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乙型肝炎病毒阳性和丙型肝炎病毒阳性肝细胞癌之间存在显著的基因相似性。

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

作者信息

Tornillo L, Carafa V, Richter J, Sauter G, Moch H, Minola E, Gambacorta M, Bianchi L, Vecchione R, Terracciano L M

机构信息

Institute of Pathology, University of Basel, Basel, Switzerland.

出版信息

J Pathol. 2000 Nov;192(3):307-12. doi: 10.1002/1096-9896(2000)9999:9999<::AID-PATH706>3.0.CO;2-O.

Abstract

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.

摘要

肝细胞癌(HCC)是全球最常见的肿瘤之一。已明确的风险因素包括感染两种截然不同的病毒:引起乙型肝炎的DNA病毒(HBV)和诱发丙型肝炎的RNA病毒(HCV)。为了确定HBV和HCV诱发的HCC之间是否存在基因差异,通过比较基因组杂交(CGH)对41个已知病毒感染状态的HCC样本进行了检测。分析发现1p(24%)、4q(39%)、6q(41%)、8p(44%)、9p(24%)、11q(24%)、12q(22%)和13q(39%)频繁出现缺失,同时1q(46%)、6p+(20%)、8q+(41%)、11q(27%)和17q+(37%)出现常见的增加。在25个HCV感染肿瘤和16个HBV感染肿瘤之间,染色体失衡的数量和类型没有显著差异。这与以下模型一致,即HBV和HCV通过非特异性炎症和再生过程致癌,而非通过与特定靶基因的病毒特异性相互作用致癌。染色体失衡也与HCC的分级和分期无关。这可能表明大多数明显的基因组改变发生在HCC发展的早期,并且这些肿瘤的进一步进展可能与其他类型的基因变化有关,而CGH无法检测到这些变化。总之,这些数据表明HCC中会出现特征性的明显基因组变化,但目前这些改变似乎没有诊断或预后应用价值。

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