乳腺导管上皮非典型增生actin的表达及其病理学意义

The Expression and Significance of Actin Protein in Atypical Breast Intraductal Hyperplasia

应用免疫组化技术对乳腺导管上皮轻、中度非典型增生（ＡＩＤＨ）６５例（轻中度组）、重度 ＡＩＤＨ ３０例（重度组）、浸润性导管癌 ４０例（导管癌组）和正常乳腺２０例（正常组）进行 ａｃｔｉｎ蛋白的检测。结果：（１）各组 ａｃｔｉｎ表达阳性率分别为正常组１００％（２０／２０例），轻、中度组１００％（６５／６５例），重度组７３．３％（２２／３０例），导管癌组１７．５％（７／４０例）。正常组和轻、中度组相同，其它各组之间比较均有显著性差异（ Ｐ＜ ０． ０５）。（ ２）阳性细胞（肌上皮细胞）的分布方式：正常组和轻、中度组的肌上皮细胞皆以连续性分布为主（分别占９０％和８１．４％），阴性表达率分别为１．５％和５．３％。重度组肌上皮细胞呈连续性分布者仅为２２．５％，１９．６％呈断续性分布和１８．６％呈零星散在，阴性表达率为 ３９． ３％。导管癌组的阴性表达率高达 ９６． ５％，个别呈现 ａｃｔｉｎ阳性的癌巢的上皮也多零星散在（ ２． ７％）或断续性分布（０．８％）。各组之间阳性细胞的分布方式均有显著性差异（Ｐ＜０．０５）或非常显著性差异（均Ｐ＜０．０１）。提示： ａｃｔｉｎ免疫组化检测可用作评估乳腺 ＡＩＤＨ程度及重度

For the purpose of detecting the expression and clinico-pathological significance of actin protein,65 cases of mild- mediate atypical intraductal hyperplasia (MMAIDH), 30 cases of severe atypical intraductal hyperplasia (SAIDH), 40 cases of infiltrating ductal carcinoma (IDCa) and 20 cases of normal breast (NB) were examined by immunohistochemistry technique. Results: (l)The positive expression in NB, MMAIDH, SAIDH,and IDCa for actin were 100 %, 100%, 73. 3%, and 17. 5 % respectively. There were the same rates of positive expression (100% ) in NB and MMAIDH, the significant differences in other between groups were shown (P< 0. 05 ). (2)The distribution modes of positive cells (myoepithelial cells): In NB and MMAIDH groups, the myoepithelial cells were expressed mainly as the consecutive distribution (90% and 81. 4 %, respectively), negative expression rates in ducts was 1. 5 % and 5. 3 %. In SAIDH group, the myoepithelial cells were expressed as the consecutive distribution 22. 5 %, intermittent distribution 19. 6 %, and negative expression rate 39. 3 %. In IDCa group, the negative expression rate of the myoepitehlial cells was 96. 5 %. There were significant differences between groups in the distribution modes of the positive cells (P < 0. 05 ). Conclusions: The detecting of actin by immunohistochemistry may be regarded as the reference index in evaluating the degree of breast intraductal hyperplasia and the potential power of malignant change of SAIDH.