Syrjänen K J
Unità di Citoistopatologia, Laboratorio di Epidemiologia e Biostatistica, Istituto Superiore di Sanità, Roma, Italy.
J Clin Pathol. 2002 Dec;55(12):885-91. doi: 10.1136/jcp.55.12.885.
Because of the major clinical impact of bronchial cancer worldwide, the possibility that human papillomavirus (HPV) contributes to its pathogenesis as a co-carcinogen is an intriguing one. Bronchial squamous cell carcinoma develops through well defined precursor lesions, often at the sites of squamous metaplasia. Benign squamous cell papillomas are rare but HPV DNA has been found in almost half of those studied, implicating a causal association. In invasive bronchial cancer, morphological changes seen in HPV lesions elsewhere are often seen. HPV DNA has been detected in 21.7% of the 2,468 bronchial carcinomas analysed to date and the same high risk types implicated in other squamous cell cancers have been identified. Clearly, more effort should be focused on assessing the role of HPV in bronchial carcinogenesis, by analysing the synergistic effects of carcinogenic agents (cigarette smoke, radiation, asbestos, etc) and HPV in different experimental settings.
鉴于支气管癌在全球范围内具有重大临床影响,人乳头瘤病毒(HPV)作为一种协同致癌物参与其发病机制的可能性是一个引人关注的问题。支气管鳞状细胞癌通过明确的前驱病变发展而来,这些病变常发生于鳞状化生部位。良性鳞状细胞乳头状瘤罕见,但在近半数研究病例中发现了HPV DNA,这表明存在因果关联。在浸润性支气管癌中,常可见到在其他部位HPV病变中出现的形态学改变。在迄今分析的2468例支气管癌中,21.7%检测到了HPV DNA,并且已鉴定出与其他鳞状细胞癌相关的相同高危型别。显然,应通过分析致癌物(香烟烟雾、辐射、石棉等)与HPV在不同实验环境中的协同作用,将更多精力集中于评估HPV在支气管癌发生中的作用。