Hepatitis C-associated hepatocellular carcinomas in non-cirrhotic livers.
Hepatitis C-associated hepatocellular carcinomas in non-cirrhotic livers.
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肝炎C相关的肝细胞癌在非卷肝肝脏中。
DOI：
10.1038/modpathol.2009.174
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发表时间：
2010-02
期刊：
影响因子：
--
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中科院分区：
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慢性丙型肝炎病毒感染可导致肝硬化和肝细胞癌。一般认为，丙型肝炎感染本身不是致癌的，但肝硬化的存在决定了肝细胞癌风险的增加。然而，对2001-2008年两个大型三级护理中心的手术病理学文件进行检索，共发现18例慢性丙型肝炎感染的非肝硬化肝细胞癌。在6例病例中，背景肝脏显示桥接纤维化，而其余病例显示较轻的纤维化阶段。病例的临床和血清学证据均为阴性，B型肝炎合并感染，并且通过福尔马林固定的石蜡包埋组织中的PCR检测隐性B型肝炎为阴性。肿瘤也阴性的TP 53，外显子7，密码子249突变，一个特征性的突变与黄曲霉毒素暴露密切相关。肝细胞癌具有典型的组织学特征，没有异常生长模式或组织学特征的富集。在这段时间内，所有切除的肝细胞癌中的非肝硬化肝脏，HCV感染的患病率为16%，显着高于预期的机会。总之，这些结果表明，肝细胞癌可以出现在肝脏慢性感染丙型肝炎，但没有肝硬化。这些发现提高了在某些情况下丙型肝炎感染和炎症可以直接致癌的可能性。在某些情况下，已建立的肝硬化也可能消退。无论机制如何，这些发现都强调了没有肝硬化的丙型肝炎感染个体发生肝细胞癌的重要和以前未被认识到的风险。
Chronic hepatitis C viral infection can lead to cirrhosis and hepatocellular carcinoma. It is generally believed that hepatitis C infection is not oncogeneic per se, but that the presence of cirrhosis determines the increased risk for hepatocellular carcinoma. However, a search of surgical pathology files from two large tertiary care centers for the years of 2001–2008 identified a total of 18 hepatocellular carcinomas in non-cirrhotic livers with chronic hepatitis C infection. In six cases the background livers showed bridging fibrosis while the remainder showed lesser stages of fibrosis. Cases were negative for clinical and serologic evidence of hepatitis B coinfection and occult hepatitis B testing was negative by PCR in formalin-fixed, paraffin embedded tissues. The tumors were also negative for TP53, exon 7, codon 249 mutations, a characteristic mutation strongly linked to aflatoxin exposure. The hepatocellular carcinomas had typical histology with no enrichment for unusual growth patterns or histological features. Amongst all resected hepatocellular carcinomas in non-cirrhotic livers over this time period, the prevalence of 16% with HCV infection was significantly greater than expected by chance. In conclusion, these results demonstrate that hepatocellular carcinomas can arise in livers chronically infected with hepatitis C but without cirrhosis. These findings raise the possibility that in some cases hepatitis C infection and inflammation can be directly oncogeneic. It is also possible that established cirrhosis may have regressed in some cases. Regardless of the mechanism, these findings highlight an important and previously under-recognized risk for hepatocellular carcinoma in hepatitis C infected individuals who do not have cirrhosis.
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影响因子：
13.5
作者：
Fukutomi, T;Zhou, YH;Li, JS
通讯作者：
Li, JS
影响因子：
13.5
作者：
EGUCHI, A;NAKASHIMA, O;KOJIRO, M
通讯作者：
KOJIRO, M
影响因子：
--
作者：
Evert, M.;Dombrowski, F.
通讯作者：
Dombrowski, F.
DOI：
10.1007/bf01605457
发表时间：
1993-05-01
期刊：
VIRCHOWS ARCHIV A-PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
影响因子：
--
作者：
TERADA, T;UEDA, K;NAKANUMA, Y
通讯作者：
NAKANUMA, Y
影响因子：
64.8
作者：
HSU, IC;METCALF, RA;HARRIS, CC
通讯作者：
HARRIS, CC