• 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.

• Clinical and Experimental Reproductive Medicine
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• v.30 no.2
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• pp.135-139
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• 2003

Objective: We investigated whether serum testosterone to estradiol ratio was decreased in infertile men and whether this condition can be corrected with oral aromatase inhibitor. Method: The serum testosterone to estradiol ratio of 26 men with testicular failure were compared with those of normal semen analysis parameter, 89 control reference group. All of 26 testicular failure group were diagnosed with the previous testicular biopsy. Then 46 men with oligospermia and/or asthenospermia were selected and treated with 1 mg of the aromatase inhibitor anastrozole ($Arimidex^{(R)}$) orally once daily for 3 months. Testosterone to estradiol ratio and semen analyses were evaluated during anastrozole therapy. Results: The testosterone level of testicular failure group was significantly lower and the testosterone to estradiol ratio was more decreased than normal semen parameter group. Forty six on-anastrozole group had significantly lower testosterone (4.6 versus 5.7 ng/ml, p<0.01) and higher estradiol (15.9 versus 23.4 pg/ml, p<0.01) than pre-anastrozole group, resulting in a decreased testosterone to estradiol ratio ($0.21{\pm}0.07$ versus $0.39{\pm}0.15$, p<0.01). Semen analyses before and during anastrozole treatment revealed significant increases in sperm count (35.5 versus 52.2 million sperm per ml, p<0.01) and motility (22.9% versus 29.3%, p<0.01). Conclusions: We identified infertile men with testicular failure had hormonal changes characterized by a decreased serum testosterone to estradiol ratio. The ratio can be corrected with aromatase inhibitor, resulting in a significant improvement in semen parameters.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.55 no.1
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• pp.17-22
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• 2022

Successful reproduction in vertebrates necessitates complex interactions along the brain-pituitary-gonad axis, it is determined by gonadotropin releasing hormone produced in the hypothalamus of the brain, gonadotropin synthesized in the pituitary gland, and sex hormone secreted by the gonads. The goal of this study was to secure and test technology for controlling (inhibiting) sexual maturation hormones such as maturation hormones through hormone regulation. We studied the effect on sexual maturation of zebrafish Danio rerio by tamoxifen, anastrozole, exemestane and dopamine 4 kinds of sexual maturation inhibitors to feed and after administration. As a result, 4 kinds of sexual maturation inducing substances were mixed with zebrafish feed, it could be concluded that all of them were effective in inhibiting sexual maturation by reducing mRNA levels of genetic materials related to sexual maturation.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7111-7116
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• 2013

Introduction: Trastuzumab, an HER2-targeting agents, has shown efficacy in metastatic HER2-positive breast cancer patients. Single-agent clinical trials have evaluated therapeutic regimens using trastuzumab for metastatic breast cancer patients. The aim of our study is to evaluate the efficacy and safety of trastuzumab in combination with chemotherapy or hormone therapy in HER2-positive metastatic breast cancer patients. Methods: A literature research was conducted in PubMed and to identify appropriate studies from relevant reviews. Randomized controlled trials comparing chemotherapy or hormone therapy regimens in combination with trastuzumab were eligible. Dadta on clinical outcomes, including safety, efficacy, and patient characteristics were collected. Results: Seven articles describing five trials were included in our systematic review and meta-analysis. Partners of trastuzumab included in trials were anthracycline, paclitaxel, docetaxel, anastrozole and letrozole. The addition of trastuzumab to chemotherapy improved the overall survival (HR=0.79, 95%CI 0.65-0.96), while to hormone therapy did not (HR=0.85 95%CI 0.56-1.30). All trastuzumab-containing regimens increased cardiac toxicity (RR=3.37, 95%CI 1.26-9.02) and grade III-IV adverse events. Conclusions: Our study supports the addition of trastuzumab to chemotherapy which is effective and tolerated for metastatic breast cancer with HER2+ patients. Of note, more adverse events will occur followed the use of trastuzumab, especially cardiac toxicity, with two treatment regimens.

• Genomics & Informatics
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• v.21 no.2
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• pp.20.1-20.10
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• 2023

Aromatase inhibitors (AI) are drugs that are widely used in treating estrogen receptor (ER)-positive breast cancer patients. Drug resistance is a major obstacle to aromatase inhibition therapy. There are diverse reasons behind acquired AI resistance. This study aims at identifying the plausible cause of acquired AI resistance in patients administered with non-steroidal AIs (anastrozole and letrozole). We used genomic, transcriptomic, epigenetic, and mutation data of breast invasive carcinoma from The Cancer Genomic Atlas database. The data was then separated into sensitive and resistant sets based on patients' responsiveness to the non-steroidal AIs. A sensitive set of 150 patients and a resistant set of 172 patients were included for the study. These data were collectively analyzed to probe into the factors that might be responsible for AI resistance. We identified 17 differentially regulated genes (DEGs) among the two groups. Then, methylation, mutation, miRNA, copy number variation, and pathway analyses were performed for these DEGs. The top mutated genes (FGFR3, CDKN2A, RNF208, MAPK4, MAPK15, HSD3B1, CRYBB2, CDC20B, TP53TG5, and MAPK8IP3) were predicted. We also identified a key miRNA - hsa-mir-1264 regulating the expression of CDC20B. Pathway analysis revealed HSD3B1 to be involved in estrogen biosynthesis. This study reveals the involvement of key genes that might be associated with the development of AI resistance in ER-positive breast cancers and hence may act as a potential prognostic and diagnostic biomarker for these patients.