Bailey-Wilson J E, Sellers T A, Elston R C, Evens C C, Rothschild H
Dept of Biometry and Genetics, Stanley S. Scott Cancer Center, New Orleans.
J La State Med Soc. 1993 Apr;145(4):157-62.
Genetic segregation analyses that allowed for variable age of onset of lung cancer and smoking history were performed on 337 families, each ascertained through a lung cancer patient. Results indicated compatibility of the data with Mendelian codominant inheritance of a rare major autosomal gene that acts in concert with smoking to predispose carriers to lung cancer, by producing earlier onset of the cancer when controlling for equivalent smoking levels. Segregation at this locus could account for 69% and 47% of the cumulative incidence of lung cancer in individuals up to ages 50 and 60 respectively, but only 22% of all lung cancers in persons up to age 70. This decrease in the importance of the gene's contribution to overall lung cancer rates at later ages is most likely a reflection of an increasing proportion of noncarriers succumbing to the effects of long-term exposure to tobacco. A significant cohort effect was found, most likely due to differing smoking patterns before and after World War I, but in both cohorts the effect of a major locus could not be rejected.
对337个家庭进行了遗传分离分析，这些家庭均通过肺癌患者确诊，分析考虑了肺癌发病年龄的变化和吸烟史。结果表明，数据与一种罕见的主要常染色体基因的孟德尔共显性遗传相符，该基因与吸烟共同作用，使携带者易患肺癌，在控制同等吸烟水平时会使癌症发病更早。该位点的分离分别可解释50岁和60岁以下个体肺癌累积发病率的69%和47%，但在70岁以下人群的所有肺癌中仅占22%。该基因对后期总体肺癌发病率贡献的重要性降低，很可能反映了非携带者因长期接触烟草影响而死亡的比例增加。发现了显著的队列效应，很可能是由于第一次世界大战前后吸烟模式不同，但在两个队列中，主要位点的效应均不能被排除。
