Marked genetic similarities between hepatitis B virus-positive and hepatitis C virus-positive hepatocellular carcinomas

被引:12
作者
Tornillo, L
Carafa, V
Richter, J
Sauter, G
Moch, H
Minola, E
Gambacorta, M
Bianchi, L
Vecchione, R
Terracciano, LM
机构
[1] Univ Basel, Inst Pathol, Basel, Switzerland
[2] Osped Niguarda Ca Granda, Dept Pathol, Milan, Italy
[3] Univ Naples Federico II, Dept Pathol, Naples, Italy
关键词
liver; hepatocellular carcinoma; cytogenetics; comparative genomic hybridization; hepatitis; HBV; HCV;
D O I
10.1002/1096-9896(2000)9999:9999<::AID-PATH706>3.0.CO;2-O
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Hepatocellular carcinoma (HCC) is one of the most common neoplasms worldwide. Well-established risk factors include infections with two very different viruses: the DNA virus causing hepatitis B (HBV) and the RNA virus inducing hepatitis C (HCV). In order to determine whether genetic differences exist between HBV- and HCV-induced HCC, 41 HCC samples of known vival status were examined by comparative genomic hybridization (CGH), The analysis revealed frequent deletions of 1p (24%), 4q (39%), 6q (41%), 8p (44%), 9p (24%), 11q (24%), 12q (22%), and 13q (39%), as well as common gains of 1q (46%), 6p + (20%), 8q + (41%), 11q (27%), and 17q + (37%). There was no significant difference in the number and type of chromosomal imbalances between 25 HCV- and 16 HBV-infected tumours. This is consistent with models suggesting that HBV and HCV cause cancer through non-specific inflammatory and regenerative processes, rather than through virus-specific interactions with defined target genes. Chromosomal imbalances were also unrelated to the grade and stage of HCC. This may suggest that most gross genomic alterations occur early during HCC development and that further progression of these tumours may be associated with other types of genetic changes, not detectable by CGH. In summary, these data show that characteristic gross genomic changes occur in HCC, but these alterations at present do not appear to have diagnostic or prognostic applications. Copyright (C) 2000 John Wiley & Sons, Ltd.
引用
收藏
页码:307 / 312
页数:6
相关论文
共 43 条
[1]
In situ detection of hepatitis B, C, and G virus nucleic acids in human hepatocellular carcinoma tissues from different geographic regions [J].
Abe, K ;
Edamoto, Y ;
Park, YN ;
Nomura, AMY ;
Taltavull, TC ;
Tani, M ;
Thung, SN .
HEPATOLOGY, 1998, 28 (02) :568-572
[2]
Ashida K, 1997, J CANCER RES CLIN, V123, P489
[3]
Frequency of mutation and deletion of the tumor suppressor gene CDKN2A (MTS1/p16) in hepatocellular carcinoma from an Australian population [J].
Biden, K ;
Young, J ;
Buttenshaw, R ;
Searle, J ;
Cooksley, G ;
Xu, DB ;
Leggett, B .
HEPATOLOGY, 1997, 25 (03) :593-597
[4]
Brechot C, 1998, HEPATO-GASTROENTEROL, V45, P1189
[5]
Impact of HBV HCV and GBV-C/HGV on hepatocellular carcinomas in Europe:: results of a European concerted action [J].
Bréchot, C ;
Jaffredo, F ;
Lagorce, D ;
Gerken, G ;
zum Büschenfelde, KM ;
Papakonstontinou, A ;
Hadziyannis, S ;
Romeo, R ;
Colombo, M ;
Rodes, J ;
Bruix, J ;
Williams, R ;
Naoumov, N .
JOURNAL OF HEPATOLOGY, 1998, 29 (02) :173-183
[6]
Bringuier PP, 1996, ONCOGENE, V12, P1747
[7]
LOSS OF HETEROZYGOSITY SUGGESTS TUMOR SUPPRESSOR GENE RESPONSIBLE FOR PRIMARY HEPATOCELLULAR-CARCINOMA [J].
BUETOW, KH ;
MURRAY, JC ;
ISRAEL, JL ;
LONDON, WT ;
SMITH, M ;
KEW, M ;
BLANQUET, V ;
BRECHOT, C ;
REDEKER, A ;
GOVINDARAJAH, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (22) :8852-8856
[8]
CELL-PROLIFERATION IN CARCINOGENESIS [J].
COHEN, SM ;
ELLWEIN, LB .
SCIENCE, 1990, 249 (4972) :1007-1011
[9]
Lineage- and stage-specific expression of runt box polypeptides in primitive and definitive hematopoiesis [J].
Corsetti, MT ;
Calabi, F .
BLOOD, 1997, 89 (07) :2359-2368
[10]
HEPATITIS-B VIRUS-DNA INTEGRATION IN A SEQUENCE HOMOLOGOUS TO V-ERB-A AND STEROID-RECEPTOR GENES IN A HEPATOCELLULAR-CARCINOMA [J].
DEJEAN, A ;
BOUGUELERET, L ;
GRZESCHIK, KH ;
TIOLLAIS, P .
NATURE, 1986, 322 (6074) :70-73