JCP

eISSN 2288-3657
pISSN 2288-3649

Table 1

Components of AOP 46

Component	Description
MIE	Formation of pro-mutagenic DNA adducts
KE1	Insufficient repair or mis-repair of pro-mutagenic DNA adducts
KE2	Induced mutation in cancer critical genes
KE3	Cellular proliferation, clonal expansion of mutant cells, and progression to form AHF
AO	Hepatocellular carcinoma
pre-MIEa	Metabolism of AFB1 leads to formation of pro-mutagenic DNA adducts
KER1	pro-mutagenic DNA adducts lead to insufficient repair or mis-repair of pro-mutagenic DNA adducts
KER2	Insufficient repair or mis-repair of pro-mutagenic DNA adducts leads to induced mutation in cancer critical gene
KER3	Induced mutation in cancer critical gene leads to cell proliferation and clonal expansion to form AHF
KER4	Cell proliferation and clonal expansion to form AHF lead to HCC
naKER1 (MIE to KE2)	Formation of pro-mutagenic DNA adducts leads to induced mutation in cancer critical gene
naKER2 (MIE to KE3)	Formation of pro-mutagenic DNA adducts leads to cell proliferation and clonal expansion to form AHF
naKER3 (MIE to AO)	Formation of pro-mutagenic DNA adducts leads to HCC
naKER4 (KE2 to AO)	Induced mutation in cancer critical gene leads to HCC

AOP, adverse outcome pathway; MIE, molecular initiating event; KE, key event; AO, adverse outcome; KER, key event relationship; AHF, Altered Hepatic Foci; AFB1, aflatoxin B1; HCC, hepatocellular carcinoma.

pre-MIE is a term we use randomly.

There is no term to describe the relationship between the stressor and induction of a MIE because the first KER is defined as the relationship between the MIE and KE1.

Journal of Cancer Prevention 2018;23:126~133 https://doi.org/10.15430/JCP.2018.23.3.126