Thun Michael J, Henley S Jane, Gansler Ted
Epidemiology and Surveillance Research, American Cancer Society, 1599 Clifton Road, Atlanta, GA 30329-4251, USA.
Novartis Found Symp. 2004;256:6-21; discussion 22-8, 49-52, 266-9.
Many chronic inflammatory conditions increase the risk of cancer in affected tissues. Clinical conditions that involve both inflammation and increased cancer risk include a broad range of immunological disorders, infections (bacterial, helminthic, viral), and chronic chemical and mechanical irritation. For example, the inflammatory bowel diseases, ulcerative colitis and Crohn's disease, predispose to the development of cancers of the large bowel and/or terminal ileum; chronic infection with the bacterium Helicobacter pylori causes atrophic gastritis, dysplasia, adenocarcinoma and an unusual form of gastric lymphoma; and parasitic infection with schistosomes and other trematodes cause cancers of the urinary bladder and the intrahepatic and extrahepatic biliary tract. Chronic reflux of gastric acid and bile into the distal oesophagus causes chemical injury, Barrett's oesophagus and oesophageal adenocarcinoma. Chronic cholecystitis and gallstones predispose to cancer of the gallbladder. Besides these clinical syndromes, subclinical inflammation may promote the development of certain tumours. The expression of COX-2 and lipid mediators of inflammation increases during the multistage progression of these tumours. Non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit COX-2 activity and tumour development in many experimental and clinical settings, are inversely associated with certain cancers in epidemiological studies. Despite their promise, however, anti-inflammatory drugs are not yet recommended for the prevention or treatment of any cancers. Numerous questions must be resolved concerning their molecular and cellular targets of action, efficacy, safety, treatment regimen, indications, and the balance of risks and benefits from treatment in designated patient populations.
许多慢性炎症性疾病会增加受影响组织患癌的风险。涉及炎症和癌症风险增加的临床病症包括广泛的免疫紊乱、感染（细菌、蠕虫、病毒）以及慢性化学和机械刺激。例如，炎症性肠病、溃疡性结肠炎和克罗恩病易引发大肠和/或回肠末端癌症；幽门螺杆菌慢性感染会导致萎缩性胃炎、发育异常、腺癌以及一种罕见的胃淋巴瘤；血吸虫和其他吸虫的寄生虫感染会引发膀胱癌以及肝内和肝外胆管癌。胃酸和胆汁长期反流至食管远端会造成化学损伤、巴雷特食管和食管腺癌。慢性胆囊炎和胆结石易引发胆囊癌。除了这些临床综合征外，亚临床炎症可能促进某些肿瘤的发展。在这些肿瘤的多阶段进展过程中，COX - 2和炎症脂质介质表达增加。在许多实验和临床环境中抑制COX - 2活性和肿瘤发展地非甾体抗炎药（NSAIDs），在流行病学研究中与某些癌症呈负相关。然而，尽管它们前景广阔，但抗炎药物尚未被推荐用于预防或治疗任何癌症。关于它们的分子和细胞作用靶点、疗效、安全性、治疗方案、适应症以及特定患者群体治疗的风险和益处平衡，仍有许多问题需要解决。
