Denaro N, Lo Nigro C, Natoli G, Russi E G, Adamo V, Merlano M C
Oncology Department, ASO Santa Croce e Carle Cuneo, Via Michele Coppino 21, 12100 Cuneo, Italy.
ISRN Otolaryngol. 2011 Dec 7;2011:931813. doi: 10.5402/2011/931813. Print 2011.
Head and neck cancer is a complex disorder that includes mostly squamous cell carcinomas that can develop in the throat, larynx, nose, sinuses, and mouth. Etiopathogenesis is due to tobacco and alcohol consumption and to infection by human papillomavirus (HPV) type 16/18. Tumors often develop within preneoplastic fields of genetically altered cells. Most head and neck cancers result from multistep accumulation of genetic alterationsm resulting in clonal outgrowth of transformed cells. These DNA changes are caused by a variety of mechanisms like endogenous mutations and exogenous mutations. Dysregulated molecular pathway includes alterations of critical inhibitor of cyclin CDK complexes, inactivating mutations of p53 gene, and activation of oncogenes and growth factors. This paper attempts to review the role of p53 and MDM2 genetic aberrations and pathways in head and neck cancer.
头颈癌是一种复杂的疾病,主要包括可发生于咽喉、喉、鼻、鼻窦和口腔的鳞状细胞癌。其病因发病机制归因于烟草和酒精消费以及人乳头瘤病毒16/18型(HPV)感染。肿瘤通常在基因改变细胞的癌前区域内发展。大多数头颈癌是由基因改变的多步骤积累导致的,从而引起转化细胞的克隆性生长。这些DNA变化是由多种机制引起的,如内源性突变和外源性突变。失调的分子途径包括细胞周期蛋白CDK复合物关键抑制剂的改变、p53基因的失活突变以及癌基因和生长因子的激活。本文试图综述p53和MDM2基因畸变及途径在头颈癌中的作用。