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PubMed1996

Ifosfamide combined with toremifene in the treatment of non-small cell lung cancer.

The efficacy and safety of toremifene-ifosfamide as a first-line chemotherapy in non-small cell lung cancer were assessed. Sixteen patients were treated with oral toremifene (420 mg on days 1-4 and 240 mg on day 5) followed by ifosfamide infusion 5 g/m2 on day 5 every 3 weeks 1-6 times. Toremifene at the doses used did not enhance the effect or toxicity of ifosfamide in previously untreated non-small cell lung cancer patients.

Aged↗
PubMed1997

A phase III comparison of two toremifene doses to tamoxifen in postmenopausal women with advanced breast cancer. Eastern European Study Group.

Efficacy and safety of toremifene 60 and 240 mg daily (TOR60 and TOR240) are compared to 40 mg tamoxifen daily (TAM40) in postmenopausal women with advanced estrogen receptor (ER) positive or ER unknown breast cancer. The study is randomized and open label in three parallel groups. Primary efficacy variables are response rate and time to progression. WHO and ECOG criteria were used for measurable and nonmeasurable disease assessment, respectively. Safety was reported according to WHO criteria. Altogether 463 patients were randomized (157 to TOR60, 157 to TOR240, and 149 to TAM40). By data cut-off, after 20.5 months median follow-up time, over 70% of the patients had experienced disease progression. Response rates are 20.4%, 28.7%, and 20.8% in TOR60. TOR240, and TAM40, respectively. TOR60 and TAM40 show statistically equivalent efficacy and the difference between TOR240 and TAM40 is not significant (P = 0.112). Median times to progression are 4.9 (TOR60), 6.1 (TOR240), and 5.0 (TAM40) months and the corresponding hazard ratios (TAM:TOR) 1.015 and 1.124. Again, TOR60 and TAM40 are statistically equivalent and the difference between TOR240 and TAM40 is not significant (P = 0.374). All treatments were well tolerated. As a conclusion, TOR60 and TAM40 show equivalent clinical efficacy and tolerability. The higher dose of toremifene slightly but not statistically significantly improves response rate and time to progression. In postmenopausal women, toremifene 60 mg daily is an effective and safe treatment of advanced ER-positive or ER-unknown breast cancer.

Adult↗
PubMed2000

Genotoxic effects of the novel mixed antiestrogen FC-1271a in comparison to tamoxifen and toremifene.

Tamoxifen has been used for the treatment of breast cancer since the 1970s, but is considered a carcinogen because it has been linked to liver cancer in rats and an increased risk of endometrial cancer in patients. In rats, DNA adducts appear to be responsible for carcinogenesis, but their contribution to carcinogenesis in humans is not clear. FC-1271a and toremifene are mixed antiestrogens similar to tamoxifen. In order to compare the genotoxicity of these different triphenylethylenes, we treated mice for 28 days with 50 mg/kg of either tamoxifen, toremifene, FC- 1271 a or vehicle control. DNA from liver and uterus was assayed by standard 32P-postlabeling and thin layer chromatography for the presence of DNA adducts. Two methods of drug administration (oral and subcutaneous) and two strains of mice were compared and the plasma and tissue concentrations of the drugs and three metabolites of tamoxifen and toremifene were determined. Regardless of the conditions, only tamoxifen-treated mice showed DNA adducts in the liver. Adduct levels did not correlate with drug or metabolite levels and adducts were present even when drug was not detectable. Mice were also treated orally with either 50, 100, or 200 mg/kg of drug for 7 days. Again, adducts were found only in liver tissue of mice treated with tamoxifen, and adduct levels were dose-dependent. In conclusion, the chlorinated triphenylethylene FC-1271a did not cause DNA adducts under various conditions in mice, suggesting a low carcinogenic potential.

Administration, Oral↗
PubMed2001

Synthesis and secretion of transforming growth factor-beta1 by human desmoid fibroblast cell line and its modulation by toremifene.

