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dc.contributor.authorKast, Richard E.es_ES
dc.contributor.authorSkuli, Nicolases_ES
dc.contributor.authorCos Corral, Samuel es_ES
dc.contributor.authorKarpel Massler, Georges_ES
dc.contributor.authorShiozawa, Yusukees_ES
dc.contributor.authorGoshen, Ranes_ES
dc.contributor.authorHalatsch, Marc-Erices_ES
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2018-01-23T18:33:55Z
dc.date.available2018-01-23T18:33:55Z
dc.date.issued2017es_ES
dc.identifier.issn1179-1314es_ES
dc.identifier.urihttp://hdl.handle.net/10902/12918
dc.description.abstractBreast cancer metastatic to bone has a poor prognosis despite recent advances in our understanding of the biology of both bone and breast cancer. This article presents a new approach, the ABC7 regimen (Adjuvant for Breast Cancer treatment using seven repurposed drugs), to metastatic breast cancer. ABC7 aims to defeat aspects of epithelial-to-mesenchymal transition (EMT) that lead to dissemination of breast cancer to bone. As add-on to current standard treatment with capecitabine, ABC7 uses ancillary attributes of seven already-marketed noncancer treatment drugs to stop both the natural EMT process inherent to breast cancer and the added EMT occurring as a response to current treatment modalities. Chemotherapy, radiation, and surgery provoke EMT in cancer generally and in breast cancer specifically. ABC7 uses standard doses of capecitabine as used in treating breast cancer today. In addition, ABC7 uses 1) an older psychiatric drug, quetiapine, to block RANK signaling; 2) pirfenidone, an anti-fibrosis drug to block TGF-beta signaling; 3) rifabutin, an antibiotic to block beta-catenin signaling; 4) metformin, a first-line antidiabetic drug to stimulate AMPK and inhibit mammalian target of rapamycin, (mTOR); 5) propranolol, a beta-blocker to block beta-adrenergic signaling; 6) agomelatine, a melatonergic antidepressant to stimulate M1 and M2 melatonergic receptors; and 7) ribavirin, an antiviral drug to prevent eIF4E phosphorylation. All these block the signaling pathways ? RANK, TGF-beta, mTOR, beta-adrenergic receptors, and phosphorylated eIF4E ? that have been shown to trigger EMT and enhance breast cancer growth and so are worthwhile targets to inhibit. Agonism at MT1 and MT2 melatonergic receptors has been shown to inhibit both breast cancer EMT and growth. This ensemble was designed to be safe and augment capecitabine efficacy. Given the expected outcome of metastatic breast cancer as it stands today, ABC7 warrants a cautious trial.es_ES
dc.format.extent20 p.es_ES
dc.language.isoenges_ES
dc.publisherDove Medical Presses_ES
dc.rights© 2017 Kast et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution -Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/).es_ES
dc.sourceBreast Cancer (Dove Med Press). 2017 Jul 11;9:495-514es_ES
dc.titleThe ABC7 regimen: a new approach to metastatic breast cancer using seven common drugs to inhibit epithelial-to-mesenchymal transition and augment capecitabine efficacy.es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttps://www.dovepress.com/the-abc7-regimen-a-new-approach-to-metastatic-breast-cancer-using-seve-peer-reviewed-article-BCTTes_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.2147/BCTT.S139963. eCollection 2017es_ES
dc.type.versionpublishedVersiones_ES


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