or benign tumour. Only three of seven cases of HCC revealed trisomy 8 whereas the five benign liver tumours and all normal liver tissues examined had disomy 8. Our results confirm conventional cytogenetic findings in terms of chromosome 1 aberrations in HCC although they are not specific for these types of malignant liver tumours. Since alpha-satellite probes were used in our study, only gains or losses including the centromeric regions of the chromosomes 1 and 8 could be detected. Nevertheless, our findings suggest that FISH may help in the differential diagnosis of malignant versus benign neoplasms of the liver.

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Section: Introductionmentioning

confidence: 94%

Trisomy 1 and 8 occur frequently in hepatocellular carcinoma but not in liver cell adenoma and focal nodular hyperplasia. A fluorescence in situ hybridization study

Nasarek

Werner

Nolte

et al. 1995

Vichows Archiv A Pathol Anat

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“…The scant karyotypic information on HCC has been largely due to the difficulty in achieving tumor metaphase cells with good chromosome morphology from short-term cultures. By use of classical cytogenetics, frequent aneuploidy in HCC was described, but the only recurring structural abnormality reported was on chromosome 1 (Simon et al, 1982(Simon et al, , 1991Pinto et al, 1985;Wuu et al, 1987;Parada et al, 1998). Karyotypic precision has been greatly facilitated in recent years by the development of powerful molecular cytogenetic techniques such as spectral karyotyping (SKY) and comparative genomic hybridization (CGH).…”

Section: Introductionmentioning

confidence: 94%

Consistent chromosome 10 rearrangements in four newly established human hepatocellular carcinoma cell lines

Pang

Wong

Lai

et al. 2001

Genes Chromosomes & Cancer

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Cancer cell lines represent an invaluable resource for isolation of novel genes relevant to tumor pathogenesis and as in vitro models. In this study, we report on the successful establishment of four cell lines from hepatocellular carcinoma tissue. These cell lines, designated HKCI-1, HKCI-2, HKCI-3, and HKCI-4, have been growing continuously for more than 24 months and have been passaged more than 50 times. A comprehensive cytogenetic characterization on the primary tumors and the derived cell lines was achieved by the combined approach of spectral karyotyping and comparative genomic hybridization. Chromosomal imbalances from the primary tumors were also maintained in the cell lines and included gains of 1q, 6p, 7, 10p, 17q, and 20 and loss of 4q. Recurring translocations included t(X;11), t(1;10), t(4;16), i(5)(p10), t(7;21), t(8;17), t(9;22), i(10)(p10), t(14;20), t(16;22), and t(17;19). It was noteworthy that consistent chromosome 10 aberrations, in particular t(1;10)(q10;p10), were detected in all four cell lines. Furthermore, microsatellite analysis on primary tumor and derived cell lines indicated a common deleted region of 10q23-q26. The functional importance of chromosome 10 aberrations in relation to the pathogenesis of HCC is unknown; however, the high frequency with which such aberrations were maintained in the cell lines suggests proliferative advantages of 10q loss or 10p gain in the multistep development of hepatic neoplasia.

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Cytogenetic analysis of human hepatocarcinoma cell line PLC-PRF-5 and its mutant clones with different degrees of cell differentiation

Grabovskaya¹,

Tugizov²,

Glukhova³

et al. 1993

Cancer Genetics and Cytogenetics

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Karyotypic characterization of an established human hepatoma cell line HA22T/VGH

Cited by 6 publications

References 8 publications

Trisomy 1 and 8 occur frequently in hepatocellular carcinoma but not in liver cell adenoma and focal nodular hyperplasia. A fluorescence in situ hybridization study

Trisomy 1 and 8 occur frequently in hepatocellular carcinoma but not in liver cell adenoma and focal nodular hyperplasia. A fluorescence in situ hybridization study

Consistent chromosome 10 rearrangements in four newly established human hepatocellular carcinoma cell lines

Cytogenetic analysis of human hepatocarcinoma cell line PLC-PRF-5 and its mutant clones with different degrees of cell differentiation

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