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机构地区:[1]浙江省肿瘤医院,杭州310022
出 处:《实用肿瘤学杂志》2004年第3期175-177,共3页Practical Oncology Journal
摘 要:目的探讨c-fms癌基因与肝癌的关系及意义,为进一步阐明肝癌的发生机制提供依据。方法通过PCR-SSCP方法检测肝癌c-fms第301密码子的突变,并对肝癌组织行Ed-mondson分级来探讨与肝癌的临床关系。结果PCR扩增产物长度与预期一致,特异性高。SSCP检测发现18例肝癌组织第301位密码子DNA单链出现泳动变位,第969位密码子片段未出现异常泳动单链。测序示CSF-IR第301位密码子发生亮氨酸Leu(TTG)→丝氨酸Sel(TCG)置换,发生该位点突变的肝癌组织学分类为EdmondsonⅢ级11例、Ⅳ级7例,具有恶性程度高、发病年龄轻的特点。结论c-fms癌基因第301位密码子突变是肝癌发生发展的一种分子机制。Objective To study the clinical singificance and relationship between c-fms oncogene and hepatocellular carcinogensis, to further clarify the pathogenesis of hepatocellular carcinoma (HCC). Methods PCR- SSCP was performed, abnormal single strand band was cut off under ultraviolet, PCR was performed using the abnormal single band as template, PCR product was cloned into T vector to be sequenced. Histologi-cal classification was based on Edmondson standards Ⅰ-Ⅳ scale. Results The lengths of PCR products were consistent with the prediction with high specificity. SSCP showed two abnormal single strands in 18 HCC tissues of 301th codon PCR products. No abnormal single strands were observed in the 969th codon PCR products. DNA sequencing showed transition of Leu (TTG)→Ser (TCG) at 301st codon of CSF- 1R. Histological classification of the tumors were Edmondson Ⅲ in 11 case and Edmondson Ⅳ in 7 cases. The rumors had the characters of high degree malignancy and young age. Conclusion Mutation of c-fms codon at site 301 implied a molecular mechanism leading to hepatocellular carcinogenesis.
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