The present study provides evidence that the in vitro cultured fibroblast cell line from desmoid tumors differs from normal fibrobasts in its extracellular matrix (ECM) macromolecule composition and is modulated by treatment with toremifene, an antiestrogen that reduces tumor mass by an unknown mechanism. The results showed increased transforming growth factor-beta 1 (TGF-beta1) production, TGF-beta1 mRNA expression, and TGF-beta1 receptor number in desmoid fibroblasts compared with normal cells. As desmoid fibroblasts did not produce tumor necrosis factor-alpha (TNF-alpha) but were sensitive to it, which enhanced glycosaminoglycans (GAG) accumulation, we assessed the TGF-beta1 effects on TNF-alpha production by human monocytes. Our results showed TGF-beta1 significantly increased TNF-alpha secretion by monocytes. Toremifene mediated its effects in desmoid fibroblasts via an estrogen receptor-independent pathway. It inhibited GAG accumulation and the secretion of both latent and active forms of TGF-beta1 and had an inhibitory effect on TNF-alpha production by monocytes. Our results suggest that in reducing TGF-beta1 production by desmoid fibroblasts and TNF-alpha production by monocytes, toremifene may restore the balance between the two growth factors.

Antineoplastic Agents, Hormonal↗
PubMed1993

Antiestrogenic potency of toremifene and tamoxifen in postmenopausal women.

In this nonblinded, controlled multicenter trial, postmenopausal women were randomly assigned to receive graded doses of toremifene and tamoxifen or no antiestrogen to assess dose-response levels and evaluation methodology. For standardization, transdermal estradiol (Estraderm-Ciba Geigy) was applied to all women for 38 days. The antiestrogens were added on days 29-38. For control and all treatment groups, there were no significant changes in serum chemistries or serum hormone levels, nor were there differences in adverse effects. The use of continuous estradiol precluded any meaningful assessment of the estrogenicity of tamoxifen or toremifene. As measured by vaginal superficial cytologic cell count changes, the antiestrogenic activity of toremifene doses ranging from 20 to 200 mg/day could not be distinguished from that of 20 mg/day of tamoxifen, the clinically recommended dose in North America.

Adult↗
PubMed2005

A highly vascular intracranial solitary fibrous tumor treated with radiotherapy and toremifene: case report.

OBJECTIVE AND IMPORTANCE: A case of an unusual intracranial solitary fibrous tumor with features of high vascularity and resultant difficulty at resection is presented. The use of surgery, radiotherapy, and toremifene has been successful with no recurrence after 18 months. CLINICAL PRESENTATION: A 33-year-old male patient presented with a 1-year history of loss of vision on the left side and a 3-month history of headache and lethargy. Magnetic resonance imaging showed a lobulated mass (7.6 x 4.5 cm) in the left temporal fossa and left parasellar, sellar, and suprasellar regions, with a "dural tail" more typical of meningioma. Vascular supply was from both the internal carotid arteries and the left middle meningeal artery, precluding embolization. INTERVENTION: At the time of the craniotomy, a highly vascular tumor was found. Intraoperative hemorrhage limited resection to 20% of the tumor. The histological diagnosis was of a solitary fibrous tumor with an unusually angiomatoid architecture. After the operation, radiotherapy and toremifene were administered. A dramatic reduction in the size of the tumor was seen with no recurrence to date. CONCLUSION: The use of surgery, radiotherapy, and toremifene in treatment of a vascular intracranial solitary fibrous tumor has been successful and warrants further research.

12E7 Antigen↗
PubMed1997

Anti-proliferative effect of toremifene and tamoxifen on estrogen receptor-lacking anaplastic thyroid carcinoma cell lines.

The antitumor effects of toremifene were studied in vitro using 10 anaplastic thyroid carcinoma cell lines and were compared with those of tamoxifen. The antitumor effect of toremifene was dose-dependent and the IC50 values for these cell lines ranged 20.1-58.5 microM. Although the cell lines expressed multidrug resistance gene mRNA, multidrug resistance-associated protein gene mRNA and insulin-like growth factor-1 (IGF-1) receptor mRNA to various degrees, nine of them lacked estrogen receptor expression as evaluated by immunocytochemistry. These data indicate that toremifene, as well as tamoxifen, is cytolytic at relatively high doses for multidrug-resistant anaplastic thyroid carcinoma cell lines.

Antineoplastic Agents, Hormonal↗
PubMed1999

[Endocrine chemotherapy (high-dose toremifene + 5'-DFUR) found markedly effective for 2 cases of metastatic breast cancer].

