摘要
目的:探讨角质形成细胞(KC)增生行为与p16INK4a蛋白表达及其基因失活的相关性。方法:对20例皮肤鳞状细胞癌、24例基底细胞癌、18例Bowen病、12例光线性角化病以及8例脂溢性角化病共计82例患者中具不同增生行为的KC,分别应用免疫组化检测其p16INK4a蛋白表达;应用聚合酶链反应(PCR)、PCR-单链构象多态性以及PCR-限制性内切酶分析方法分别检测p16INK4a基因外显子1和外显子2的缺失、突变和甲基化。结果:p16INK4a蛋白表达的阳性率和表达强度随着KC恶性程度的增加而降低,基因缺失和甲基化是皮肤癌p16INK4a基因失活的主要方式,p16INK4a蛋白失表达与其基因失活是一致的。结论:p16INK4a基因失活在KC恶性转化中起重要作用;p16INK4a基因有可能成为皮肤癌诊断与治疗的一种新靶位。
Objective: To elucidate the p16INK4a protein expression and gene inactivation mechanism in human keratinocytic tumors. Methods: A collection of 82 cases of keratinocytic tumors with different proliferative behavior were screened in our study, including 20 cases of cutaneous squamous cell carcinoma, 24 basal cell carcinoma, 18 Bowen's disease, 12 actinic keratosis, and 8 seborrheic keratosis. p16INK4a protein expression was detected by immunohistochemistry. p16INK4a gene extron 1 and extron 2 inactivation was detected by PCR for gene deletion, PCR-SSCP for gene mutation, and PCR-restriction enzyme assay for gene methylation respectively. Results: We found p16INK4a protein expression was markedly decreased in basal cell carcinoma and cutaneous squamous cell carcinoma, and gene deletion and methylation were the main mechanisms of p16INK4a gene inactivation, and p16INK4a protein expression was consistent with its gene inactivation in keratinocytic tumors. Conclusions: The results suggest that p16INK4a gene inactivation plays an important role in malignant transformation of keratinocytes, and p16INK4a gene might be a novel target for the diagnosis and treatment of skin cancers.
出处
《临床皮肤科杂志》
CAS
CSCD
北大核心
2005年第4期211-214,共4页
Journal of Clinical Dermatology
基金
江苏省重点学科基金资助项目(135-03)
