Da Silva Leonard, Parry Suzanne, Reid Lynne, Keith Patricia, Waddell Nic, Kossai Myriam, Clarke Catherine, Lakhani Sunil R, Simpson Peter T
Molecular and Cellular Pathology, Mayne Medical School, University of Queensland, Brisbane, Australia.
Am J Surg Pathol. 2008 May;32(5):773-83. doi: 10.1097/PAS.0b013e318158d6c5.
Invasive lobular carcinoma (ILC) and lobular carcinoma in situ characteristically show loss of E-cadherin expression and so immunohistochemistry for E-cadherin is being increasingly used as a tool to differentiate between lobular and ductal lesions in challenging situations. However, misinterpretation of "aberrant" positive staining may lead some to exclude a diagnosis of lobular carcinoma. E-cadherin and beta-catenin immunohistochemistry was analyzed in 25 ILCs. E-cadherin "positive" ILCs were subjected to molecular analysis including comparative genomic hybridization. Different morphologic components of case 25, showing heterogenous E-cadherin expression, were analyzed by E-cadherin gene sequencing, methylation, and DASL gene expression profiling. Four ILCs were positive for E-cadherin, but each also had neoplastic cells with aberrant staining. Two of these ILCs were positive for beta-catenin, again with some aberrantly stained neoplastic cells, and 2 were negative. The solid component of case 25 was positive for E-cadherin whereas the classic and alveolar areas were negative. All components harbored an in-frame deletion in exon 7 (867del24) of the E-cadherin gene and loss of the wild type allele. Comparative genomic hybridization demonstrated evidence of clonal evolution from E-cadherin-positive to E-cadherin-negative components. E-cadherin down-regulation seems to be through transcriptional repression via activation of transforming growth factor-beta/SMAD2 rather than methylation. Positive staining for E-cadherin should not preclude a diagnosis of lobular in favor of ductal carcinoma. Molecular evidence suggests that even when E-cadherin is expressed, the cadherin-catenin complex maybe nonfunctional. Misclassification of tumors may lead to mismanagement of patients in clinical practice, particularly in the context of in situ disease at margins.
浸润性小叶癌(ILC)和小叶原位癌的特征是E-钙黏蛋白表达缺失,因此在具有挑战性的情况下,E-钙黏蛋白免疫组化正越来越多地被用作区分小叶和导管病变的工具。然而,对“异常”阳性染色的错误解读可能会导致一些人排除小叶癌的诊断。对25例ILC进行了E-钙黏蛋白和β-连环蛋白免疫组化分析。对E-钙黏蛋白“阳性”的ILC进行了包括比较基因组杂交在内的分子分析。对病例25中显示E-钙黏蛋白表达异质性的不同形态学成分进行了E-钙黏蛋白基因测序、甲基化和DASL基因表达谱分析。4例ILC的E-钙黏蛋白呈阳性,但每例也有异常染色的肿瘤细胞。其中2例ILC的β-连环蛋白呈阳性,同样有一些异常染色的肿瘤细胞,2例为阴性。病例25的实性成分E-钙黏蛋白呈阳性,而经典区和腺泡区为阴性。所有成分的E-钙黏蛋白基因外显子7(867del24)均存在框内缺失,野生型等位基因丢失。比较基因组杂交显示了从E-钙黏蛋白阳性成分到E-钙黏蛋白阴性成分的克隆进化证据。E-钙黏蛋白下调似乎是通过转化生长因子-β/SMAD2激活导致的转录抑制,而非甲基化。E-钙黏蛋白阳性染色不应排除小叶癌而支持导管癌的诊断。分子证据表明,即使E-钙黏蛋白表达,钙黏蛋白-连环蛋白复合物可能也无功能。肿瘤的错误分类可能导致临床实践中患者的管理不当,尤其是在切缘原位疾病的情况下。