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Table 1 Key characteristics of carcinogens (from Smith et al. [6])

From: Causality in cancer research: a journey through models in molecular epidemiology and their philosophical interpretation

1. Is electrophilic or can be metabolically activated
 Parent compound or metabolite with an electrophilic structure (e.g. epoxide, quinone, etc.), formation of DNA and protein adducts
2. Is genotoxic
 DNA damage (DNA strand breaks, DNA protein cross-links, unscheduled DNA synthesis), intercalation, gene mutations, cytogenetic changes (e.g. chromosome aberrations, micronuclei)
3. Alters DNA repair or causes genomic instability
 Alterations of DNA replication or repair (e.g. topoisomerase II, base-excision or double-strand break repair)
4. Induces epigenetic alterations
 DNA methylation, histone modification, microRNA expression
5. Induces oxidative stress
 Oxygen radicals, oxidative stress, oxidative damage to macromolecules (e.g. DNA, lipids)
6. Induces chronic inflammation
 Elevated white blood cells, myeloperoxidase activity, altered cytokine and/or chemokine production
7. Is immunosuppressive
 Decreased immunosurveillance, immune system dysfunction
8. Modulates receptor-mediated effects
 Receptor in/activation (e.g. ER, PPAR, AhR) or modulation of exogenous ligands (including hormones)
9. Causes immortalization
 Inhibition of senescence, cell transformation
10. Alters cell proliferation, cell death or nutrient supply
 Increased proliferation, decreased apoptosis, changes in growth factors, energetics and signaling pathways related to cellular replication or cell cycle