Shalin Sara C, Sakharpe Aniket, Lyle Stephen, Lev Dina, Calonje Eduardo, Lazar Alexander J
Department of Pathology, Baylor College of Medicine, Houston, TX, USA.
Am J Dermatopathol. 2012 Apr;34(2):129-35; quiz 136-8. doi: 10.1097/DAD.0b013e3181ed39f9.
Sebaceous neoplasms are commonly considered in their relationship to the Muir-Torre syndrome and the now well-documented loss of DNA mismatch repair proteins leading to microsatellite instability. However, sebaceous neoplasms showing microsatellite instability comprise only a subset of this group of tumors, and thus, alternative tumorigenic mechanisms must exist. This article explores the relationship of p53, a tumor suppressor implicated in other cutaneous malignancies, and sebaceous neoplasia. We examined 94 sebaceous tumors from 92 patients. Tumors with strong nuclear p53 staining were significantly associated with the diagnosis of sebaceous carcinoma compared with benign sebaceous lesions, most notably for periocular carcinomas. Importantly, nuclear mismatch repair protein expression was intact in all lesions showing p53 alterations, suggesting that p53 dysfunction may represent a divergent pathway in the molecular pathogenesis of these tumors.
皮脂腺肿瘤通常被认为与穆尔-托里综合征以及现已充分记录的DNA错配修复蛋白缺失导致微卫星不稳定性有关。然而,表现出微卫星不稳定性的皮脂腺肿瘤仅占这组肿瘤的一个子集,因此,必然存在其他致瘤机制。本文探讨了p53(一种与其他皮肤恶性肿瘤相关的肿瘤抑制因子)与皮脂腺肿瘤形成之间的关系。我们检查了来自92例患者的94个皮脂腺肿瘤。与良性皮脂腺病变相比,核p53染色强的肿瘤与皮脂腺癌的诊断显著相关,尤其是眼周癌。重要的是,在所有显示p53改变的病变中,核错配修复蛋白表达均完整,这表明p53功能障碍可能代表了这些肿瘤分子发病机制中的一条不同途径。