口腔疾病防治 ›› 2021, Vol. 29 ›› Issue (1): 65-68.DOI: 10.12016/j.issn.2096-1456.2021.01.011

• 综述 • 上一篇    下一篇

人类乳头瘤病毒阳性口咽癌对放疗敏感的研究进展

陈永菊(),黄子贤,陈睿,陈伟良()   

  1. 中山大学孙逸仙纪念医院口腔颌面外科,广东 广州(510120)
  • 收稿日期:2020-03-07 修回日期:2020-08-25 出版日期:2021-01-20 发布日期:2020-11-18
  • 通讯作者: 陈伟良
  • 作者简介:陈永菊,医师,博士研究生在读,Email: 282530449@qq.com
  • 基金资助:
    国家自然科学基金面上项目(81772888)

Research progress on HPV-positive oropharyngeal carcinoma sensitive to radiation therapy

CHEN Yongju(),HUANG Zixian,CHEN Rui,CHEN Weiliang()   

  1. Department of Oral and Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China
  • Received:2020-03-07 Revised:2020-08-25 Online:2021-01-20 Published:2020-11-18
  • Contact: Weiliang CHEN
  • Supported by:
    general program of National Natural Science Foundation of China(81772888)

摘要:

口咽癌(oropharyngeal carcinoma)是一种高度异质性疾病,其主要病因是烟草、酒精的滥用或高危人类乳头瘤病毒(human papillomavirus,HPV)感染的结果。HPV阳性口咽癌与HPV阴性口咽癌存在明显的病因、流行病学、预后等方面的差异,因此治疗上应采取不同的方法。目前已知HPV阳性口咽癌对放射治疗敏感,认为其对放疗敏感可能通过多种机制共同完成。HPV阳性口咽癌存在低表达的野生肿瘤蛋白p35(tumor protein p53,TP53)基因,放射治疗可通过DNA双链断裂损伤方式激活p53并诱导细胞发生凋亡;细胞对DNA损伤存在常见的非同源末端连接(non-homologous end joining,NHEJ)修复路径,HPV癌蛋白抑制该路径可使肿瘤对放疗更为敏感;此外,免疫应答在放疗作用下进一步激活也参与对肿瘤的消除作用。本文就HPV阳性口咽癌对放疗敏感的研究进行综述,为未来临床上针对口咽癌不同致病因素及临床分期采取针对性的治疗手段提供科学依据。

关键词: 口咽癌, 人类乳头瘤病毒, 放疗敏感, DNA损伤, 肿瘤蛋白p35, 非同源末端连接, 免疫应答, 细胞凋亡

Abstract:

Oropharyngeal carcinoma is a highly heterogeneous disease that is mainly caused by tobacco and alcohol abuse or high-risk human papillomavirus (HPV) infection. HPV-positive oropharyngeal carcinoma and HPV-negative oropharyngeal carcinoma have obvious differences in etiology, epidemiology and prognosis; therefore, different methods should be adopted for treatment. It is known that the TP53 gene is not mutated in HPV-positive oropharyngeal carcinoma, and radiation therapy can activate it and induce cell apoptosis via DNA damage. There are common repair pathways to DNA damage, such as nonhomologous end joining, and this pathway is more sensitive to radiotherapy under the inhibition of HPV oncoprotein. In addition, the further activation of the immune response under the effect of radiation also participates in the elimination of tumors. In this paper, we reviewed the research on the sensitivity of HPV-positive oropharyngeal cancer to radiotherapy to provide a scientific basis for targeted treatment for various pathogenic factors and clinical stages of oropharyngeal cancer in the future.

Key words: oropharyngeal carcinoma, human papillomavirus, radiosensitization, DNA damage, tumor protein p53, non-homologous end joining, immune response, apoptosis

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