DOI . ORG {}

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We began analyzing https://link.springer.com/article/10.1007/s10911-008-9098-0, but it redirected us to https://link.springer.com/article/10.1007/s10911-008-9098-0. The analysis below is for the second page.

Title[redir]:
Crosstalk Between IGF1R and Estrogen Receptor Signaling in Breast Cancer | Journal of Mammary Gland Biology and Neoplasia
Description:
After the discovery that depriving certain breast tumors of estrogen promoted tumor regression, therapeutic strategies aimed at depriving tumors of this hormone were developed. The tumorigenic properties of estrogen are regulated through the estrogen receptor-α (ER), making understanding the mechanisms that activate this receptor highly relevant. In addition to estrogen activating the ER, other growth factor pathways, such as the insulin-like growth factors (IGFs), can activate the ER. This review will examine the interaction between these two pathways. Estrogen can activate the growth stimulatory properties of the IGF pathway via ER’s genomic and non-genomic functions. Further, blockade of ER function can inhibit IGF-mediated mitogenesis and blocking IGF action can inhibit estrogen stimulation of breast cancer cells. Collectively, these observations suggest that the two growth regulatory pathways are tightly linked and a more thorough understanding of the mechanism of this crosstalk could lead to improved therapeutic strategies in breast cancer.

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🌠 Phenomenal Traffic: 5M - 10M visitors per month

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Keywords {🔍}

google, scholar, cas, pubmed, article, cancer, receptor, growth, breast, estrogen, insulinlike, factor, cells, res, human, mol, yee, activation, endocrinol, cell, receptors, insulin, biol, signaling, igf, protein, usa, igfi, factors, role, kinase, douglas, hormone, pathways, action, factori, steroid, expression, doime, clin, endocrinology, estradiol, privacy, cookies, content, journal, search, mammary, pathway, mechanism,

Topics {✒️}

month download article/chapter luteinizing hormone-releasing hormone tamoxifen-resistant breast cancer mitogen-activated protein kinase hormone-responsive breast cancer igf receptor signalling estrogen-dependent breast cancer small-cell lung cancer inhibit igf-mediated mitogenesis growth hormone-induced igf c-fos/jun mrna early breast cancer estrogen receptor-sp1 interactions full article pdf c-myc oncogene expression estrogen-dependent growth human breast cancer privacy choices/manage cookies growth factor-1 receptor growth factor receptor breast cancer cells drug-induced apoptosis igf-binding proteins growth factor-ii breast cancer res tyrosine kinase activity combination therapy enhances estrogen-responsive element growth factor signaling breast cancer published article fagan growth factor pathways steroid hormone receptors therapeutic strategies aimed improved therapeutic strategies endometrial cancer cells breast cancers leads growth factor system estrogen receptor alpha breast cancer er inhibit estrogen stimulation clin cancer res nuclear estrogen receptors induce distinct conformational estrogen receptor-α estrogen receptor requires unliganded estrogen receptor estrogen receptor status masonic cancer center semin cancer biol

Questions {❓}

Can the insulin-like growth factors regulate breast cancer growth?

Schema {🗺️}

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         headline:Crosstalk Between IGF1R and Estrogen Receptor Signaling in Breast Cancer
         description:After the discovery that depriving certain breast tumors of estrogen promoted tumor regression, therapeutic strategies aimed at depriving tumors of this hormone were developed. The tumorigenic properties of estrogen are regulated through the estrogen receptor-α (ER), making understanding the mechanisms that activate this receptor highly relevant. In addition to estrogen activating the ER, other growth factor pathways, such as the insulin-like growth factors (IGFs), can activate the ER. This review will examine the interaction between these two pathways. Estrogen can activate the growth stimulatory properties of the IGF pathway via ER’s genomic and non-genomic functions. Further, blockade of ER function can inhibit IGF-mediated mitogenesis and blocking IGF action can inhibit estrogen stimulation of breast cancer cells. Collectively, these observations suggest that the two growth regulatory pathways are tightly linked and a more thorough understanding of the mechanism of this crosstalk could lead to improved therapeutic strategies in breast cancer.
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