Mastronikolis Nicholas, Ragos Vasileios, Kyrodimos Efthymios, Chrysovergis Aristeidis, Papanikolaou Vasileios, Mastronikolis Stylianos, Stamatelopoulos Athanasios, Tsiambas Evangelos
Department of Pathology, Anticancer Oncologic Hospital "Saint Savvas", Athens, Greece.
J BUON. 2019 Nov-Dec;24(6):2242-2244.
Laryngeal squamous cell carcinoma (LSCC) demonstrates increased rates due to pathogenetic factors including tobacco, chronic alcohol consumption and also viral-mediated deregulation. During carcinogenetic process, laryngeal epithelia accumulate gross chromosome and specific gene aberrations. Oncogenes’ overactivation is a crucial genetic event in malignant and pre-malignant neoplastic epithelia. Among oncogenes, C-myc (gene locus: 8q24.12-q24.13) acts as a strong transcription factor, implicated in the control of cell differentiation and apoptosis. Upregulation of the gene - due to increased copy numbers (amplification) - seems to be correlated with aggressive biological behaviour in LSCCs. In the current special molecular article we explored the role of C-myc deregulation in LSCC.
喉鳞状细胞癌(LSCC)的发病率因包括烟草、长期饮酒以及病毒介导的失调等致病因素而上升。在致癌过程中,喉上皮细胞会累积大量染色体和特定基因畸变。癌基因的过度激活是恶性和癌前肿瘤上皮细胞中的关键遗传事件。在癌基因中,C-myc(基因位点:8q24.12-q24.13)作为一种强大的转录因子,参与细胞分化和凋亡的调控。由于拷贝数增加(扩增)导致该基因上调,似乎与LSCC的侵袭性生物学行为相关。在当前这篇特别的分子文章中,我们探讨了C-myc失调在LSCC中的作用。