实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
9期
1391-1394
,共4页
贺琪%岳青%皮先明%石全%陈宏翔%李家文
賀琪%嶽青%皮先明%石全%陳宏翔%李傢文
하기%악청%피선명%석전%진굉상%리가문
p53%p33ING1b%银屑病%基底细胞癌%ING1
p53%p33ING1b%銀屑病%基底細胞癌%ING1
p53%p33ING1b%은설병%기저세포암%ING1
p53%p33ING1b%Psoriasis%Basal cell carcinoma%Inhibitor of growth 1 gene
目的:探讨肿瘤抑制因子p53和生长抑制因子p33ING1b在人类银屑病和基底细胞癌(basal cell carcinoma, BCC)中的表达情况及临床意义。方法:采用免疫组织化学Envision方法检测p53和p33ING1b在36例寻常型银屑病皮损(银屑病组)、28例BCC皮损(BCC组)和14例正常表皮(正常对照组)中的蛋白表达。结果:p53在正常对照组、银屑病组和BCC组中表达递增,p33ING1b在3组中表达递减,组间比较差异均有显著性(均P<0.05)。银屑病组和BCC组中,p53与p33ING1b之间均存在显著正相关(均P<0.05)。结论:p53和p33ING1b协同作用于增生性皮肤病的局部皮损,是细胞异常增殖的重要机制之一。
目的:探討腫瘤抑製因子p53和生長抑製因子p33ING1b在人類銀屑病和基底細胞癌(basal cell carcinoma, BCC)中的錶達情況及臨床意義。方法:採用免疫組織化學Envision方法檢測p53和p33ING1b在36例尋常型銀屑病皮損(銀屑病組)、28例BCC皮損(BCC組)和14例正常錶皮(正常對照組)中的蛋白錶達。結果:p53在正常對照組、銀屑病組和BCC組中錶達遞增,p33ING1b在3組中錶達遞減,組間比較差異均有顯著性(均P<0.05)。銀屑病組和BCC組中,p53與p33ING1b之間均存在顯著正相關(均P<0.05)。結論:p53和p33ING1b協同作用于增生性皮膚病的跼部皮損,是細胞異常增殖的重要機製之一。
목적:탐토종류억제인자p53화생장억제인자p33ING1b재인류은설병화기저세포암(basal cell carcinoma, BCC)중적표체정황급림상의의。방법:채용면역조직화학Envision방법검측p53화p33ING1b재36례심상형은설병피손(은설병조)、28례BCC피손(BCC조)화14례정상표피(정상대조조)중적단백표체。결과:p53재정상대조조、은설병조화BCC조중표체체증,p33ING1b재3조중표체체감,조간비교차이균유현저성(균P<0.05)。은설병조화BCC조중,p53여p33ING1b지간균존재현저정상관(균P<0.05)。결론:p53화p33ING1b협동작용우증생성피부병적국부피손,시세포이상증식적중요궤제지일。
Objective To discuss the expressions and clinical significance of p53 and p33ING1b in human psoriasis and basal cell carcinoma (BCC). Methods Immunohistochemistry EnVision technique was used to detect the expressions of p53 and p33ING1b in samples of 36 psoriasis vulgaris, 28 BCC and 14 normal skins. Results The expression of p53 increased while p33ING1b had a degressive expression in the control group, the psoriasis group and the BCC group. It was found significant statistical difference between the two groups (all P < 0.05). Prominent positive correlation between p53 and p33ING1b were found in both psoriasis group and BCC group (all P<0.05). Conclusions p53 coacts with p33ING1b at local lesions of abnormal proliferative diseases . It′s one of the most prominent mechanisms contributing to deviant cell proliferation.