From the article:
That means they inserted a gene into mice that expresses human aromatase in the animal’s mammary tissue – a gene the researchers can turn on or off.
They compared this new mouse model to one they had developed several years ago – a conditional mouse model in which a gene that produces estrogen receptors (ER) could also be turned on and off.
While they study found that both mouse models experienced the earliest stages of tumor formation, known as preneoplasia, the aromatase over-expressing mice model exhibited both increased preneoplasia and outright development of cancer. These mice also expressed proteins that are tightly linked to cancer, Furth says.
The researchers also found, to their surprise, that aromatase over-expressing mice expressed more estrogen receptors than did the ER-conditional mice. “Increased aromatase produced both more estrogen and the receptors that the hormone needs to enter breast cells,” says Díaz-Cruz. “This is obviously a greater risk for development of breast cancer than just over-expression of estrogen receptors.”
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These mice also over-expressed progesterone receptors, downstream targets of estrogen receptors that can be cancer-promoting in some settings, as shown in this study in the context of aromatase over-expression.
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Finally, they tested the effect of local versus systemic estrogen on development of preneoplasia. The researchers made three comparisons: between mice in which the ER was over-expressed; mice that had excess estrogen due to aromatase; and mice that were given more estrogen systemically. “If we give extra systemic estrogen, we don’t see any increased risk of breast cancer, but the risk increases with extra expression of ER, and is higher still with local production of aromatase,” says Díaz-Cruz. “That suggests that estrogen production in the breast is an important risk factor for development of breast cancer.”