Simooka Hanako, Oyama Tetsunari, Sano Takaaki, Horiguchi Jun, Nakajima Takashi
Department of Tumor Pathology, Gunma University, Graduate School of Medicine, Gunma, Japan.
Pathol Int. 2004 Aug;54(8):595-602. doi: 10.1111/j.1440-1827.2004.01668.x.
In order to confirm the role of 14-3-3 sigma (sigma) as a tumor suppressor in breast carcinogenesis, we have studied the expression of 14-3-3sigma immunohistochemically in usual ductal hyperplasia (UDH), ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) breast lesions. Immunostaining for estrogen receptor alpha (ERalpha), p53 and estrogen-responsive RING finger protein (Efp) was also carried out. Immunohistochemically, expression of 14-3-3sigma was seen in 92% UDH lesions and gradually decreased from 65% in DCIS to 23% in IDC. The expression of ERalpha decreased gradually from UDH to DCIS to IDC, while p53 showed an inverse staining pattern to that of ERalpha. The expression of Efp showed no significant difference among the three breast lesions. Hence, the present immunohistochemical study confirmed 14-3-3sigma as a tumor suppressor in breast carcinogenesis. A similar immunohistochemical analysis was then carried out on columnar cell hyperplasia with atypia (CCHA), in which the expression pattern of tumor suppressor 14-3-3sigma, ERalpha and p53 suggested that it might be possible that CCHA is a precancerous lesion.
为了证实14-3-3σ在乳腺癌发生过程中作为肿瘤抑制因子的作用,我们采用免疫组织化学方法研究了14-3-3σ在普通导管增生(UDH)、导管原位癌(DCIS)和浸润性导管癌(IDC)乳腺病变中的表达情况。同时还进行了雌激素受体α(ERα)、p53和雌激素反应性环指蛋白(Efp)的免疫染色。免疫组织化学结果显示,14-3-3σ在92%的UDH病变中表达,从DCIS的65%逐渐下降至IDC的23%。ERα的表达从UDH到DCIS再到IDC逐渐降低,而p53的染色模式与ERα相反。Efp在三种乳腺病变中的表达无显著差异。因此,本免疫组织化学研究证实14-3-3σ在乳腺癌发生过程中是一种肿瘤抑制因子。随后对非典型柱状细胞增生(CCHA)进行了类似的免疫组织化学分析,其中肿瘤抑制因子14-3-3σ、ERα和p53的表达模式表明CCHA可能是一种癌前病变。