Utikal Jochen, Leiter Ulrike, Udart Martin, Kaskel Peter, Peter Ralf Uwe, Krähn Gertraud M
Department of Dermatology, University Hospital of Mannheim, Ruprecht-Karls University, Heidelberg, 68135 Mannheim, Germany.
Cancer Invest. 2002;20(7-8):914-21. doi: 10.1081/cnv-120005904.
Apoptosis is an important co-factor in the pathogenesis of a plethora of malignancies. Enhanced c-myc activation can result either in proliferation or apoptosis. Coexpression with antiapoptotic bcl-2, which abrogates the apoptotic function of c-myc might lead to an enormous growth advantage of cells. In order to elucidate the role of c-myc and bcl-2 as well as the coexpression of both genes in human melanoma, their expression was studied in four samples of normal skin (SK), 15 surgical margins (SM), 20 benign melanocytic nevi (MN), 20 primary melanomas (MM), and 30 melanoma metastases (MMET) by RT-PCR. These results were compared with immunohistochemistry (IH) in 7 SK, 7 SM, 26 MN, 50 MM, and 34 MMET. Similar results were found with both methods. However, MMET expressed c-myc (PCR 28/30, IH 23/34) as well as bcl-2 (PCR 27/30, IH 24/34) more frequently. Primary melanomas showed a similar expression pattern as SM and nevi. Moreover, in contrast to SK, SM, MN, and MM coexpression of bcl-2 and c-myc was found more frequently in MMET (PCR 25/30, p < 0.01, IH 19/34, p < 0.01). These results indicate that coexpression of c-myc and bcl-2 appears to be associated with advanced melanoma and contributes to the malignant phenotype.
细胞凋亡是众多恶性肿瘤发病机制中的一个重要辅助因素。增强的c-myc激活可导致增殖或细胞凋亡。与抗凋亡的bcl-2共表达可消除c-myc的凋亡功能，这可能导致细胞具有巨大的生长优势。为了阐明c-myc和bcl-2的作用以及这两个基因在人类黑色素瘤中的共表达情况，通过逆转录聚合酶链反应（RT-PCR）对4份正常皮肤样本（SK）、15份手术切缘样本（SM）、20份良性黑素细胞痣样本（MN）、20份原发性黑色素瘤样本（MM）和30份黑色素瘤转移样本（MMET）进行了它们的表达研究。并将这些结果与7份SK、7份SM、26份MN、50份MM和34份MMET样本的免疫组织化学（IH）结果进行了比较。两种方法得到了相似的结果。然而，MMET更频繁地表达c-myc（PCR检测为28/30，IH检测为23/34）以及bcl-2（PCR检测为27/30，IH检测为24/34）。原发性黑色素瘤显示出与SM和痣相似的表达模式。此外，与SK、SM、MN和MM不同的是，在MMET中更频繁地发现bcl-2和c-myc的共表达（PCR检测为25/30，p<0.01；IH检测为19/34，p<0.01）。这些结果表明，c-myc和bcl-2的共表达似乎与晚期黑色素瘤相关，并有助于恶性表型的形成。
