Molecular pathogenesis of head and neck squamous cell carcinoma
Molecular pathogenesis of head and neck squamous cell carcinoma
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DOI：
10.1007/s00405-003-0581-3
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发表时间：
2003-10-01
影响因子：
2.6
通讯作者：
Hardisson, D
中科院分区：
文献类型：
--
作者：
Hardisson, D
头颈鳞状细胞癌 (HNSCC) 占所有癌症的 6%。此类癌症患者的总体 5 年生存率是主要癌症类型中最低的，并且在过去十年中没有显着改善。病理分期，特别是淋巴结分期，是 HNSCC 最重要的因素。头颈肿瘤学缺乏进展强调了分子遗传学研究的重要性，以定义可能与肿瘤行为相关的改变。在 HNSCC 中观察到的分子改变主要是由于癌基因激活和抑癌基因失活，导致细胞增殖失调。这些改变包括基因扩增和癌基因（如 ras、myc、EGFR 和细胞周期蛋白 D1）的过度表达，以及导致 p16 和 TP53 肿瘤抑制基因失活的突变和缺失。本文回顾了 HNSCC 中常见的分子变化。讨论了这些标记物的生物学功能和潜在的临床应用。对 HNSCC 分子基础了解的进展将有助于识别新的分子标志物，这些标志物可用于更准确的诊断和预后评估，并可能为新的治疗和预防方法开辟道路。
Head and neck squamous cell carcinoma (HNSCC) represents 6% of all cancers. The overall 5-year survival rate for patients with this type of cancer is among the lowest of the major cancer types and has not improved dramatically during the last decade. The pathological staging, in particular the nodal stage, is the most important factor in HNSCC. The lack of progress in head and neck oncology emphasizes the importance of molecular genetic studies to define alterations that may correlate with tumor behavior. The molecular alterations observed in HNSCC are mainly due to oncogene activation and tumor suppressor gene inactivation, leading to deregulation of cell proliferation. These alterations include gene amplification and overexpression of oncogenes such as ras, myc, EGFR and cyclin D1, and mutations and deletions leading to p16 and TP53 tumor suppressor genes inactivation. This article reviews the molecular changes commonly observed in HNSCC. The biological function of these markers and the potential clinical application are discussed. Advances in the understanding of the molecular basis of HNSCC will help in the identification of new molecular markers that could be used for a more accurate diagnosis and assessment of prognosis and may open the way for novel approaches to treatment and prevention.