Abstract 4348: A prospective study of smoking habit and risk of synchronous colorectal cancers

Abstract

Abstract Background: Synchronous colorectal cancers (CRC) (2 or more distinct primary carcinomas simultaneously identified in one patient) may arise as a result of a “field effect” or shared etiologic factors. Synchronous CRC has been associated with somatic epigenetic changes; cigarette smoking has been associated with DNA methylation in CRC. Thus, we examined the association between cigarette smoking and risk of synchronous CRC. Methods: Among men and women enrolled in the Health Professionals Follow-up Study and Nurses’ Health Study over 24 and 32 years, respectively, we examined the association of smoking with CRC. We examined the differential risk of developing synchronous CRC compared with solitary CRC, classified based on review of pathology reports, through duplication-method Cox proportional hazards regression. Results: During 3,477,211 person-years of follow-up of 45,691 men and 88,614 women, we documented 1,960 individuals with solitary CRC and 45 individuals with synchronous CRC. The association of smoking with CRC differed significantly according to the presence of synchronous compared with solitary tumors (Pheterogeneity = 0.0008). Compared with never smokers, current smokers experienced a higher risk of synchronous CRC (multivariable HR = 5.26; 95% CI, 2.08-13.32). In contrast, current smokers did not experience an elevated risk of solitary cancer (multivariable HR = 0.97; 95% CI, 0.83-1.13). Similar differences in the association of cumulative pack-years smoked with CRC according to tumor synchronicity status were also observed (Pheterogeneity = 0.006). Smoking cessation for ≥10 years was significantly associated with reduced risk of synchronous tumors (multivariable HR = 0.44; 95% CI, 0.20-1.00), but not solitary tumors (multivariable HR = 1.07; 95% CI, 0.91-1.25) (Pheterogeneity = 0.003). Conclusion: Current cigarette smoking is associated with an increased risk of synchronous but not solitary CRC. These data support a model in which smoking contributes to an etiologic field effect predisposing individuals to the development of synchronous CRC. Citation Format: David A. Drew, Reiko Nishihara, Paul Lochhead, Aya Kuchiba, Zhi Rong Qian, Kosuke Mima, Katsuhiko Nosho, Kana Wu, Molin Wang, Donna Spiegelman, Edward L. Giovannucci, Charles S. Fuchs, Shuji Ogino, Andrew T. Chan. A prospective study of smoking habit and risk of synchronous colorectal cancers. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4348.