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Genetic Polymorphisms in Catechol-O-Methyltransferase, Menopausal Status, and Breast Cancer Risk

TLDR
The association of risk with at least one low-activity COMT(Met) allele was strongest among the heaviest premenopausal women and among the leanest post menopausal women, suggesting that COMT, mediated by body mass index, may be playing differential roles in human breast carcinogenesis, dependent upon menopausal status.
Abstract
Polymorphic catechol- O -methyltransferase (COMT) catalyzes the O -methylation of estrogen catechols. In a case-control study, we evaluated the association of the low-activity allele ( COMT Met) with breast cancer risk. Compared to women with COMT Val/Val, COMT Met/Met was associated with an increased risk among premenopausal women [odds ratio (OR), 2.1; confidence interval (CI), 1.4–4.3] but was inversely associated with postmenopausal risk (OR, 0.4; CI, 0.2–0.7). The association of risk with at least one low-activity COMT Met allele was strongest among the heaviest premenopausal women (OR, 5.7; CI, 1.1–30.1) and among the leanest postmenopausal women (OR, 0.3; CI, 0.1–0.7), suggesting that COMT, mediated by body mass index, may be playing differential roles in human breast carcinogenesis, dependent upon menopausal status.

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Multifactor-Dimensionality Reduction Reveals High-Order Interactions among Estrogen-Metabolism Genes in Sporadic Breast Cancer

TL;DR: In this article, the authors introduced multifactor dimensionality reduction (MDR) as a method for reducing the dimensionality of multilocus information, to improve the identification of polymorphism combinations associated with disease risk.
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Catechol-O-methyltransferase (COMT): biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors.

TL;DR: The enzyme responsible for the O- methylation, catechol- O -methyltransferase (COMT) was partly purified and characterized by the same group as EC, which first described the enzyme-catalyzed O-methylation of catechlamines and other catechols in the late 1950s.
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A Systematic Review Of Genetic Polymorphisms and Breast Cancer Risk

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Methylation pharmacogenetics: catechol O-methyltransferase, thiopurine methyltransferase, and histamine N-methyltransferase.

TL;DR: Experimental strategies used to study methylation pharmacogenetics illustrate the rapid evolution of biochemical, pharmacologic, molecular, and genomic approaches that have been used to determine the role of inheritance in variation in drug metabolism, effect, and toxicity.
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Chapter 3: Endogenous Estrogens as Carcinogens Through Metabolic Activation

TL;DR: Evidence shows that the catechols themselves are signaling molecules that work through the estrogen receptor that give rise to reactive quinones capable of forming direct adducts with glutathione and purines in DNA and of redox cycling to generate reactive oxygen species that can cause oxidative damage.
References
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Journal ArticleDOI

Human catechol-O-methyltransferase pharmacogenetics: description of a functional polymorphism and its potential application to neuropsychiatric disorders.

TL;DR: The identification of a gentic marker associated with significant alterations in enzyme activity will facilitate the analysis of a possible role for the COMT gene in neuropsychiatric conditions in which abnormalities in catecholamine neurotransmission are believed to occur.
Journal ArticleDOI

Functional role of estrogen metabolism in target cells: review and perspectives.

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Journal ArticleDOI

Molecular origin of cancer: Catechol estrogen-3,4-quinones as endogenous tumor initiators

TL;DR: 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.
Journal ArticleDOI

Molecular Mechanisms of Estrogen Carcinogenesis

TL;DR: The examples demonstrate that the parent compounds and their metabolites cause both nongenotoxic cell proliferative effects as well as direct and indirect genotoxic effects, which illustrates the complex nature of estrogen carcinogenesis.
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