Markers for Sebaceoma Show a Spectrum of Cell Cycle Regulators, Tumor Suppressor Genes, and Oncogenes.
Markers for Sebaceoma Show a Spectrum of Cell Cycle Regulators, Tumor Suppressor Genes, and Oncogenes.
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DOI：
10.4103/1947-2714.159338
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发表时间：
2015-06
期刊：
影响因子：
--
通讯作者：
Googe PB
中科院分区：
文献类型：
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作者：
Abreu Velez AM;Howard MS;Kim J;Googe PB
皮脂瘤是一种致癌基因尚不清楚的肿瘤。皮脂腺瘤的组织病理学特征与基底细胞癌相似，如栅栏状边缘和基底样细胞，以及泡沫状胞浆和锯齿状细胞核。我们检测了多种细胞周期、癌基因和抑癌基因标记物在皮脂腺瘤中的表达，试图找到适合该肿瘤的生物学标记物，并与其他已发表的研究进行比较。我们研究了一组对细胞信号传导非常重要的免疫组化（IHC）染色，包括我们的皮脂瘤队列中的细胞周期调节因子、肿瘤抑制基因、癌基因、激素受体和基因组稳定性标记物。我们从三个独立的美国皮肤病理学实验室收集了30个皮脂瘤。以下IHC组：我们的病例检测了上皮细胞膜抗原（EMA）/CD 227、细胞角蛋白AE 1/AE 3、细胞周期蛋白D1、人乳腺癌1蛋白（BRCA-1）、C-erb-2、Bcl-2、人雄激素受体（AR）、细胞周期蛋白依赖性激酶抑制剂1B（p27 kip 1）、p53、拓扑异构酶II α、增殖细胞核抗原和Ki-67。EMA/CD 227在高分化皮脂瘤中呈阳性表达（13/30）。细胞周期蛋白依赖性激酶抑制剂1B在中分化肿瘤中呈阳性表达（22/30）。分化较差的肿瘤不能用EMA和AR染色。在分化良好的栅栏状区的肿瘤中，拓扑异构酶II α、p27 kip 1和p53大多呈阳性表达，在肿瘤基底样区呈阳性表达（22/30）。许多肿瘤是局灶性阳性的多种标志物，表明在整个组中的变异性的显着程度。癌基因、肿瘤抑制基因、细胞周期调节因子和激素受体在皮脂瘤中表达异常。我们的研究结果表明，在这些肿瘤中，选择的标记物染色似乎与肿瘤分化相关;即，分化良好的肿瘤作为一个组，EMA和AR染色，栅栏区表现出一致的p53，拓扑异构酶II α和p27 kip 1染色。相比之下，分化较差的区域用不同谱的标记物染色。
Sebaceoma is a tumor for which the causative oncogenes are not well-understood. Sebaceomas demonstrate some histopathologic features similar to basal cell carcinoma (BCC), such as palisading borders and basaloid cells with additional features, including foamy cytoplasm and indented nuclei. We examine multiple cell-cycle, oncogene, and tumor suppressor gene markers in sebaceomas, to try to find some suitable biological markers for this tumor, and compare with other published studies. We investigated a panel of immunohistochemical (IHC) stains that are important for cellular signaling, including a cell cycle regulator, tumor suppressor gene, oncogene, hormone receptor, and genomic stability markers in our cohort of sebaceomas. We collected 30 sebaceomas from three separate USA dermatopathology laboratories. The following IHC panel: Epithelial membrane antigen (EMA)/CD227, cytokeratin AE1/AE3, cyclin D1, human breast cancer 1 protein (BRCA-1), C-erb-2, Bcl-2, human androgen receptor (AR), cyclin-dependent kinase inhibitor 1B (p27kip1), p53, topoisomerase II alpha, proliferating cell nuclear antigen, and Ki-67 were tested in our cases. EMA/CD227 was positive in the well-differentiated sebaceomas (13/30). Cyclin-dependent kinase inhibitor 1B was positive in tumors with intermediate differentiation (22/30). The less well-differentiated tumors failed to stain with EMA and AR. Most of the tumors with well-differentiated palisaded areas demonstrated positive staining for topoisomerase II alpha, p27kip1, and p53, with positive staining in tumoral basaloid areas (22/30). Numerous tumors were focally positive with multiple markers, indicating a significant degree of variability in the complete group. Oncogenes, tumor suppressor genes, cell cycle regulators, and hormone receptors are variably expressed in sebaceomas. Our results suggest that in these tumors, selected marker staining seems to correlate with tumor differentiation; that is, well-differentiated tumors as a group stained with EMA and AR, and palisaded areas demonstrated consistent p53, topoisomerase II alpha and p27kip1 staining. In contrast, less well-differentiated areas stained with a different spectrum of markers.