We are analyzing https://link.springer.com/chapter/10.1007/978-0-387-78818-0_13.

Title:
Selective Estrogen Modulators as an Anticancer Tool: | SpringerLink
Description:
The majority of breast cancers are estrogen receptor (ER) positive and depend on estrogen for growth. Therefore, blocking estrogen mediated actions remains the strategy of choice for the treatment and prevention of breast cancer. The selective estrogen receptor...
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Keywords {🔍}

google, scholar, cancer, pubmed, cas, article, breast, estrogen, receptor, tamoxifen, jordan, res, growth, natl, action, cells, inst, treatment, endocrinol, resistance, activity, cell, therapy, human, chapter, mol, serm, effect, biol, activation, endocrine, rev, antiestrogens, model, adjuvant, athymic, trial, endocrinology, selective, effects, treat, signaling, molecular, study, mice, raloxifene, omalley, coactivator, clin, factor,

Topics {✒️}

phosphatidylinositol 3-kinase/akt-mediated activation mitogen-activated protein kinase tamoxifen-induced er-alpha-src-3 interaction tamoxifen-bound estrogen receptor-alpha er/her2-positive breast cancer month download article/chapter raloxifene-estrogen receptor-alpha complex aberrantly activated pi3k/akt tamoxifen-resistant tumorigenic growth distinct chromatin-modifying complexes growth factor pathways tamoxifen-dependent gene expression estrogen receptor-selective coregulator long-term estrogen withdrawal estrogen receptor beta-isoform long-term tissue culture estrogen receptor/coactivator recognition tamoxifen-complexed estrogen receptor tamoxifen-resistant mcf-7 cells long-term antiestrogen administration 2/neu-positive breast cancer rat mammary tumours long-term estrogen deprivation estrogen receptor-regulated transcription n-cor-regulated genes raloxifene-resistant mcf-7 cells breast cancer—96-month follow selective receptor modulators high-dose estrogen treatment tamoxifen-stimulated endometrial cancer springer science+business media raloxifene-stimulated breast cancer human breast cancer estrogen receptor status selective estrogen modulators nuclear receptor coactivators nuclear receptor corepressor estrogen receptor-positive privacy choices/manage cookies estrogen receptor alpha oestrogen receptor beta breast tumor growth tamoxifen-stimulated growth early breast cancer erbb2-targeting strategies estrogen receptor activity estradiol-stimulated growth endometrial tumor growth lewis js resistant breast cancer

Schema {🗺️}

ScholarlyArticle:
      headline:Selective Estrogen Modulators as an Anticancer Tool:
      pageEnd:219
      pageStart:206
      image:https://media.springernature.com/w153/springer-static/cover/book/978-0-387-78818-0.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Innovative Endocrinology of Cancer
         isbn:
            978-0-387-78818-0
            978-0-387-78817-3
         type:Book
      publisher:
         name:Springer New York
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Surojeet Sengupta
            affiliation:
                  name:Fox Chase Cancer Center
                  address:
                     name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:V. Craig Jordan
            affiliation:
                  name:Fox Chase Cancer Center
                  address:
                     name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      keywords:Breast Cancer, Estrogen Receptor, Breast Cancer Cell, Natl Cancer Inst, Athymic Mouse
      description:The majority of breast cancers are estrogen receptor (ER) positive and depend on estrogen for growth. Therefore, blocking estrogen mediated actions remains the strategy of choice for the treatment and prevention of breast cancer. The selective estrogen receptor modulators (SERMs) are molecules that block estrogen action in breast cancer but can still potentially maintain the beneficial effects of estrogen in other tissues, such as bone and cardiovascular system. Tamoxifen, the prototypical drug of this class has been used extensively for the past 30 years to treat and prevent breast cancer. The target of drug action, ERs alpha and beta, are the two receptors which are responsible for the first step in estrogen and SERM action. The SERM binds to the ERs and confers a unique conformation to the complex. In a target site which expresses antiestrogenic actions, the conformation of the ER is distinctly different from estrogen bound ER. The complex recruits protein partners called corepressors to prevent the transcription of estrogen responsive genes. In contrast, at a predominantly estrogenic site coactivators for estrogen action are recruited. Unfortunately at an antiestrogenic site such as breast cancer, long term SERM therapy causes the development of acquired resistance. The breast and endometrial tumor cells selectively become SERM stimulated. Overexpression of receptor tyro sine kinases, HER-2, EGRF and IGRF and the signaling cascades following their activation are frequently involved in SERM resistant breast cancers. The aberrantly activated PI3K/AKT and MAPK pathways and their cross talk with the genomic components of the ER action are implicated in SERM resistance. Other down stream factors of HER-2 and EGRF signaling, such as PI3K/AKT, MAPK or mTOR pathways has also been found to be involved in resistance mechanisms. Blocking the actions of HER-2 and EGRF represent a rational strategy for treating SERM resistant phenotypes and may in fact restore the sensitivity to the SERMs. Another approach exploits the discovery that low dose estrogen will induce apoptosis in the SERM resistant breast cancers. Numerous clinical studies are addressing these issues.
      datePublished:2008
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Book:
      name:Innovative Endocrinology of Cancer
      isbn:
         978-0-387-78818-0
         978-0-387-78817-3
Organization:
      name:Springer New York
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Fox Chase Cancer Center
      address:
         name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
         type:PostalAddress
      name:Fox Chase Cancer Center
      address:
         name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Surojeet Sengupta
      affiliation:
            name:Fox Chase Cancer Center
            address:
               name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
               type:PostalAddress
            type:Organization
      name:V. Craig Jordan
      affiliation:
            name:Fox Chase Cancer Center
            address:
               name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
      name:Alfred G. Knudson Chair of Cancer Research, Fox Chase Cancer Center, Philadelphia, USA
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