Inflammation and apoptosis in malignant transformation of sinonasal inverted papilloma: the role of the bridge molecules, cyclooxygenase-2, and nuclear factor κB
Inflammation and apoptosis in malignant transformation of sinonasal inverted papilloma: the role of the bridge molecules, cyclooxygenase-2, and nuclear factor κB
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DOI：
10.1016/j.amjoto.2012.07.008
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发表时间：
2013-01-01
影响因子：
2.5
通讯作者：
Roh, Hwan-Jung
中科院分区：
文献类型：
--
作者：
Yoon, Bit-Na;Chon, Kyong-Myong;Roh, Hwan-Jung
目的：本研究从慢性炎症和细胞凋亡的角度探讨了鼻窦内翻性乳头状瘤向鳞状细胞癌肿瘤进展的早期事件。 材料和方法：总共 118 张来自 45 名患者的苏木精和伊红染色存档玻片根据组织病理学进行分级（I-IV 级）。将其代表性部分转移到组织微阵列中，对切片进行环氧合酶2、p53、bax、bcl-2和核因子κB的免疫组化染色。结果：环氧合酶2表达与组织病理学分级呈正相关，高级分级中表达较高。 p53 在高级年级（III、IV）的所有核心中均检测到，但在早期年级（I、II）中未检测到。核因子kappa B、bax、bcl-2的表达与分级无关。结论：p53突变可能是鼻腔鼻窦内翻性乳头状瘤恶变的关键事件。由于 p53 突变而激活的 Cyclooxygenase-2 介导的炎症信号可能有助于促进晚期鼻腔内翻性乳头状瘤的增殖。 (C) 2013 Elsevier Inc. 保留所有权利。
Purpose: This study examined the early events in the neoplastic progression of the sinonasal inverted papilloma to squamous cell carcinoma from the viewpoint of chronic inflammation and apoptosis.Materials and methods: In total, 118 archival slides stained with hematoxylin and eosin from 45 patients were graded according to histopathology (grades I-IV). Their representative portions were transferred to a tissue microarray, sections of which were stained immunohistochemically for cyclooxygenase-2, p53, bax, bcl-2, and nuclear factor kappa B.Results: Cyclooxygenase-2 expression was positively correlated with histopathologic grade, with higher expression in advanced grades. p53s were detected in all cores from advanced grades (III, IV), but not in early grades (I, II). The expressions of nuclear factor kappa B, bax, and bcl-2 were not correlated with the grade.Conclusions: A p53 mutation seems be a critical event for the malignant transformation of the sinonasal inverted papilloma. Cyclooxygenase-2 mediated inflammatory signals, activated as a consequence of the p53 mutation, may contribute to promoting the proliferation of the advanced sinonasal inverted papilloma. (C) 2013 Elsevier Inc. All rights reserved.