Shimada M, Taguchi K, Hasegawa H, Gion T, Shirabe K, Tsuneyoshi M, Sugimachi K
Department of Surgery II, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Liver. 1998 Oct;18(5):337-42. doi: 10.1111/j.1600-0676.1998.tb00815.x.
AIMS/BACKGROUND: Decreased expression of nm23, a putative metastasis suppressor gene, has been reported to be related to either intrahepatic metastasis or a poor prognosis in hepatocellular carcinoma (HCC). The aim of this study was to elucidate the true role of nm23-H1 expression in both intrahepatic and distant metastases of HCC.
Thirteen patients with single-nodule HCC, seven patients with HCC having satellite nodules and seven patients with HCCs having extrahepatic metastases were included in this study. The expression of nm23-H1 protein was immunohistochemically examined in both primary and metastatic nodules.
Ten of 13 single-nodule HCCs were found to overexpress nm23-H1 protein. All main tumors, having satellite nodules, were found to overexpress nm23-H protein, except for two HCCs, which only partially expressed nm23-H1 protein. Regarding the nm23-H1 expression in intrahepatic metastases, most nodules overexpressed the protein. The expression of nm23-H1 was found to be low in only one intrahepatic metastasis specimen, while its primary tumor was also found to show a low expression of nm23-H1 protein. Microscopic portal vein invasion was found in three of the five patients studied, and all cancer cells in portal invasion overexpressed nm23-H1 protein. Nm23-H1 protein was expressed in all distant metastatic tumors and the staining intensity of most metastatic nodules was similar to that of the primary tumors.
Our study demonstrated that nm23-H1 expression did not always decrease but instead tended to increase at both intrahepatic and extrahepatic metastatic sites. Based on these findings, nm23-H1 expression is not considered to be a reliable indicator of either intrahepatic or distant metastasis in HCC.
目的/背景：据报道，假定的转移抑制基因nm23表达降低与肝细胞癌（HCC）的肝内转移或预后不良有关。本研究的目的是阐明nm23-H1表达在HCC肝内和远处转移中的真正作用。
本研究纳入了13名单发结节性HCC患者、7名伴有卫星结节的HCC患者和7名伴有肝外转移的HCC患者。通过免疫组织化学方法检测原发性和转移性结节中nm23-H1蛋白的表达。
13名单发结节性HCC中有10例被发现nm23-H1蛋白过度表达。所有伴有卫星结节的主要肿瘤均被发现nm23-H蛋白过度表达，但有2例HCC仅部分表达nm23-H1蛋白。关于肝内转移灶中nm23-H1的表达，大多数结节过度表达该蛋白。仅在1例肝内转移标本中发现nm23-H1表达较低，而其原发性肿瘤也显示nm23-H1蛋白低表达。在研究的5例患者中有3例发现镜下门静脉侵犯，门静脉侵犯中的所有癌细胞均过度表达nm23-H1蛋白。所有远处转移瘤均表达nm23-H1蛋白，大多数转移结节的染色强度与原发性肿瘤相似。
我们的研究表明，nm23-H1表达并非总是降低，而是在肝内和肝外转移部位均倾向于增加。基于这些发现，nm23-H1表达不被认为是HCC肝内或远处转移的可靠指标。
