Raju U, Crissman J D, Zarbo R J, Gottlieb C
Department of Pathology, Henry Ford Hospital, Detroit, MI 48202.
Am J Surg Pathol. 1990 Oct;14(10):939-47. doi: 10.1097/00000478-199010000-00007.
Epitheliosis is a benign intraluminal proliferation in the breast ducts and lobules that needs to be distinguished from ductal carcinoma in situ (DCIS). The histogenesis and differentiation of cells comprising epitheliosis have been the subject of some controversy. We evaluated the expression of a high-molecular-weight keratin (34 beta E12), muscle-specific actin (HHF-35), and S-100 protein immunoreactivity in formalin-fixed sections of the breast with epitheliosis and DCIS. In 28 of 30 cases of epitheliosis, there was strong HMW keratin immunoreactivity in the streaming sheetlike intraluminal proliferations. In contrast, 35 of 40 cases of DCIS (nonpapillary and papillary) were nonreactive for HMW keratin; the other five were weakly reactive. Furthermore, in 10 cases of DCIS, some ducts had isolated or small aggregates of HMW keratin-positive benign cells on the luminal aspects of the neoplastic proliferation that were reminiscent of a pagetoid pattern. Muscle actin-stained sections were analyzed to assess myoepithelial (ME) cell participation in epitheliosis. Muscle actin-positive ME cells were present at the periphery of the involved ducts but were absent or rare within epitheliosis. The distribution of ME cells--i.e., at the periphery of the spaces involved--was similar in DCIS and epitheliosis. S-100 protein was weakly but relatively consistently expressed by epitheliosis, but all cases of DCIS were negative. Six cases of atypical ductal hyperplasia included in the study were negative for HMW keratin, muscle actin, and S-100 protein. The immunohistochemical profile of epitheliosis indicates that it is primarily an epithelial proliferation with strong HMW keratin and weak S-100 protein expression but without ME cell participation. The distinct differences in HMW keratin expression of epitheliosis and intraductal carcinoma appear to reflect a consistent antigenic difference in these two biologically distinct forms of proliferation.
上皮组织增生是乳腺导管和小叶内的一种良性腔内增殖，需要与导管原位癌（DCIS）相鉴别。构成上皮组织增生的细胞的组织发生和分化一直存在一些争议。我们评估了高分子量角蛋白（34βE12）、肌肉特异性肌动蛋白（HHF-35）和S-100蛋白免疫反应性在伴有上皮组织增生和DCIS的乳腺福尔马林固定切片中的表达。在30例上皮组织增生病例中的28例，在流式片状腔内增殖中有强烈的高分子量角蛋白免疫反应性。相比之下，40例DCIS（非乳头状和乳头状）病例中的35例对高分子量角蛋白无反应；另外5例反应较弱。此外，在10例DCIS中，一些导管在肿瘤增殖的腔内方面有孤立的或小聚集的高分子量角蛋白阳性良性细胞，这让人联想到派杰样模式。分析肌肉肌动蛋白染色切片以评估肌上皮（ME）细胞在上皮组织增生中的参与情况。肌肉肌动蛋白阳性的ME细胞存在于受累导管的周边，但在上皮组织增生内不存在或罕见。ME细胞的分布——即在受累空间的周边——在DCIS和上皮组织增生中相似。上皮组织增生微弱但相对一致地表达S-100蛋白，但所有DCIS病例均为阴性。该研究中纳入的6例非典型导管增生对高分子量角蛋白、肌肉肌动蛋白和S-100蛋白均为阴性。上皮组织增生的免疫组织化学特征表明，它主要是一种上皮增殖，具有强烈的高分子量角蛋白和微弱的S-100蛋白表达，但没有ME细胞参与。上皮组织增生和导管内癌在高分子量角蛋白表达上的明显差异似乎反映了这两种生物学上不同的增殖形式在抗原性上的一致差异。
