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The 3,4-Quinones of Estrone and Estradiol Are the Initiators of Cancer whereas Resveratrol and N-acetylcysteine Are the Preventers

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Publisher

MDPI
DOI: 10.3390/ijms22158238

Keywords

cancer initiation; cancer prevention; estrogens; estrogen-DNA adducts; N-acetylcysteine; resveratrol

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This article reviews evidence suggesting that many prevalent types of cancer share a common initiation mechanism, with endogenous estrogens playing a central role. It explains the role of estrogen-DNA adducts in cancer initiation and highlights two potential cancer prevention compounds, resveratrol and N-acetylcysteine.
This article reviews evidence suggesting that a common mechanism of initiation leads to the development of many prevalent types of cancer. Endogenous estrogens, in the form of catechol estrogen-3,4-quinones, play a central role in this pathway of cancer initiation. The catechol estrogen-3,4-quinones react with specific purine bases in DNA to form depurinating estrogen-DNA adducts that generate apurinic sites. The apurinic sites can then lead to cancer-causing mutations. The process of cancer initiation has been demonstrated using results from test tube reactions, cultured mammalian cells, and human subjects. Increased amounts of estrogen-DNA adducts are found not only in people with several different types of cancer but also in women at high risk for breast cancer, indicating that the formation of adducts is on the pathway to cancer initiation. Two compounds, resveratrol, and N-acetylcysteine, are particularly good at preventing the formation of estrogen-DNA adducts in humans and are, thus, potential cancer-prevention compounds.

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