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作 者:张帆[1] 马鸿达[1] 赵天如[1] 曹群[1] 王欣[1] 任志勇 张乃鑫[1]
出 处:《天津医药》1999年第7期387-389,共3页Tianjin Medical Journal
基 金:国家教委优秀青年教师基金
摘 要: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.
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