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Journal ArticleDOI

Fulvestrant ('Faslodex')--a new treatment option for patients progressing on prior endocrine therapy.

C Morris, +1 more
- 01 Dec 2002 - 
- Vol. 9, Iss: 4, pp 267-276
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TLDR
Fulvestrant has recently gained US Food and Drug Administration approval for the treatment of hormone receptor-positive metastatic breast cancer in postmenopausal women with disease progression following antiestrogen therapy and these new hormonal treatments expand the choice of endocrine therapy for women with advanced breast cancer.
Abstract
Since its introduction more than 30 years ago, tamoxifen has been the most widely used endocrine therapy for the treatment of women with advanced breast cancer. More recently, a number of alternative endocrine treatments have been developed, including several selective estrogen receptor modulators (SERMs), aromatase inhibitors (AIs) and, most recently, fulvestrant ('Faslodex'). Fulvestrant is an estrogen receptor (ER) antagonist, which, unlike the SERMs, has no known agonist (estrogenic) effect and downregulates the ER protein. Tamoxifen is effective and well tolerated, although the non-steroidal AIs, anastrozole and letrozole, are more effective treatments for advanced disease than tamoxifen. Fulvestrant has recently gained US Food and Drug Administration approval for the treatment of hormone receptor-positive metastatic breast cancer in postmenopausal women with disease progression following antiestrogen therapy. In two global phase III clinical trials fulvestrant was at least as effective and as equally well tolerated as anastrozole for the treatment of postmenopausal women with advanced and metastatic breast cancer. In a retrospective analysis of the combined data from these trials, mean duration of response was significantly greater for fulvestrant compared with anastrozole. These new hormonal treatments expand the choice of endocrine therapy for women with advanced breast cancer and offer new options for sequencing and combining treatments.

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Journal ArticleDOI

Mechanisms of tumor regression and resistance to estrogen deprivation and fulvestrant in a model of estrogen receptor-positive, HER-2/neu-positive breast cancer.

TL;DR: The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib significantly delayed the emergence of resistance to both estrogen deprivation and fulvestrant, but reactivation of HER-2/neu and signaling through AKT leads to tumor regrowth.
Journal ArticleDOI

Advanced concepts in estrogen receptor biology and breast cancer endocrine resistance: implicated role of growth factor signaling and estrogen receptor coregulators.

TL;DR: Compelling experimental and clinical evidence suggest that the epidermal growth factor/her2/neu receptor (EGFR/HER2) pathway might play a distinct role in endocrine resistance, and especially in resistance to selective estrogen receptor modulators (SERMs) such as tamoxifen.
Journal ArticleDOI

The DEAD-box protein p72 regulates ERα-/oestrogen-dependent transcription and cell growth, and is associated with improved survival in ERα-positive breast cancer

TL;DR: A crucial role for p72 is highlighted in ERα co-activation and oestrogen-dependent cell growth and evidence in support of distinct but important roles for both p68 and p72 in regulating ERα activity in breast cancer is provided.
Journal ArticleDOI

Insights into the molecular biology of the estrogen receptor define novel therapeutic targets for breast cancer.

TL;DR: The molecular mechanisms through which ER activates transcription of target genes and through which available anti-estrogens mediate their therapeutic effects are reviewed.
References
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Journal ArticleDOI

Megestrol Acetate in Advanced Breast Carcinoma

Marc Espié
- 01 Jul 1994 - 
TL;DR: In randomized trials, efficacy of megestrol acetate is comparable with tamoxifen and with other hormonal treatments, and studies are ongoing to evaluate if high doses of megesin acetate may increase the response rate with acceptable toxicity.
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