Kelly Karen, Kittelson John, Franklin Wilbur A, Kennedy Timothy C, Klein Catherine E, Keith Robert L, Dempsey Edward C, Lewis Marina, Jackson Mary K, Hirsch Fred R, Bunn Paul A, Miller York E
Pulmonary 111A, Denver VA Medical Center, 1055 Clermont Street, Denver, CO 80220, USA.
Cancer Prev Res (Phila). 2009 May;2(5):440-9. doi: 10.1158/1940-6207.CAPR-08-0136. Epub 2009 Apr 28.
No chemoprevention strategies have been proven effective for lung cancer. We evaluated the effect of 13-cis retinoic acid (13-cis RA), with or without alpha tocopherol, as a lung cancer chemoprevention agent in a phase II randomized controlled clinical trial of adult subjects at high risk for lung cancer as defined by the presence of sputum atypia, history of smoking, and airflow obstruction, or a prior surgically cured nonsmall cell lung cancer (disease free, >3 years). Subjects were randomly assigned to receive either 13-cis RA, 13-cis RA plus alpha tocopherol (13-cis RA/alpha toco) or observation for 12 months. Outcome measures are derived from histologic evaluation of bronchial biopsy specimens obtained by bronchoscopy at baseline and follow-up. The primary outcome measure is treatment "failure" defined as histologic progression (any increase in the maximum histologic score) or failure to return for follow-up bronchoscopy. Seventy-five subjects were randomized (27/22/26 to observations/13-cis RA/13-cis RA/alpha toco); 59 completed the trial; 55 had both baseline and follow-up bronchoscopy. The risk of treatment failure was 55.6% (15 of 27) and 50% (24 of 48) in the observation and combined (13 cis RA plus 13 cis RA/alpha toco) treatment arms, respectively (odds ratio adjusted for baseline histology, 0.97; 95% confidence interval, 0.36-2.66; P = 0.95). Among subjects with complete histology data, maximum histology score in the observation arm increased by 0.37 units and by 0.03 units in the treated arms (difference adjusted for baseline, -0.18; 95% confidence interval, -1.16 to 0.81; P = 0.72). Similar (nonsignificant) results were observed for treatment effects on endobronchial proliferation as assessed by Ki-67 immunolabeling. Twelve-month treatment with 13-cis RA produced nonsignificant changes in bronchial histology, consistent with results in other trials. Agents advancing to phase III randomized trials should produce greater histologic changes. The addition of alpha tocopherol did not affect toxicity.
尚无化学预防策略被证明对肺癌有效。我们在一项II期随机对照临床试验中,评估了13 - 顺式维甲酸(13 - cis RA)联合或不联合α - 生育酚作为肺癌化学预防剂的效果,该试验的成年受试者为肺癌高危人群,其定义为存在痰异型性、吸烟史和气流阻塞,或既往有手术治愈的非小细胞肺癌(无疾病,>3年)。受试者被随机分配接受13 - 顺式维甲酸、13 - 顺式维甲酸加α - 生育酚(13 - cis RA/α - 生育酚)或观察12个月。结局指标来自于在基线和随访时通过支气管镜检查获得的支气管活检标本的组织学评估。主要结局指标是治疗“失败”,定义为组织学进展(最大组织学评分的任何增加)或未返回进行随访支气管镜检查。75名受试者被随机分组(27/22/26分别进入观察/13 - 顺式维甲酸/13 - 顺式维甲酸/α - 生育酚组);59名完成试验;55名有基线和随访支气管镜检查结果。观察组和联合治疗组(13 - 顺式维甲酸加13 - 顺式维甲酸/α - 生育酚)的治疗失败风险分别为55.6%(27例中的15例)和50%(48例中的24例)(根据基线组织学调整的优势比为0.97;95%置信区间为0.36 - 2.66;P = 0.95)。在有完整组织学数据的受试者中,观察组的最大组织学评分增加了0.37个单位,治疗组增加了0.03个单位(根据基线调整的差异为 - 0.18;95%置信区间为 - 1.16至0.81;P = 0.72)。通过Ki - 67免疫标记评估的对支气管内增殖的治疗效果也观察到了类似(无统计学意义)的结果。13 - 顺式维甲酸治疗12个月对支气管组织学产生了无统计学意义的变化,这与其他试验结果一致。进入III期随机试验的药物应产生更大的组织学变化。添加α - 生育酚不影响毒性。