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Characterization of hepatocellular carcinoma developed after achieving sustained virological response to interferon therapy for hepatitis C
Author(s) -
Sanefuji Kensaku,
Kayashima Hiroto,
Iguchi Tomohiro,
Sugimachi Keishi,
Yamashita Yoichi,
Yoshizumi Tomoharu,
Soejima Yuji,
Nishizaki Takashi,
Taketomi Akinobu,
Maehara Yoshihiko
Publication year - 2008
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21176
Subject(s) - hepatocellular carcinoma , medicine , gastroenterology , hccs , pathological , hepatitis c virus , hepatectomy , immunohistochemistry , interferon , hepatitis c , carcinoma , oncology , immunology , virus , surgery , resection
Background Interferon (IFN) reduces the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C (CHC). However, HCC develops in the some patients who have achieved a sustained virological response (SVR). The aim of this study was to clarify the features and prognosis of SVR patients who developed HCC. Materials and Methods Twenty‐six patients who underwent curative hepatectomy for initial HCC after IFN therapy were closely investigated. Twenty patients who were seropositive for HCV‐RNA (non‐SVR), and a further 6 patients who achieved SVRs (SVR) were included. We analyzed the clinicopathological features, immunological expression levels of p53 and whether HCV‐RNA is present in the excised liver. Results The liver functions of the SVR group were almost better than those of the non‐SVR group. However, there was no significant difference in pathological features, surgical factors and prognosis between the groups. In one case with SVR out of eight specimens tested was HCV‐RNA detected in the non‐cancerous tissue. Immunohistochemistry revealed overexpression of p53 in eight HCCs (100%) from SVR patients. Conclusion Recurrent HCC still developed after the curative hepatectomy, even if viral elimination had been successful. And molecular alterations in hepatocarcinogenesis of SVR patients might be different from those of CHC patients. J. Surg. Oncol. 2009;99:32–37. © 2008 Wiley‐Liss, Inc.