Murphy M, Mabruk M J E M F, Lenane P, Liew A, McCann P, Buckley A, O Flatharta C, Hevey D, Billet P, Robertson W, Javed S, Leader M, Kay E, Murphy G M
Department of Pathology, Royal College of Surgeons in Ireland, Dublin, Ireland.
J Clin Pathol. 2002 Nov;55(11):829-33. doi: 10.1136/jcp.55.11.829.
Ultraviolet light (UV) is known to cause DNA damage in the epidermis. The damaged DNA is repaired or deleted by apoptosis to prevent the generation of cancer. It has been suggested that a deficient apoptotic mechanism may predispose individuals to skin cancer. Therefore, the response of normal controls and patients with basal cell carcinoma (BCC) to UV irradiation was investigated.
The buttock skin from normal volunteers and patients with BCC was irradiated using solar simulated radiation (SSR). SSR mimics the effect of natural sunlight. Skin biopsies were excised and examined for p53, p21, and Bax protein expression and for the induction of apoptosis.
At 33 hours after UV irradiation, the induction of apoptosis was significantly higher (p = 0.04) in patients with BCC than in normal volunteers (Mann Whitney test). A trend towards higher p21 expression was found at 33 hours in patients with BCC (mean, 18.69 positive cells/field) than in normal volunteers (mean, 9.89), although this difference was not significant (p = 0.05 positive cells/field).
These results may imply that patients with BCC have enhanced sensitivity to UV irradiation or that there is some defect in the cell arrest or repair pathways, which results in damaged cells been pushed into apoptosis rather than repair.
紫外线(UV)已知会导致表皮中的DNA损伤。受损的DNA通过凋亡被修复或清除,以防止癌症的发生。有人提出,凋亡机制缺陷可能使个体易患皮肤癌。因此,研究了正常对照者和基底细胞癌(BCC)患者对紫外线照射的反应。
使用太阳模拟辐射(SSR)照射正常志愿者和BCC患者的臀部皮肤。SSR模拟自然阳光的效果。切除皮肤活检组织,检查p53、p21和Bax蛋白表达以及凋亡诱导情况。
紫外线照射后33小时,BCC患者的凋亡诱导率显著高于正常志愿者(p = 0.04)(Mann Whitney检验)。BCC患者在33小时时p21表达有升高趋势(平均,18.69个阳性细胞/视野),高于正常志愿者(平均,9.89个),尽管这种差异不显著(p = 0.05个阳性细胞/视野)。
这些结果可能意味着BCC患者对紫外线照射的敏感性增强,或者细胞停滞或修复途径存在某些缺陷,导致受损细胞被推向凋亡而非修复。