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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.