Editing Carcinogen (section)

===Breast cancer===
[[Breast cancer]] is the second most common cancer [(1.4 million cases, 10.9%), but ranks 5th as cause of death (458,000, 6.1%)].<ref name=Ferlay />  Increased risk of breast cancer is associated with persistently elevated blood levels of [[estrogen]].<ref>{{cite journal | vauthors = Yager JD, Davidson NE | title = Estrogen carcinogenesis in breast cancer | journal = The New England Journal of Medicine | volume = 354 | issue = 3 | pages = 270–282 | date = January 2006 | pmid = 16421368 | doi = 10.1056/NEJMra050776 | s2cid = 5793142 }}</ref>  Estrogen appears to contribute to breast carcinogenesis by three processes; (1) the metabolism of estrogen to genotoxic, [[4-Hydroxyestrone|mutagenic carcinogens]], (2) the stimulation of tissue growth, and (3) the repression of phase II [[detoxification]] enzymes that metabolize [[Reactive oxygen species|ROS]] leading to increased oxidative DNA damage.<ref>{{cite journal | vauthors = Ansell PJ, Espinosa-Nicholas C, Curran EM, Judy BM, Philips BJ, Hannink M, Lubahn DB | title = In vitro and in vivo regulation of antioxidant response element-dependent gene expression by estrogens | journal = Endocrinology | volume = 145 | issue = 1 | pages = 311–317 | date = January 2004 | pmid = 14551226 | doi = 10.1210/en.2003-0817 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Belous AR, Hachey DL, Dawling S, Roodi N, Parl FF | title = Cytochrome P450 1B1-mediated estrogen metabolism results in estrogen-deoxyribonucleoside adduct formation | journal = Cancer Research | volume = 67 | issue = 2 | pages = 812–817 | date = January 2007 | pmid = 17234793 | doi = 10.1158/0008-5472.CAN-06-2133 | s2cid = 24602808 | doi-access =  }}</ref><ref>{{cite journal | vauthors = Bolton JL, Thatcher GR | title = Potential mechanisms of estrogen quinone carcinogenesis | language = EN | journal = Chemical Research in Toxicology | volume = 21 | issue = 1 | pages = 93–101 | date = January 2008 | pmid = 18052105 | pmc = 2556295 | doi = 10.1021/tx700191p }}</ref>

The major estrogen in humans, [[estradiol]], can be metabolized to quinone derivatives that form [[DNA adduct|adducts]] with DNA.<ref name=Yue>{{cite journal | vauthors = Yue W, Santen RJ, Wang JP, Li Y, Verderame MF, Bocchinfuso WP, Korach KS, Devanesan P, Todorovic R, Rogan EG, Cavalieri EL | title = Genotoxic metabolites of estradiol in breast: potential mechanism of estradiol induced carcinogenesis | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 86 | issue = 3–5 | pages = 477–486 | date = September 2003 | pmid = 14623547 | doi = 10.1016/s0960-0760(03)00377-7 | s2cid = 31885800 }}</ref>  These derivatives can cause depurination, the removal of bases from the phosphodiester backbone of DNA, followed by inaccurate repair or replication of the apurinic site leading to mutation and eventually cancer.  This genotoxic mechanism may interact in synergy with estrogen receptor-mediated, persistent cell proliferation to ultimately cause breast cancer.<ref name=Yue /> Genetic background, dietary practices and environmental factors also likely contribute to the incidence of DNA damage and breast cancer risk.

Consumption of [[Alcohol (drug)|alcohol]] has also been linked to an increased risk for breast cancer.<ref>{{cite journal | vauthors = McDonald JA, Goyal A, Terry MB | title = Alcohol Intake and Breast Cancer Risk: Weighing the Overall Evidence | journal = Current Breast Cancer Reports | volume = 5 | issue = 3 | pages = 208–221 | date = September 2013 | pmid = 24265860 | pmc = 3832299 | doi = 10.1007/s12609-013-0114-z }}</ref>