非类固醇抗炎药物和结直肠癌的分子致癌
G Huls1, J J Koornstra, J H Kleibeuker
1Department of Internal Medicine, University Hospital Groningen, Groningen, Netherlands. g.huls@int.azg.nl <g.huls@int.azg.nl>
Lancet (London, England)
|July 30, 2003
概括
包括阿司匹林在内的非类固醇抗炎药物 (NSAIDs) 在中等风险人群中对结直肠癌表现出中度的化学预防作用. 需要进一步研究以了解分子机制,如p21在NSAID中介癌症预防中的作用.
科学领域:
- 在瘤学瘤学.
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 结肠直肠癌是癌症死亡的主要原因,需要有效的预防策略.
- 非类固醇抗炎药物 (NSAIDs) 显示出对结直肠癌的化学预防性质.
- 以前的研究表明,NSAIDs如sulindac和celecoxib在家族腺瘤多重症患者中是有效的.
研究的目的:
- 评估阿司匹林在患有结直肠癌中等风险人群中的化学预防作用.
- 探索潜在的分子机制,在NSAID介导的结直肠癌化学预防的基础上.
主要方法:
- 分析了两个随机的安慰剂对照试验,研究阿司匹林对结直肠腺瘤复发的影响.
- 对NSAID机制的体外,动物,流行病学和干预研究的审查.
主要成果:
- 阿司匹林 (每天325毫克) 降低了之前患有结直肠癌的患者的复发腺瘤风险35%.
- 与安慰剂相比,较低剂量的阿司匹林 (81毫克) 也显示出减少腺瘤发病率的趋势.
- NSAIDs可能会诱导瘤细胞的亡,并可能涉及细胞循环调节器p21.
结论:
- 阿司匹林在患有中等结直肠癌风险的人群中表现出适度的化学预防作用.
- 细胞循环调节蛋白p21可能是NSAID化学预防作用的关键分子媒介.
- 了解这些机制可能会导致改善结直肠癌预防策略.
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