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. Author manuscript; available in PMC: 2022 Jan 5.
Published in final edited form as: Semin Cancer Biol. 2021 Jul 7;76:3–16. doi: 10.1016/j.semcancer.2021.07.001

Figure 5.

Figure 5.

Differential roles of CYP1A1 and 1A2 in PAH carcinogenesis. Compared to WT mice, Cyp1a1(−/−) showed a significantly lower pulmonary tumor count following exposure to 3-methylcholanthrene (3-MC). Cyp1a2(−/−) mice demonstrated a significantly higher pulmonary tumor count compared to WT mice. These results strongly indicate a protective function of hepatic CYP1A2 enzymes against pulmonary carcinogenesis. This protective mechanism may occur due to CYP1A2-induced suppression of CYP1A1 enzyme following PAH exposure. In Cyp1a2(−/−) mice, CYP1A1 is not suppressed, allowing for increased DNA adduct formation and resulting lung tumor development.