CAJ | 학술논문

目的探讨肿瘤转移抑制基因 KAI1/ CD82、细胞黏附分子 CD44v6在人喉鳞状细胞癌（LSCC）、癌前病变、息肉以及正常黏膜中的表达。方法应用免疫组化法检测64例LSCC、21例喉癌前病变、15例喉息肉和15例正常喉黏膜组织中 KAI1/ CD82、CD44v6蛋白的表达水平。结果①KAI1/ CD82蛋白在正常喉黏膜及喉息肉组织中呈高表达，喉癌前病变及 LSCC 组织中呈低表达，阳性表达率分别为86.67%（13/15）、80.00%（12/15）、38.10%（8/21）、37.50%（24/64），正常喉黏膜与 LSCC 两者之间比较差异有统计学意义（P <0.05）。② CD44v6蛋白在正常喉黏膜及喉息肉中呈低表达，在喉癌前病变及 LSCC 组织中呈高表达，阳性表达率分别为26.67%（4/15）、33.33%（5/15）、80.95%（17/21）、75.00%（48/64），正常喉黏膜与 LSCC 两者之间比较差异有统计学意义（P <0.05）。结论① KAI1/ CD82表达下调、缺失及 CD44v6表达上调与 LSCC 的发生、发展相关。②联合检测 KAI1/ CD82和 CD44v6可为 LSCC 的早期诊断提供临床依据。
목적탐토종류전이억제기인 KAI1/ CD82、세포점부분자 CD44v6재인후린상세포암（LSCC）、암전병변、식육이급정상점막중적표체。방법응용면역조화법검측64례LSCC、21례후암전병변、15례후식육화15례정상후점막조직중 KAI1/ CD82、CD44v6단백적표체수평。결과①KAI1/ CD82단백재정상후점막급후식육조직중정고표체，후암전병변급 LSCC 조직중정저표체，양성표체솔분별위86.67%（13/15）、80.00%（12/15）、38.10%（8/21）、37.50%（24/64），정상후점막여 LSCC 량자지간비교차이유통계학의의（P <0.05）。② CD44v6단백재정상후점막급후식육중정저표체，재후암전병변급 LSCC 조직중정고표체，양성표체솔분별위26.67%（4/15）、33.33%（5/15）、80.95%（17/21）、75.00%（48/64），정상후점막여 LSCC 량자지간비교차이유통계학의의（P <0.05）。결론① KAI1/ CD82표체하조、결실급 CD44v6표체상조여 LSCC 적발생、발전상관。②연합검측 KAI1/ CD82화 CD44v6가위 LSCC 적조기진단제공림상의거。
Objective To study the expression of metastasic suppressor gene( KAI1 / CD82)and cell adhesion molecules(CD44v6)in human laryngeal squamous cell carcinoma(LSCC),precancerous lesion,polyps,and normal mucosa. Methods Immunohistochemical technique( Envision)was used to detect the expression of KAI1 / CD82 protein and CD44v6 protein in 64 cases of LSCC,21 cases of laryngeal precancerous lesion(LPL),15 cases of polyp of larynx(LP)and 15 cases of normal laryngeal mucosa(NLM). Results The result turned out to be as follows:①KAI1 / CD82 protein was highly expressed in NLM and LP,and lowly expressed in LPL and LSCC,the positive rates of KAI1 / CD82 protein expression were 86. 67%(13 / 15),80. 00%(12 / 15),38. 10%(8 / 21)and 37. 50%(24 /64),respectively. There was statistically significant difference in NLM and LSCC. ② CD44v6 protein was lowly ex-pressed in NLM and LP and highly expressed in LPL and LSCC,the positive rates of CD44v6 protein expression were 26. 67%(4 / 15),33. 33%(5 / 15),80. 95%(17 / 21)and 75. 00%(48 / 64),respectively. There was statisti-cally significant difference in NLM and LSCC. Conclusion ① The down-regulation or deletion of KAI1 / CD82 and the up-regulation of CD44v6 are related to carcinogenesis,development of LSCC. ② The combined detection of KAI1 / CD82 and CD44v6 may provide clinical basis for the early diagnosis of LSCC.