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机构地区:[1]复旦大学附属华山医院皮肤科,上海200040
出 处:《国际皮肤性病学杂志》2008年第1期37-39,共3页International Journal of Dermatology and Venereology
摘 要:p16是抑制CDK4和6的肿瘤抑制蛋白。高危型HPV中的致癌基因E7可使p16^INK4a失去pRb的反馈性抑制而过度表达且功能异常。低危型HPV感染相关的尖锐湿疣中p16^INK4a免疫活性表现为离散、点状分布的阳性。中高危HPV感染相关的鲍恩样丘疹病中p16^INK4a免疫活性表现为弥漫强阳性。p16^INK4a较HPV型别能更客观地推测尖锐湿疣、鲍恩样丘疹病恶变的可能。p16 protein is a tumor suppressor protein inhibiting cyclin-dependent kinases (CDK) 4 and 6. The E7 gene, an oncogene in high-risk types of HPV, could induce the overexpression and functional abnormality of P16^INK4a by inhibiting the phosphorylation of pRb and withdrawing the negative feedback of it. P16^INK4a is dispersedly or punctiformly situated in the lesions of condyloma acuminatum related to low risk types of HPV infection, diffusely and massively distributed in the lesions of Bowenoid papulosis related to high- or intermediate-risk types of HPV infection. Compared with the typing of HPV, the detection of P16^INK4a could more objectively speculate the possibility of canceration of condyloma acuminatum and Bowenoid papulosis.
关 键 词:P16^INK4A基因 乳头瘤病毒 人 尖锐湿疣 鲍恩样丘疹病
分 类 号:R752[医药卫生—皮肤病学与性病学]
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