PHASE II CLINICAL TRIAL OF CELECOXIB IN PERSONS WITH GE

塞来昔布在 GE 患者中的 II 期临床试验

• 批准号: 6357838
• 负责人: PATRICK M. LYNCH
• 金额: $ 325.11万
• 依托单位: UNIVERSITY OF TX MD ANDERSON CAN CTR
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-09-30 至 2005-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6357838
• 关键词: adenomatous polyps; clinical research; colon neoplasms; drug screening /evaluation; enzyme inhibitors; gene expression; genetic susceptibility; human subject; neoplasm /cancer chemotherapy; neoplasm /cancer genetics; preneoplastic state; prostaglandin endoperoxide synthase

Familial adenomatous polyposis (FAP) is an inherited susceptibility to diffuse colorectal adenomas and to colorectal carcinoma, occurring in close to 100% of unresected colons and is caused by a germline mutation in the APC gene. Most subjects who develop FAP show evidence of early adenomas between ages 10 and 15. The mutated APC gene also predisposes to duodenal polyps and to periampullary carcinoma. Although the standard of care has long been considered to be colectomy at diagnosis, practitioners and patients have been increasingly willing to undergo surveillance until there is evidence of progressive polyp burden. A recent trial demonstrated the activity of celecoxib in regressing prevalent adenomas in FAP patients with advanced adenomatous disease. This study will examine the natural history of the colorectal mucosa in young, asymptomatic carriers of APC mutations, and explore the role of celecoxib in suppressing emergence of the adenomatous phenotype. In addition, a number of ancillary evaluations will examine the relative impact of this potential preventive approach on the psychosocial status of patients.

家族性腺瘤性息肉病（FAP）是一种对弥漫性结直肠腺瘤和结直肠癌的遗传易感性，发生在接近100%未切除的结肠中，由APC基因的种系突变引起。大多数发生FAP的受试者在10至15岁之间表现出早期腺瘤的迹象。突变的APC基因也易患十二指肠息肉和壶腹周围癌。虽然诊断时的治疗标准一直被认为是结肠切除术，但医生和患者越来越愿意接受监测，直到有证据表明有进展性息肉负担。最近的一项试验表明，塞来昔布在FAP晚期腺瘤性疾病患者中消退流行腺瘤的活性。本研究将研究APC突变的年轻无症状携带者结肠黏膜的自然历史，并探讨塞来昔布在抑制腺瘤表型出现中的作用。此外，一些辅助评估将检查这种潜在的预防方法对患者心理社会状况的相对影响。