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作 者:焦杨[1] 班克臣[2] 曹骥[2] 岳海英[2] 罗元[2] 苏建家[2]
机构地区:[1]广西医科大学药理学教研室,广西南宁530021 [2]广西医科大学附属肿瘤医院病理研究室,广西南宁530021
出 处:《癌症》2007年第10期1085-1089,共5页Chinese Journal of Cancer
基 金:国家人事部留学人员科技活动择优资助项目(No2004-37)~~
摘 要:背景与目的:广西南部是肝细胞癌(hepatocellular carcinoma,HCC)高发地区,也是粮食受黄曲霉毒素B1(aflatoxin B1,AFB1)污染较重的地区。β-Catenin的异常表达与多种肿瘤有关,而AFB1是诱发HCC的重要因素。本研究旨在探讨AFB1高暴露地区HCC患者癌组织中β-Catenin基因突变及表达情况。方法:用基因直接测序、RT-PCR、免疫组化和Western blot等方法,检测52例来自广西南部AFB1高暴露地区HCC患者癌、癌旁组织和18例非肝癌肝组织中β-Catenin基因的表达。结果:癌组织中未见β-Catenin基因第三外显子的突变。β-Catenin mRNA在癌、癌旁和正常肝组织中的表达分别为0.42±0.24、0.20±0.16和0.23±0.12,癌组织中的表达显著高于癌旁组织或正常肝组织(P<0.01);免疫组化染色癌组织中阳性率为55.8%(29/52),显著高于癌旁组织[36.5%(19/52)](P<0.05)。β-Catenin蛋白表达与肝外转移、术后复发、门静脉癌栓和临床分期有关(P<0.05),而mRNA的表达与上述临床参数均无明显关系(P>0.05)。结论:β-Catenin在HCC组织中高表达,但其异常表达不是由基因第三外显子上GSK-3β磷酸化位点的突变引起。 BACKGROUND & OBJECTIVE: South Guangxi is an area with high incidence of hepatocellular carcinoma (HCC), and with severe contamination of dietary aflatoxin B1 (AFB1). The activation of β-Catenin is involved in many cancers. AFB1 may play a key role in hepatocarcinogenesis. This study was to explore the expression and mutation of β-Catenin in HCC patients from the area with high exposure level of AFB1. METHODS: The expression of β-Catenin in 52 specimens of HCC and para-HCC tissues, and 18 specimens of non-cancerous liver tissues from South Guangxi were detected by direct sequencing, reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot. RESULTS: No mutation in exon 3 of β-Catenin gene was found in HCC tissues. The mRNA level of β-Catenin was significantly higher in HCC tissues than in para-HCC tissues and non-cancerous tissues (0.42±0.24 vs. 0.20±0.16 and 0.23±0.12, P〈0.01). The positive rate of β-Catenin was significantly higher in HCC tissues than in para-HCC tissues (55.8% vs. 36.5%, P〈0.05). The expression of β-Catenin mRNA showed no significant correlation to clinicopathologic parameters of HCC (all P〉0.05), while the expression of β-Catenin protein was significantly correlated to metastasis, relapse, portal vein embolus, and clinical stage (all P〈0.05). CONCLUSION: β-Catenin is overexpressed in HCC, but its overexpression has no correlation to gene mutation at GSK-3β phosphorylation sites in exon 3.
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