Two cases of metastatic breast cancer are reported in which endocrine chemotherapy with Toremifene + 5'-DFUR proved markedly effective. Case 1: A 69-year-old female. After CAF therapy as a adjuvant chemotherapy, Tamoxifen and Tegafur had been administered. At the 5th postoperative year, multiple metastases to lung and a rise in the tumor marker were found. Since the patient was not desirous of intensive chemotherapy, administration of Toremifene 120 mg/day and 5'-DFUR 800 mg/day was initiated. The patient showed PR 9 months after and achieved CR 14 months later. Case 2: A 48-year-old female. CAF therapy for a total of 6 cycles was performed as adjuvant chemotherapy. The patient was administered Tamoxifen and followed. On bone scintigrams 3.5 years after surgery, an abnormal accumulation appeared in the left sternoclavicular joint, and an infiltrative tumor mass was formed in the skin of that region. Administration of Toremifene + 5'-DFUR was initiated. After 6 months, the infiltrative mass disappeared. These findings are suggestive of the effectiveness of this combined chemotherapy.

Aged↗
PubMed2002

[A case of locally recurrent breast cancer in which phlebothrombosis of the right leg after hormonal therapy using a high dose of toremifene citrate].

A 72-year-old female had undergone mastectomy at the age of 67 for right breast cancer (T2a, n1 alpha, positive for ER). In the surgery the pectoralis muscle was preserved. For adjuvant therapy, 20 mg/day of tamoxifen was orally administered for 5 years. Six years after surgery, relapse was detected in the right major pectoralis muscle. Irradiation at this site and oral administration of 120 mg/day of toremifene citrate were started. The patient had a medical history of diabetes, and the control of her blood sugar was poor. About 2 months after oral administration of toremifene citrate was started, flares with blebs and swelling were observed in the right lower leg, suggesting acute phlebothrombosis of the right lower limb. The symptoms were ameliorated by intravenous administration of heparin and an antibiotic. In administering a high dose of toremifene citrate to patients with complications, careful follow-up is needed.

Aged↗
PubMed2002

[Synergistic effect of toremifene and cisplatin on human lung cancer cell line A549].

OBJECTIVE: To study the toxic effect of toremifene (TOR) and its synergistic effect with cisplatin (DDP) on human lung adenocarcinoma cell line A549. METHODS: The cytotoxic effects of these agents on human lung cancer cell line A549 were monitored by a tetrazolium-based colorimetric assay (MTT assay). The cell cycle and DNA content were detected by flow cytometer technic. p21 expression level was monitored by Western blot. RESULTS: Toremifene inhibited the growth of A549 cell, with > or = 5 micromol/L significantly enhancing the chemosensitivity of cisplatin. TOR enhanced the antitumor activity of DDP at S, G(2) and M phases of cells. And p21 expression was increased after TOR and DDP had been given. CONCLUSION: Toremifene (> or = 5 micromol/L) combined with cisplatin shows significant synergistic anti-tumor effect on A549 cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

Toremifene resistance in a rat mammary tumour model.

The effect of Toremifene on cell growth in vitro was tested on the R3230AC rat mammary adenocarcinoma as model. Toremifene differed from Tamoxifen in that it did not induce resistance; some cross-resistance was observed in Tamoxifen tolerant tumour cell lines. Toremifene does not influence P-glycoprotein expression in this model and at the levels studied.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2004

[A case of breast cancer with multiple bone metastases demonstrating complete remission with high-dose toremifene therapy].

We report a 64-year-old woman who underwent mastectomy for stage II (T2N1M0) advanced breast cancer, in whom multiple spine metastases developed 18 months postoperatively. She received 6 cycles of CA (cyclophosphamide 500 mg/m2, ADM 50 mg/m2 3 wq) therapy and oral tamoxifen (20 mg/body) administration for adjuvant therapy. The multiple bone metastases of the spine were revealed by technetium bone scan. The level of serum tumor marker CA15-3 increased two times over the normal range 18 months after surgery. She also developed osteoporosis a few years later, so we selected high-dose toremifene administration (120 mg/body) as a second-line therapy. No adverse effects have occurred and bone metastases disappeared. Moreover, the tumor marker was also normalized 6 months after toremifene therapy started. It was shown that high-dose treatment of toremifene was useful for recurrent breast cancer with bone metastasis.

Antineoplastic Agents, Hormonal↗
PubMedDate not supplied

Phase II study of high dose toremifene in advanced breast cancer progressing during tamoxifene treatment.

Thirty-five (34 evaluable) consecutive postmenopausal women with estrogen receptor positive (greater than or equal to 10 fmol/mg) or unknown advanced breast cancer were treated with high dose toremifene in a phase II study. All patients had progressed during prior adjuvant or palliativ antiestrogen treatment. The dose of toremifene was 240 mg per day. No complete or partial responders were registered. Nine patients (26%) were considered to have stable disease (NC). The time to progression for these patients was 5-27+ months with a mean time of twelve months and median time of eight months. Two patients are still on treatment after twelve and 24 months respectively. There seems to be a relationship with receptor value; however, there are two few patients for a safe statistical analysis. The side effects were insignificant. The conclusion is that the efficiency of toremifene as second line hormonal treatment is restricted, although it may be one additional choice.

