Luo Shi-Min, Tan Wei-Min, Deng Wei-Xiong, Zhuang Si-Min, Luo Jian-Wei
Department of Cadre Surgery, The First Municipal People's Hospital of Guangzhou, Guangzhou 510180, Guangdong Province, China.
World J Gastroenterol. 2005 Jul 21;11(27):4272-6. doi: 10.3748/wjg.v11.i27.4272.
To explore the expression of albumin (ALB), insulin-like growth factor (IGF)-1, and insulin-like growth factor binding protein (IGFBP)-3 in tumor tissues and adjacent non-tumor tissues of hepatocellular carcinoma (HCC) patients with cirrhosis.
Twenty-four HCC patients with cirrhosis who underwent hepatectomy were studied. ALB mRNA, IGF-1 mRNA, and IGFBP-3 mRNA in liver tissues (including tumor tissues and adjacent non-tumor tissues) were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Liver Ki67 immunohistochemistry staining was studied. At the same time, 12 patients with cholelithiasis or liver angioma who underwent operation were segregated as normal control.
In HCC patients with cirrhosis, hepatic ALB mRNA, IGF-1 mRNA, and IGFBP-3 mRNA of tumor tissues or adjacent non-tumor tissues were lower than the normal liver tissues, while in tumor tissues, hepatic ALB mRNA and IGFBP-3 mRNA were lower, hepatic IGF-1 mRNA was higher than in adjacent non-tumor tissues. Liver Ki67 labeling index (Ki67 LI) in tumor tissues or adjacent non-tumor tissues were higher than that in the normal liver tissues, while in tumor tissues it was higher than that in adjacent non-tumor tissues.
Imbalance of IGF-1 and IGFBP-3 may play a role in hepatocarcinogenesis and tumor development of liver cirrhosis patients.
探讨肝硬化肝细胞癌(HCC)患者肿瘤组织及癌旁非肿瘤组织中白蛋白(ALB)、胰岛素样生长因子(IGF)-1和胰岛素样生长因子结合蛋白(IGFBP)-3的表达情况。
对24例行肝切除术的肝硬化HCC患者进行研究。采用逆转录聚合酶链反应(RT-PCR)检测肝组织(包括肿瘤组织和癌旁非肿瘤组织)中的ALB mRNA、IGF-1 mRNA和IGFBP-3 mRNA。研究肝脏Ki67免疫组化染色情况。同时,将12例行手术的胆石症或肝血管瘤患者作为正常对照。
肝硬化HCC患者中,肿瘤组织或癌旁非肿瘤组织的肝脏ALB mRNA、IGF-1 mRNA和IGFBP-3 mRNA均低于正常肝组织,而在肿瘤组织中,肝脏ALB mRNA和IGFBP-3 mRNA较低,肝脏IGF-1 mRNA高于癌旁非肿瘤组织。肿瘤组织或癌旁非肿瘤组织的肝脏Ki67标记指数(Ki67 LI)高于正常肝组织,而在肿瘤组织中高于癌旁非肿瘤组织。
IGF-1与IGFBP-3的失衡可能在肝硬化患者肝癌发生及肿瘤发展中起作用。