• Title, Summary, Keyword: Fulvestrant

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Fulvestrant 250mg versus Anastrozole 1 mg in the Treatment of Advanced Breast Cancer: a Meta-Analysis of Randomized Controlled Trials

  • Gong, Dan-Dan;Man, Chang-Feng;Xu, Juan;Fan, Yu
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.5
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    • pp.2095-2100
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    • 2014
  • Objective: Most patients with advanced breast cancer experience resistance to endocrine treatment and eventual disease progression. This meta-analysis was designed to compare the efficacy and tolerability of fulvestrant 250mg with anastrozole 1mg in postmenopausal women with advanced breast cancer. Methods: Electronic literature databases (Cochrane Library, Medline, and Embase) were searched for randomized controlled trials (RCTs) published prior to August 2013. Only RCTs that compared fulvestrant 250mg to anastrozole 1mg in postmenopausal women with advanced breast cancer were selected. The main outcomes were time to treatment failure (TTF), time to progression (TTP), duration of response (DOR), clinical benefit rate, and tolerability. Results: Four RCTs covering 1,226 patients (fulvestrant, n=621; anastrozole, n=605) were included in the meta-analysis. Fulvestrant increased the DOR compared to anastrozole (HR =1.31, 95% confidence interval [CI] 1.13-1.51). There was no statistically significant difference between fulvestrant and anastrozole in terms of TTF (HR=1.02, 95%CI 0.89-1.17), complete response (RR=1.79, 95%CI, 0.93-3.43), and partial response (RR=0.91, 95%CI 0.69-1.21). As for safety, there was no statistical significance between the two groups for common adverse events. Conclusion: Fulvestrant 250mg is as effective and well-tolerated as anastrozole 1mg treatment for advanced breast cancer in postmenopausal women whose disease progressed after prior endocrine treatment. Thus, fulvestrant may serve as a reasonable alternative to anastrozole when resistance is experienced in breast cancer cases.

Fulvestrant Does Not Have Antagonistic Effect on 17β-estradiol's Anti-proliferative Action in Cultured Chinese Hamster Ovarian Cell Line (17β-Estradiol의 CHO 세포 항 증식작용에 대한 fulvestrant의 효과)

  • Kim, Hyun Hee;Park, Hyeong Cheol;Min, Gyesik
    • Journal of Life Science
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    • v.24 no.2
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    • pp.173-180
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    • 2014
  • Estrogen can promote or inhibit cellular proliferation depending on tissue cell types and physiological condition and acts through the signal transduction pathways mediated primarily by estrogen receptors. This study examined the effects of fulvestrant (Ful), a well-known antagonist for the estrogen receptor, on the action of $17{\beta}$-estradiol (E2) with respect to the proliferation and apoptosis of Chinese hamster ovarian (CHO) cells. We used different concentrations of E2, Ful, and E2 plus Ful during different treatment durations. Treatment with 15-40 ${\mu}M$ E2 significantly inhibited proliferation in a time-dependent manner, although it had no influence in concentrations up to 1 ${\mu}M$. Interestingly, Ful at 10-40 ${\mu}M$ also inhibited cellular proliferation in both a concentration- and time-dependent manner. In addition, Ful enhanced rather than decreased the inhibitory effect on cellular proliferation by E2 in combined treatment for 10 days. Thus, Ful does not appear to have an antagonistic effect on estrogen's anti-proliferative action in CHO cells. In TUNEL assays to confirm DNA fragmentation by E2 and/or Ful, CHO cells treated with 20 ${\mu}M$ E2 showed a TUNEL-positive reaction in most DAPI-stained nuclei, and cells treated with either 40 ${\mu}M$ Ful or 40 ${\mu}M$ Ful plus 20 ${\mu}M$ E2 also exhibited a TUNEL-positive reaction but at a lower rate compared to the E2-treated cells. These results indicate that Ful does not have an antagonistic effect on estrogen's anti-proliferative action in CHO cells, suggesting that the anti-proliferative and apoptosis-related mechanism(s) through DNA fragmentation by E2 and Ful may be mediated by different signal transduction pathways.

Estrogen Receptor α Roles in Breast Cancer Chemoresistance

  • Xu, Chao-Yang;Jiang, Zhi-Nong;Zhou, Ying;Li, Jia-Jia;Huang, Li-Ming
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.7
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    • pp.4049-4052
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    • 2013
  • Resistance to chemotherapy treatment, which may lead to limited efficacy of systemic therapy in breast cancer patients, is multifactorial. Among the mechanisms of resistance to chemotherapy treatment, there are those closely related to estrogen receptor ${\alpha}$, P-glycoprotein, multidrug resistance-related protein, glutathione S-transferase pi and topoisomerase-II. $ER{\alpha}$ is ligand-activated transcription factor that regulates gene expression and plays a critical role in endocrine signaling. In previous preclinical and clinical studies, positive $ER{\alpha}$ expression in breast cancer cells was correlated with decreased sensitivity to chemotherapy. This article reviews current knowledge on the predictive value of $ER{\alpha}$ with regard to response to chemotherapy. Better understanding of its role may facilitate patient selection of therapeutic regimens and lead to optimal clinical outcomes.