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Estrogens as endogenous genotoxic agents--DNA adducts and mutations.
- E. Cavalieri, K. Frenkel, J. Liehr, E. Rogan, D. Roy
- Biology, ChemistryJournal of the National Cancer Institute…
- 1 July 2000
It is concluded that estrogens, including the natural hormones estradiol and estrone, must be considered genotoxic carcinogens on the basis of the evidence outlined in this chapter.
Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators.
- E. Cavalieri, D. Stack, E. Rogan
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 30 September 1997
The hypothesis that CE-3,4-Q are endogenous tumor initiators is supported, supported by data that indicates that depurinating hydrocarbon-DNA adducts generate oncogenic mutations found in mouse skin papillomas.
Catechol estrogen quinones as initiators of breast and other human cancers: implications for biomarkers of susceptibility and cancer prevention.
Deficiency of either cyclooxygenase (COX)-1 or COX-2 alters epidermal differentiation and reduces mouse skin tumorigenesis.
Both COX-1 andCOX-2 have roles in keratinocyte differentiation, and it is proposed that the absence of either isoform causes premature terminal differentiation of initiated keratinocytes and reduced tumor formation.
Metabolism and DNA binding studies of 4-hydroxyestradiol and estradiol-3,4-quinone in vitro and in female ACI rat mammary gland in vivo.
Results demonstrate that the 4-CE are metabolized to CE-3,4-Q, which react with DNA to form primarily depurinating adducts, which can generate the critical mutations that initiate cancer.
Central role of radical cations in metabolic activation of polycyclic aromatic hydrocarbons.
It is demonstrated that formation of quinones and phenols occurs via an initial electron transfer from BP to P450 and subsequent transfer of oxygen from the iron-oxo complex of P450 to BP.
IDH2R172 mutations define a unique subgroup of patients with angioimmunoblastic T-cell lymphoma.
Target resequencing on 92 cases of PTCL and frequent mutations affecting RHOA, TET2, DNMT3A, and isocitrate dehydrogenase 2 (IDH2) revealed recurrently hypermethylated genes involved in T-cell receptor signaling and T- cell differentiation that likely contribute to lymphomagenesis in AITL.
Molecular characteristics of catechol estrogen quinones in reactions with deoxyribonucleosides.
- D. Stack, J. Byun, M. Gross, E. Rogan, E. Cavalieri
- Chemistry, BiologyChemical research in toxicology
- 15 July 1996
Four estrogen-deoxyribonucleoside adducts were synthesized and provide insight into the type of DNA damage that can be caused by o-quinones of the catechol estrogens.
Unbalanced metabolism of endogenous estrogens in the etiology and prevention of human cancer
Relative imbalances in estrogen metabolism and conjugation in breast tissue of women with carcinoma: potential biomarkers of susceptibility to cancer.
The level of catechol estrogen quinone conjugates in cases was three times that in controls, suggesting in the cases a higher probability for the quinones to react with DNA and generate mutations that may initiate cancer.