Epidemiologic Architedure of Lung Cancer and Smoking

肺癌与吸烟的流行病学结构

• 批准号: 7933321
• 负责人: Christopher I. Amos
• 金额: $ 29.24万
• 依托单位: UNIVERSITY OF TX MD ANDERSON CAN CTR
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7933321
• 关键词: 15q25; Accounting; Adenocarcinoma; African; Age; Architecture; Area; Aromatic Hydrocarbons; Asbestos; Asia; Asians; Australia; Behavioral Genetics; Biochemical; Biological; Biological Markers; Breast; Breathing; Calibration; Cancer Etiology; Cancer Model; Carcinogen exposure; Case-Control Studies; Categories; Cells; Cessation of life; Characteristics; Chemoprevention; Chromosomes, Human, Pair 5; Chronic Obstructive Airway Disease; Chronic lung disease; Cigar Smoking; Cigarette; Cohort Studies; Colon Carcinoma; Comorbidity; Complex; Consensus; Country; Data; Detection; Development; Diagnosis; Diet; Discrimination; Disease; Dose; Ensure; Environment; Environmental Exposure; Environmental Risk Factor; Environmental Tobacco Smoke; Epidemiologic Studies; Epidemiology; Ethnic Origin; Europe; European; Exposure to; Family Cancer History; Family history of; Gender; Gene Frequency; General Population; Genes; Genetic; Genetic Polymorphism; Genetic Risk; Genetic Variation; Geographic Locations; Goals; Grant; Health Benefit; Heavy Metals; Heterogeneity; Iceland; Individual; Intake; Intervention; Joints; Lung; Malignant Neoplasms; Malignant neoplasm of lung; Maps; Measurement; Measures; Medical; Medical History; Meta-Analysis; Metric; Modeling; Nicotine; Nicotine Dependence; North America; Occupational Exposure; Participant; Patient Self-Report; Performance; Phenotype; Population; Population Attributable Risks; Population Heterogeneity; Predisposition; Probability; Procedures; Process; Prostate; Public Health; Publishing; Race; Radon; Recording of previous events; Relative (related person); Research; Research Design; Residual state; Resources; Risk; Risk Factors; Sample Size; Sampling; Screening procedure; Sex Characteristics; Signal Transduction; Smoke; Smoker; Smoking; Smoking Behavior; Smoking Status; Specimen; Squamous Cell; Stage at Diagnosis; Staging; Structure; Subgroup; Survival Rate; Testing; Time; Tobacco smoke; Tobacco-Associated Carcinogen; Variant; Work; base; cancer risk; case control; cell type; cohort; cost; disease characteristic; disorder risk; follow-up; fruits and vegetables; gene environment interaction; genetic association; genome wide association study; high risk; improved; indexing; insight; lung carcinogenesis; melanoma; mortality; non-smoker; population based; programs; prospective; racial and ethnic; residence; sex; tool; urinary

Finally, in area 3 we propose to perform detailed studies to charaderize the effeds of genetic variation on risk for lung cancer, allowing for effects from tobacco smoke and a limited set of additional environmental exposures that have been collected as a part of ILCCO. We will also explore the effects of genetic variation on smoking phenotypes. Area 3 analyses will allow a careful assessment of the joint effects of smoking and genetic exposures for a range of populations having different smoking behaviors, genetic backgrounds and effects from potential confounding fadors such as diet that have been measured in many cases, but with imprecision. In addition, we will be evaluating existing procedures for characterizing the risk for lung cancer according to age, sex, smoking behavior and demographic and medical history factors. We will also extend these models to include the results from the proposed genetic studies that we are conduding. The final product will be the development of a clearer view of lung carcinogenesis as well as better tools for identifying individuals at high risk to develop lung cancer. Identifying such people is an important goal, since there remain no approved screening mortalities for lung cancer in asymptomatic individuals because of a low positive predidive value of such approaches in the general population, and concern about the potential risks and costs associated with screening.

最后，在第 3 领域，我们建议进行详细研究，以描述遗传变异对肺癌风险的影响，考虑烟草烟雾和作为 ILCCO 一部分收集的有限的一组额外环境暴露的影响。我们还将探讨遗传变异对吸烟表型的影响。区域 3 分析将允许仔细评估吸烟和遗传暴露对一系列具有不同吸烟行为、遗传背景的人群的联合影响，以及潜在的混杂因素（例如饮食）的影响，这些影响在许多情况下都得到了测量，但并不精确。此外，我们将评估现有程序，根据年龄、性别、吸烟行为以及人口和病史因素来表征肺癌风险。我们还将扩展这些模型，以包含我们正在进行的拟议基因研究的结果。最终产品将是开发出更清晰的肺癌发生机制，以及更好的工具来识别肺癌高危人群。识别这些人是一个重要的目标，因为由于这种方法在普通人群中的阳性预测值较低，并且对与筛查相关的潜在风险和成本的担忧，目前还没有批准对无症状个体进行肺癌死亡率筛查。