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人肝细胞癌的窦状毛细血管化:成纤维细胞生长因子可能的促进作用。

Sinusoidal capillarization of human hepatocellular carcinoma: possible promotion by fibroblast growth factor.

作者信息

Motoo Y, Sawabu N, Yamaguchi Y, Terada T, Nakanuma Y

机构信息

Department of Internal Medicine, Kanazawa University, Japan.

出版信息

Oncology. 1993 Jul-Aug;50(4):270-4. doi: 10.1159/000227194.

DOI:10.1159/000227194
PMID:8388557
Abstract

Expression of acidic and basic fibroblast growth factors (aFGF and bFGF) and von Willebrand factor (vWF) was immunohistochemically investigated in 55 nodules of human hepatocellular carcinoma (HCC), 15 nodules of adenomatous hyperplasia (AH) of the liver and 10 cirrhotic livers (LC). AH, a putative preneoplastic lesion in the cirrhotic liver, was subdivided into ordinary and atypical types: the former was characterized by little cellular and structural atypia and the latter had some atypia equivocal as to benignity and malignancy. The positive rates of FGF (aFGF and/or bFGF) were as follows: 0% in LC, 20% in AH (ordinary and atypical) and 42% in HCC, whereas the positivity of vWF was 10% in LC, 20% in ordinary AH, 30% in atypical AH and 40% in HCC. There was no correlation between the expression of FGF or vWF and the size of HCC. No correlation was also found between the positivity of FGF and that of vWF in HCC and atypical AH. While vWF was not constantly expressed in the vicinity of FGF-positive HCC cells, capillarized sinusoids were significantly more numerous in FGF-positive cases than in FGF-negative cases (p < 0.01). These data indicate that FGF may be pathogenetically linked to the multistep development of HCC in relation to sinusoidal capillarization.

摘要

采用免疫组织化学方法研究了55例人类肝细胞癌(HCC)结节、15例肝腺瘤样增生(AH)结节和10例肝硬化肝脏(LC)中酸性和碱性成纤维细胞生长因子(aFGF和bFGF)以及血管性血友病因子(vWF)的表达情况。AH是肝硬化肝脏中一种假定的癌前病变,分为普通型和非典型型:前者的特征是细胞和结构异型性小,后者有一些难以判定良恶性的异型性。FGF(aFGF和/或bFGF)的阳性率如下:LC中为0%,AH(普通型和非典型型)中为20%,HCC中为42%,而vWF的阳性率在LC中为10%,普通AH中为20%,非典型AH中为30%,HCC中为40%。FGF或vWF的表达与HCC的大小之间无相关性。在HCC和非典型AH中,FGF的阳性与vWF的阳性之间也未发现相关性。虽然vWF在FGF阳性的HCC细胞附近并非持续表达,但FGF阳性病例中的毛细血管化血窦明显多于FGF阴性病例(p<0.01)。这些数据表明,FGF可能在发病机制上与HCC的多步骤发展以及血窦毛细血管化有关。

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