Breast cancer, passive and active cigarette smoking and N-acetyltransferase 2 genotype

Citation
Rj. Delfino et al., Breast cancer, passive and active cigarette smoking and N-acetyltransferase 2 genotype, PHARMACOGEN, 10(5), 2000, pp. 461-469
Citations number
51
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Toxicology
Journal title
PHARMACOGENETICS
ISSN journal
0960-314X → ACNP
Volume
10
Issue
5
Year of publication
2000
Pages
461 - 469
Database
ISI
SICI code
0960-314X(200007)10:5<461:BCPAAC>2.0.ZU;2-Y
Abstract
The relationship of breast cancer to cigarette smoking is inconsistent in t he literature, possibly due in part to heterogeneity in carcinogen metaboli sm. N-acetyltransferase 2 (NAT2) enzyme activity is believed to play a role in the activation of tobacco smoke carcinogens. We examined the effect of NAT2 genetic polymorphisms on risk of breast cancer from active and passive smoking, Women were recruited from those who had suspicious breast masses detected clinically and/or mammographically. Questionnaire data were collec ted prior to biopsy diagnosis to blind subjects and interviewers. Histopath ology showed 113 cases with mammary carcinoma (30 carcinoma in situ) and 27 8 controls with benign breast disease. NAT2 genotype was determined using a llele-specific polymerase chain reaction amplification to detect slow acety lator mutations. Effects of passive and active tobacco smoke and of NAT2: g enotype on breast cancer risk were examined with logistic regression contro lling for known risk factors. Models first included all controls, and subse quently 107 with no or low risk (normal breast or no hyperplasia), and fina lly 148 with high risk (hyperplasia, atypical hyperplasia, complex fibroade nomas). Referents had no active or passive smoke exposure. We found no asso ciation between breast cancer risk and NAT2, smoking status (never, former, current), smoking duration, or cigarettes per day. There were no effects o f passive exposure among never-smokers, Models were unchanged across contro l groups. There were no statistical interactions between tobacco smoke expo sure and NAT2. The results were similar when restricting the analysis to in vasive cancers. These findings do not support the hypothesis that NAT2: is a risk factor for breast cancer or that it alters susceptibility to tobacco smoke, Pharmacogenetics 10:461-469 (C) 2000 Lippincott Williams & Wilkins.