目的 研究肝细胞癌（HCC）中血管内皮生长因子（VEGF）、缺氧诱生因子1 alpha（HIF-1α）和表皮生长因子（EGF）的表达情况及其临床意义。方法 采用免疫组织化学SABC法检测36例HCC组织及其癌旁肝组织和6例正常肝组织中VEGF、HIF-1α和EGF的表达情况，研究这3个因子与HCC临床病理学资料、新生血管生成以及预后的关系。结果 36例HCC中VEGF、HIF-1α和EGF表达的阳性率分别为89%（32/36），67%（24/36）和75%（27/36），均高于相应的癌旁肝组织和正常肝组织（P<0.05）。光学显微镜下有静脉浸润的HCC组织中VEGF和HIF-1α的表达率分别为96%（23/24）和88%（21/24），高于光学显微镜下无静脉浸润者（75%和25%），差异有显著意义（P<0.05）。VEGF阴性组术后1、2年生存率均为100%，弱阳性组分别为87%和22%，强阳性组分别为54%和0，三组存活率的差异具有显著意义（P<0.05）。EGF 阴性组术后1、2年存活率分别为100%和60%，弱阳性组均为70%，强阳性组分别为27%和0、三组之间存活率的差异亦具有显著意义（P<0.05）。结论 HCC组织中VEGF、HIF-1α和EGF呈过量表达。HCC组织中VEGF、EGF和HIF-1α的表达与HCC中新生血管生成以及预后不良有密切关系。

目的 研究肝细胞癌（HCC）中表皮生长因子（EGF）与血管内皮生长因子（VEGF）过量表达的关系。方法 通过免疫组化SABC法，检测36例HCC组织及其相应癌旁肝组织和6例正常肝组织中EGF、VEGF和微血管密度的表达，并对这些指标进行相关分析。离体实验中，用重组人EGF刺激人肝癌细胞系HepG2，采用半定量逆转录PCR检测VEGF的表达情况。结果 36例HCC组织中，EGF和VEGF表达阳性率分别为75.0%和88.9%。Spearman等级相关分析显示，HCC组织中EGF的表达与VEGF的表达具有明显的正相关关系（r=0.462，P<0.01) 。重组人EGF可以以浓度和时间依赖性的方式诱导HepG2细胞中VEGF的转录。结论 HCC中EGF的表达是VEGF过量表达的基本原因之一。

AIM: To study the difference in gene expression between solitary large hepatocellular carcinoma (SLHCC) and nodular hepatocellular carcinoma (NHCC). METHODS: Polymerase chain reaction (PCR) products of 8464 human genes were spotted on a chip in array. DNAswere then fixed on a glass plate. Total RNA was isolated from freshly excised human SLHCC (n=7) and NHCC (n=15) tissues, and was reversely transcribed to cDNAs with the incorporation of fluorescent dUTP for preparation of hybridization probes. The mixed probes were then hybridizedto the cDNA microarray. After highly stringent washing, cDNA microarray was scanned for the fluorescent signalsto display the difference between the two kinds of HCC. In addition, the expression of RhoC and protocadherin LKC was also detected with the reverse transcriptase polymerase chain reaction (RT-PCR) method. RESULTS: Among the 8464 human genes, 668 (7.89%)genes were expressed differentially at the mRNA levels between SLHCC and NHCC. Three hundred and fifty five (4.19%) genes, including protocadherin LKC, were upregulated,whereas 313 (3.70%) genes, including RhoC, were down-regulated. The mRNA expression levels of RhoC and protocadherin LKC were confirmed by RT-PCR. Analysis of differentially expressedgenes confirmed that our molecular data obtained by cDNA microarray were consistent with the published biochemical and clinical observations ofSLHCC and NHCC. CONCLUSION: cDNA microarray is an effective technique in screening the difference in gene expression between SLHCC and NHCC. Many of these differentially expressed genes are involved in the invasion and metastasis of HCC.Further analysis of these genes will help to understand thedifferent molecular mechanisms of SLHCC and NHCC.

AIM: To study the relationship between hypoxia or epidermal growth factor (EGF) and the overexpression of vascular endothelial growth factor (VEGF) in hepatocellular carcinoma (HCC) and the signal transduction pathway of the transcription of VEGF in hepatoma cells. METHODS: Cobalt chloride and recombinant human EGF were used to stimulate the hepatoma cell lines HepG2. VEGF mRNA was detected by using of semi-quantitative polymerase chain reaction (RT-PCR). Specific inhibitors of phosphatidylinositol 3-kinase (PI3K) and p42/p44 mitogen activated protein kinase (MAPK) were used to observe the effects of the two kinases on the regulation of the transcription of VEGF in hepatoma cells. RESULTS: The expression of VEGF mRNA in HepG2 cells cultured in serum-free mediumwas 0.117. However, 100 nmol/L cobalt chloride for 24 h increased the expression of VEGF mRNA and VEGF mRNA increased gradually with the increase of the concentration and duration of cobalt chloride. Also, 25ng/mL recombinant human EGF stimulated the expression of VEGF in HepG2 cells and the expression increased with the increase of EGF concentration. 5nmol/L LY294002 inhibited the expression of VEGF stimulated by cobalt chloride or recombinant human EGF and the inhibition decreased step by step with increase of the concentration of LY294002. But even 20 mol/L LY294002 could not completely block theexpression of VEGF. In contrast, PD98059 had no inhibitory effects on the transcription of VEGF stimulated by cobalt chloride or recombinant human EGF. CONCLUSION: The overexpression of VEGF in HCC could be promoted by hypoxia and EGF expression in HCC. The signal transduction pathway of VEGF transcription in HepG2 cells may be through PI3K pathway, but not through p42/p44 MAPK pathway.

AIM: To investigate the expression of RhoC gene in hepatocellular carcinoma (HCC) and to evaluate the relationship between RhoC gene expression and invasion and metastasis of HCC. METHODS: mRNA expression level of RhoC gene was examined by reverse transcription-polymerase chain reaction (RT-PCR) in 25 cases of HCC and para-cancerous normal liver tissues. In addition, mutation of RhoC gene was examined by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). RESULTS: The mRNA expression levels of RhoC in tumor tissues were significantly higher than those in para-cancerous normal liver tissues (1.8