乳腺导管内增生性病变中ER、Ki-67和cyclin D1的表达

目的 探讨ER、Ki-67和cyclin D1在乳腺导管内增生性病变中的表达及意义。方法 采用免疫组化和免疫荧光双标记法对56例乳腺导管内增生性病变进行ER、 Ki-67和cyclin D1染色标记。结果 正常乳腺组织中仅有散在的少数上皮细胞呈ER阳性表达。在普通型导管增生（usual ductal hyperplasia，UDH）中ER表达比正常乳腺组织增加，但ER阳性细胞呈不连续分布，阳性细胞间有较多的阴性细胞。非典型性导管增生（atypical ductal hyperplasia，ADH）和低级别原位导管癌（ductal carcinoma in situ，DCIS）中ER表达比UDH明显增加（P〈0．05），ER阳性细胞呈连续的片状分布，阳性细胞间较少或没有ER阴性细胞。ADH和低级别DCIS中ER表达较高级DCIS显著（P〈0．01）。DCIS中Ki-67和cyclin D1表达高于UDH（P〈0．05），并与UDH、ADH和DCIS的组织学分组呈正相关（r=0．352，P〈0．05和r=0．390，P〈0．05）。正常乳腺组织中上皮细胞内无ER和Ki-67同时表达。在UDH中有极少数上皮细胞ER和Ki-67同时表达，而在ADH和DCIS中ER和 Ki-67同时表达的细胞明显增加。结论 从正常乳腺组织到UDH、ADH、低级DCIS的恶性转化过程中伴有ER表达的逐渐增高。ER过度表达及ER和Ki-67在上皮细胞内同时表达可能是某些乳腺癌发生过程中的早期事件。

Expression of ER, Ki-67 and cylin D1 in introductal proliferative lesions of breast

Purpose To investigate the expression and association of ER, Ki-67 and cyclin D1 in usual ductal hyperplasia (UDH), atypical ductal hyperplasia(ADH) and ductal carcinoma in situ (DCIS) in the breast. Methods Immunohistochemistry was used to determine the expression of ER, Ki-67 and cyclin D1 and double-lablling immunofluorescence technique was used to observe the coexpression of ER and Ki-67 in 56 cases of introductal proliferative lesions. Results The expression and distribution of ER-positive cells were significantly different in UDH, ADH and DCIS. The ER-positive cells were much more in UDH than in normal terminal ductal lobular units. The distribution of ER-positive cells interspersed amid ER-negative cells within UDH. However, the ER positive cells showed marked increases in ADH and low-grade DCIS(P<0.05), and distributed among almost all constituent cells. The expression of Ki-67 and cyclin D1 was significant difference between UDH and DCIS(P<0.05), and a positive correlation was found between Ki-67 and morphological classification of intraductal proliferative lesions (r=0.352, P<0.05) as well as cyclin D1(r=0.390,P<0.05). Double-labelling immunofluorescence showed that there was no coexpression of ER and Ki-67 in normal breast tissue. The coexpression of the two markers was found in ADH and increased in DCIS. Conclusions Overexpression of ER, Ki-67 and cyclin D1 is significantly associated with the transformation of normal cells and UDH into ADH and DCIS. The coexpression of ER and Ki-67 may present the early change in carcinogenesis of breast cancer.