Kiyohara Chikako, Ohno Yoshiyuki
Department of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan.
Gend Med. 2010 Oct;7(5):381-401. doi: 10.1016/j.genm.2010.10.002.
Several epidemiologic and molecular epidemiologic studies have indicated that, for a given number of cigarettes smoked, women may be at higher risk of lung cancer compared with men.
The objective of this article was to address sex differences in lung cancer susceptibility, with special emphasis on genetic, biological, and sex-related hormonal factors.
Using the search terms gender or sex difference in combination with lung cancer, susceptibility, survival, polymorphism, biomarker, and smoking, we conducted a review of the available literature in the MEDLINE, Current Contents, and Web of Science biomedical databases. Relevant English-language publications (January 1966-December 2009) on sex differences in lung cancer were identified.
Higher levels of polycyclic aromatic hydrocarbon DNA adducts were observed in female lung cancer patients compared with their male counterparts, even though the level of tobacco carcinogens was lower among women than among men. DNA repair capacity was found to be lower in female lung cancer patients than in their male counterparts. A higher frequency of G-to-T transversion mutations in the tumor suppressor protein p53 gene has been observed in women compared with men. Non-small cell lung tumors in women appeared to be more likely than those in men to harbor K-ras, c-erbB-2, or epidermal growth factor receptor mutations. Sex differences have been identified in the expression of the cytochrome P4501A1 gene and gastrin-releasing peptide receptor gene, with women exhibiting higher gene expression than men for both of these genes. Evidence supporting a possible association between estrogen and lung cancer risk based on epidemiologic studies has not been consistent, but sex hormones may influence susceptibility to lung carcinogenesis.
Women may be more susceptible to tobacco smoke and potentially more vulnerable to lung cancer development. If additional studies yield supporting evidence, researchers, the public, and policy makers should focus on ways to reduce the risk of lung cancer for women.
多项流行病学和分子流行病学研究表明，在吸烟量相同的情况下，女性患肺癌的风险可能高于男性。
本文旨在探讨肺癌易感性的性别差异，特别关注遗传、生物学和与性别相关的激素因素。
我们使用“性别差异”与“肺癌”、“易感性”、“生存率”、“多态性”、“生物标志物”及“吸烟”等组合关键词，对MEDLINE、《现刊目次》和科学网生物医学数据库中的现有文献进行了综述。确定了有关肺癌性别差异的相关英文出版物（1966年1月至2009年12月）。
与男性肺癌患者相比，女性肺癌患者体内多环芳烃DNA加合物水平更高，尽管女性体内烟草致癌物水平低于男性。发现女性肺癌患者的DNA修复能力低于男性患者。与男性相比，女性肿瘤抑制蛋白p53基因中G到T颠换突变的频率更高。女性的非小细胞肺癌似乎比男性更有可能携带K-ras、c-erbB-2或表皮生长因子受体突变。已发现细胞色素P4501A1基因和胃泌素释放肽受体基因的表达存在性别差异，女性这两个基因的表达均高于男性。基于流行病学研究支持雌激素与肺癌风险之间可能存在关联的证据并不一致，但性激素可能影响肺癌发生的易感性。
女性可能对烟草烟雾更敏感，患肺癌的可能性可能更高。如果更多研究提供支持证据，研究人员、公众和政策制定者应关注降低女性肺癌风险的方法。
