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目的:探讨瘢痕瘤的发生及其侵袭性生长失控的分子生物学基础。方法:以正常皮肤为对照,对增生性瘢痕和瘢痕瘤组织的DNA样本分别作Rb exon(14 ,27)和p53 exon (5 ~8) PCRSSCP分析。结果:26-1 %(6/23)的瘢痕瘤于Rb exon 27 处有异常电泳带,p53 exon (5 ~8)及其它标本均未见异常。结论:瘢痕瘤的发生或其侵袭性生长失控可能与Rb 肿瘤抑制基因突变或缺失有关。
Objective: To explore the molecular biological basis of the occurrence of keloid tumors and their invasive growth control. METHODS: Using normal skin as a control, DNA samples of hypertrophic scars and keloid tissues were analyzed by Rb exon (14, 27) and p53 exon (5-8) PCR-SSCP analyses, respectively. RESULTS: 26-1 % (6/23) of keloids had abnormal electrophoresis bands at Rb exon 27, and no abnormalities were found in p53 exon (5-8) and other specimens. Conclusion: The occurrence of keloid or its invasive growth may be related to the mutation or deletion of Rb tumor suppressor gene.