| pubmed-article:17085047 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17085047 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:17085047 | lifeskim:mentions | umls-concept:C0935916 | lld:lifeskim |
| pubmed-article:17085047 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:17085047 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:17085047 | lifeskim:mentions | umls-concept:C0205210 | lld:lifeskim |
| pubmed-article:17085047 | pubmed:issue | 1-5 | lld:pubmed |
| pubmed-article:17085047 | pubmed:dateCreated | 2006-11-20 | lld:pubmed |
| pubmed-article:17085047 | pubmed:abstractText | We seek to evaluate the clinical consequences of resistance to antihormonal therapy by studying analogous animal xenograft models. Two approaches were taken: (1) MCF-7 tumors were serially transplanted into selective estrogen receptor modulator (SERM)-treated immunocompromised mice to mimic 5 years of SERM treatment. The studies in vivo were designed to replicate the development of acquired resistance to SERMs over years of clinical exposure. (2) MCF-7 cells were cultured long-term under SERM-treated or estrogen withdrawn conditions (to mimic aromatase inhibitors), and then injected into mice to generate endocrine-resistant xenografts. These tumor models have allowed us to define Phase I and Phase II antihormonal resistance according to their responses to E(2) and fulvestrant. Phase I SERM-resistant tumors were growth stimulated in response to estradiol (E(2)), but paradoxically, Phase II SERM and estrogen withdrawn-resistant tumors were growth inhibited by E(2). Fulvestrant did not support growth of Phases I and II SERM-resistant tumors, but did allow growth of Phase II estrogen withdrawn-resistant tumors. Importantly, fulvestrant plus E(2) in Phase II antihormone-resistant tumors reversed the E(2)-induced inhibition and instead resulted in growth stimulation. These data have important clinical implications. Based on these and prior laboratory findings, we propose a clinical strategy for optimal third-line therapy: patients who have responded to and then failed at least two antihormonal treatments may respond favorably to short-term low-dose estrogen due to E(2)-induced apoptosis, followed by treatment with fulvestrant plus an aromatase inhibitor to maintain low tumor burden and avoid a negative interaction between physiologic E(2) and fulvestrant. | lld:pubmed |
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| pubmed-article:17085047 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17085047 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17085047 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17085047 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:17085047 | pubmed:issn | 0960-0760 | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:JordanV... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:AriaziEric... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:LiTianyuT | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:CorderaFernan... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:AriaziJennife... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:Lewis-WambiJo... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:GillShaun DSD | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:PyleJennifer... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:KimHelen RHR | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:SharmaCatheri... | lld:pubmed |
| pubmed-article:17085047 | pubmed:author | pubmed-author:ShuppHeather... | lld:pubmed |
| pubmed-article:17085047 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17085047 | pubmed:volume | 102 | lld:pubmed |
| pubmed-article:17085047 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17085047 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17085047 | pubmed:pagination | 128-38 | lld:pubmed |
| pubmed-article:17085047 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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