catechol/سرطان الثدي

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Cytochrome P450 CYP1B1 and catechol O-methyltransferase (COMT) genetic polymorphisms and breast cancer susceptibility in a Turkish population.

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Epidemiological studies indicate that most risk factors for breast cancer are related to reproductive and hormonal factors. Estrogen has been proposed to trigger breast cancer development via an initiating mechanism involving its metabolite, catechol estrogen (CE). Because of the important role of

Genetic polymorphisms in catechol-O-methyltransferase, menopausal status, and breast cancer risk.

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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 catechol estrogen metabolism as a risk factor for nonfamilial breast cancer.

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The metabolism of estrone (E1) or estradiol-17 beta (E2) to catechols seldom has been investigated in biochemical studies related to the risk of development of human breast cancer, as a result of the extreme lability and reactivity of these hormones. A method of indirect calculation was developed in

Identification of Cytosolic Protein Targets of Catechol Estrogens in Breast Cancer Cells Using a Click Chemistry-based Workflow

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Catechol estrogens (CEs) are known to be toxic metabolites and the initiators in the oncogenesis of breast cancers via forming covalent adducts with DNAs. CEs shall also react with proteins but their cellular protein targets remain un-explored. Here we reported the identification of protein targets

An association between the allele coding for a low activity variant of catechol-O-methyltransferase and the risk for breast cancer.

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Mounting evidence suggests that catechol metabolites of estradiol may contribute to the development of estrogen-induced cancers. O-Methylation, catalyzed by catechol-O-methyltransferase (COMT), inactivates catechol estrogens. COMT is polymorphic in the human population, with 25% of Caucasians being

Immunoperoxidase localization of catechol-o-methyl transferase (COMT) in human breast cancer.

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Immunoperoxidase reaction of appropriately fixed tissue with an antiserum to catechol-o-methyl transferase (COMT), as the primary step in the peroxidase-immunoglobulin bridge technique, has been utilized for the localization of COMT in biopsy specimens of human breast neoplasm and its metastases.

Src supports UDP-glucuronosyltransferase-2B7 detoxification of catechol estrogens associated with breast cancer.

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Mammary gland-distributed and ER-bound UDP-glucuronosyltransferase (UGT)-2B7 metabolizes genotoxic catechol-estrogens (CE) associated with breast cancer initiation. Although UGT2B7 has 3 PKC- and 2 tyrosine kinase (TK)-sites, its inhibition by genistein, herbimycin-A and PP2 with parallel losses in

Effect of catechol-o-methyltransferase-gene (COMT) variants on experimental and acute postoperative pain in 1,000 women undergoing surgery for breast cancer.

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BACKGROUND Catechol-O-methyltransferase (COMT) metabolizes catecholamines in different tissues. Polymorphisms in COMT gene can attenuate COMT activity and increase sensitivity to pain. Human studies exploring the effect of COMT polymorphisms on pain sensitivity have mostly included small,

Breast cancer risk reduction and membrane-bound catechol O-methyltransferase genetic polymorphisms.

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Catechol O-methyltransferase (COMT)-catalyzed methylation of catecholestrogens has been proposed to play a protective role in estrogen-induced genotoxic carcinogenesis. We have taken a comprehensive approach to test the hypothesis that genetic variation in COMT might influence breast cancer risk.

Relationship between the Val158Met polymorphism of catechol O-methyl transferase and breast cancer.

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A case-control study was performed to assess the potential influence of catechol O-methyl transferase (COMT) genotype on the risk of breast cancer in Korean women. One hundred and sixty-three histologically confirmed incident breast cancer cases and 163 age- and menopausal status-matched control

Limited association between a catechol-O-methyltransferase (COMT) polymorphism and breast cancer risk in Japan.

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BACKGROUND Catechol-O-methyltransferase (COMT) inactivates the estradiol metabolites, 2-hydroxy estradiol and 4-hydroxy estradiol. To date, three studies in Caucasians and one study in Chinese have been conducted to determine the association with breast cancer risk of a functional polymorphism

Impact of Catechol-O-Methyltransferase Val 158Met (rs4680) Polymorphism on Breast Cancer Susceptibility in Asian Population

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Background: Catechol-O-methyltransferase (COMT) is an important estrogen-metabolizing enzyme. Numerous case-control studies have evaluated the role COMT Val 158Met (rs4680;472G->A) polymorphism in the risk of breast cancer and provided inconclusive results, hence present meta-analysis was designed

Proteomics Identification and Validation of Desmocollin-1 and Catechol-O-Methyltransferase as Proteins Associated with Breast Cancer Cell Migration and Metastasis.

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Biological treatment of many cancers currently targets membrane bound receptors located on a cell surface. To identify novel membrane proteins associated with migration and metastasis of breast cancer cells, we selected and characterized a more migrating subpopulation of MDA-MB-231 breast cancer

Lack of association between catechol-O-methyltransferase Val108/158Met polymorphism and breast cancer risk: a meta-analysis of 25,627 cases and 34,222 controls.

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Epidemiological studies have evaluated the association between catechol-O-methyltransferase (COMT) Val108/158Met polymorphism and breast cancer risk. However, the results remain conflicting rather than conclusive. In order to derive a more precise estimation of the relationship, we performed this

Polymorphic catechol-O-methyltransferase gene, soy isoflavone intake and breast cancer in postmenopausal women: a case-control study.

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OBJECTIVE Genetic polymorphism Val158Met of catechol-O-methyltransferase (COMT) may contribute to estrogen-induced carcinogenesis of breast cancer. Soy isoflavones possesses chemical structure similar to endogenous estrogen and may promote the carcinogenesis of breast cancer. This study was to

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