兒茶酚氧位甲基轉移遺傳多形性為台灣乳癌致癌感受性因子
Date Issued
2000-07-31
Date
2000-07-31
Author(s)
黃俊升
DOI
892314B002221
Abstract
Both epidemiologic and cell biology
studies have documented the contribution of
estrogen to the development of breast cancer.
Well-established risk factors for breast cancer,
including age at menarche, age at menopause,
parity, and age at first full-term pregnancy (1,
2,3), are operative by way of hormonal
mechanism. Hypotheses in which estrogen is
involved in tumorigenesis are based on the
general concept that cell division plays a
crucial role in cancer development, and that
reproductive factors that increase mitotic
activity in the breast epithelium also increase
cancer risk (4). On this basis, the role of
reproductive hormones during tumorigenesis
would be largely related to epigenetic
alteration and tumor promotion. However,
recent studies showed that estrogen metabolites
can bind to DNA and trigger damage (5-7),
suggesting that estrogen might be a complete
carcinogen (8) that can directly cause genetic
alteration and effect tumor initiation. This
possibility is supported by the finding that
women with reduced amounts of the enzymes
responsible for removing reactive estrogen
metabolites are at higher risk of developing
breast cancer (9). To comprehensively
elucidate the estrogen-initiating mechanism of
tumorigenesis in breast cancer and to dissect
the contribution of individual estrogenmetabolizing
genes involved in this
mechanism, this molecular epidemiologic
study sought to determine if polymorphisms in
the genes involved in estrogen biosynthesis
(CYP17) and hydroxylation (CYP1A1) and
inactivation of the reactive metabolites
(COMT) may be associated with elevated risk
of breast cancer, and if the association between
genotypes and risk may be modified by
estrogen exposure.
SDGs
Publisher
臺北市：國立臺灣大學醫學院外科
Type
report
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