Open AccessTobacco smoking, polymorphisms in carcinogen metabolism enzyme genes, and risk of localized and advanced prostate cancer: results from the California Collaborative Prostate Cancer Study
Author(s) -
Shahabi Ahva,
Corral Román,
Catsburg Chelsea,
Joshi Amit D.,
Kim Andre,
Lewinger Juan Pablo,
Koo Jocelyn,
John Esther M.,
Ingles Sue A.,
Stern Mariana C.
Publication year - 2014
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.334
Subject(s) - prostate cancer , carcinogen , cancer , prostate , oncology , medicine , gene , enzyme , cancer research , genetics , biology , biochemistry
The relationship between tobacco smoking and prostate cancer ( PC a) remains inconclusive. This study examined the association between tobacco smoking and PC a risk taking into account polymorphisms in carcinogen metabolism enzyme genes as possible effect modifiers (9 polymorphisms and 1 predicted phenotype from metabolism enzyme genes). The study included cases ( n = 761 localized; n = 1199 advanced) and controls ( n = 1139) from the multiethnic California Collaborative Case–Control Study of Prostate Cancer. Multivariable conditional logistic regression was performed to evaluate the association between tobacco smoking variables and risk of localized and advanced PC a risk. Being a former smoker, regardless of time of quit smoking, was associated with an increased risk of localized PC a (odds ratio [ OR ] = 1.3; 95% confidence interval [ CI ] = 1.0–1.6). Among non‐Hispanic Whites, ever smoking was associated with an increased risk of localized PC a ( OR = 1.5; 95% CI = 1.1–2.1), whereas current smoking was associated with risk of advanced PC a ( OR = 1.4; 95% CI = 1.0–1.9). However, no associations were observed between smoking intensity, duration or pack‐year variables, and advanced PC a. No statistically significant trends were seen among Hispanics or African‐Americans. The relationship between smoking status and PC a risk was modified by the CYP 1A2 rs7662551 polymorphism ( P ‐interaction = 0.008). In conclusion, tobacco smoking was associated with risk of PC a, primarily localized disease among non‐Hispanic Whites. This association was modified by a genetic variant in CYP 1A2 , thus supporting a role for tobacco carcinogens in PC a risk.