Antineoplastic Agents↗
PubMed1988

The significance of estrogen receptors in tamoxifen and toremifene therapy.

Estrogen receptor (ER) concentration of breast cancer tissue is important in predicting the response of each patient to hormonal, especially antiestrogen treatment. About half of the patients with ER rich tumours respond and only about 10% of the patients with ER poor tumours respond to antioestrogen treatment. Tamoxifen is a well known and widely used drug. Toremifene is a new antioestrogen, developed in Finland. At standard doses both compounds have comparable hormonal and antitumour effects, and there is no clear difference between the compounds in the affinity to ER. The value of ER in predicting the response to tamoxifen and toremifene therapy in ER positive breast cancer is significant. It is not known, however, if the role of ER remains the same with high dose toremifene. Although ERs are an important predictive factor, the antioestrogens evidently act through them only in part. As the prediction is correct in about half of the patients, other mechanisms must influence tumour growth regulation, such as the expression of oncogenes and the synthesis and activity of growth factors.

Breast Neoplasms↗
PubMed1994

Evaluating the response to antioestrogen toremifene treatment in DMBA induced rat mammary carcinoma.

Evaluation of the treatment response to hormonal therapy in experimental mammary carcinoma models usually consists of recording the changes in tumour volume or in number of tumours. We performed quantitative histology on dimethylbenz[a]anthracene(DMBA) induced rat mammary carcinoma treated with the antioestrogen toremifene. The inhibition of growth of the treated regressing tumours was not only associated with inhibition of mitosis and reduction of the neoplastic epithelium, but toremifene seemed to reduce all main tissue components. The percentual area fractions of epithelium and stroma were equal in the untreated and the treated tumours. The estimated absolute volumes of epithelium, stroma and glandular luminae as well as the mitotic index were significantly reduced during toremifene treatment in those tumours which were responding by regression to the treatment. The findings indicate growth inhibiting effect on both epithelium and stroma or on interactions between epithelium and stroma. Adding quantitative histology to the gross response analysis in experimental animal models is feasible and may elucidate the mechanisms of action of a novel hormonal treatment.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

Cell loss in dimethylbenz(a)anthracene-induced rat mammary carcinoma treated with toremifene and ovariectomy.

The antiestrogen toremifene treatment results in regression or stabilization of dimethylbenz(a)anthracene(DMBA)-induced rat mammary tumors by reducing the mitotic activity and possibly by modifying the abundant spontaneous apoptosis seen in these tumors. A comparative study on the modes of cell loss was performed in untreated DMBA tumors and in tumors treated with toremifene and ovariectomy. Ovariectomy results in massive apoptotic cell death throughout the tumors with apoptotic cells exfoliating into the glandular lumina. Apoptosis accounts for most of the cell death also in the untreated tumors. The distinctly different morphology of the apoptotic cells in the untreated tumors (condensed apoptosis) and tumors treated with ovariectomy (blebbing apoptosis) may reflect the different type or schedule of the apoptotic process. Both morphologies of apoptotic cells were seen in the toremifene-treated tumors. Blebbing apoptosis is not easily examined in paraffin-embedded material but is best detectable in plastic sections and by electron microscopy.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Phase III trials of toremifene vs tamoxifen.

Three pivotal phase III trials conducted in North America and Europe served as the basis for the application for approval of toremifene (Fareston) by the FDA. These trials demonstrated that 60 mg/d of toremifene is safe and effective in the treatment of advanced breast cancer in postmenopausal women. The studies also indicated that, on the basis of antitumor efficacy, as well as safety, toremifene is at least equivalent to tamoxifen and may have some long-term advantages.

Antineoplastic Agents, Hormonal↗
PubMed1997

Safety assessment of tamoxifen and toremifene.

Nonclinical and clinical safety studies on the two antiestrogens, tamoxifen (Nolvadex) and toremifene (Fareston), are reviewed. Tamoxifen is genotoxic, carcinogenic in experimental animals, and carcinogenic in humans. Toremifene has yielded some positive findings for genotoxicity, but was not an initiating carcinogen in experimental animals. Thus, toremifene has a superior nonclinical safety profile, although information on its long-term effects in humans is needed to ascertain whether its use results in improved safety.

Animals↗