Relationship between 17β estradiol (17βE) levels and Catechol -O- methyltransferase (COMT) levels in ovarian cancers

Objectives: Epidemiological data show that induction of ovarian cancer is related to estrogen exposure and metabolism. In addition catechol metabolites of estrogen also contribute to carcinogenesis. O methylation by Catechol -O- methyltransferase is a phase II metabolic inactivation pathway for catechol estrogens. The goal of this study was to evaluate a potential correlation between COMT and 17$\mathrm{<i>\beta </i>}$ estradiol levels and ovarian cancer. Subjects and methods: COMT and 17$\mathrm{<i>\beta </i>}$E levels were measured in ovarian tissue and serum from 80 subjects: 30 with malignant ovarian tumors, 30 with benign ovarian tumors and 20 healthy controls. Results: Tissue and serum levels of Catechol -O- methyltransferase and 17$\mathrm{<i>\beta </i>}$ estradiol were determined using enzyme linked immunosorbant assay. According to our results Catechol -O- methyltransferase inhibition in the malignant group was associated with high levels of 17$\mathrm{<i>\beta </i>}$ estradiol, while in benign group high levels of COMT was associated with low levels of 17$\mathrm{<i>\beta </i>}$ estradiol in both serum and tissue homogenates. Conclusions: Low level of COMT and high tissue/serum levels of 17$\mathrm{<i>\beta </i>}$ estradiol may be contributory factors for the development of ovarian cancer. This supports the notion that targeting the metabolism of estrogen can be another way to reduce ovarian cancer risk.

Ovarian cancer; Catechol -O- methyltransferase; 17β estradiol (E2)

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