Toremifene in the treatment of breast cancer

Mustonen, Mika

doi:10.5306/wjco.v5.i3.393

Cited by 32 publications

(21 citation statements)

References 61 publications

(96 reference statements)

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“…The commonly used dose of toremifene in humans for treating ER ϩ breast cancer is 60 mg daily (16,39). However, several clinical studies with higher toremifene doses (200 and 240 mg/day) in humans showed no significant increase in toxic side effects compared to the standard dose of 60 mg toremifene daily (40)(41)(42)(43)(44)(45). The latter studies confirm that the toremifene dose used in this study (3 mg/kg/day) is achievable in humans.…”

supporting

confidence: 70%

“…In addition, an elevated risk of thromboembolic events, endometrial cancer (higher for tamoxifen treatment), and a prolongation of the QT interval is noticed in some cases when using ER modulators such as tamoxifen and toremifene. Besides these adverse side effects, tamoxifen and toremifene have positive effects on serum lipid levels (decreased cholesterol) and bone mineral density (16,44,45).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm Formation In Vivo

Cremer

Delattin

Brucker

et al. 2014

Antimicrob Agents Chemother

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We here report on the in vitro activity of toremifene to inhibit biofilm formation of different fungal and bacterial pathogens, including Candida albicans, Candida glabrata, Candida dubliniensis, Candida krusei, Pseudomonas aeruginosa, Staphylococcus aureus, and Staphylococcus epidermidis. We validated the in vivo efficacy of orally administered toremifene against C. albicans and S. aureus biofilm formation in a rat subcutaneous catheter model. Combined, our results demonstrate the potential of toremifene as a broad-spectrum oral antibiofilm compound.

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supporting

confidence: 70%

mentioning

confidence: 99%

Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm Formation In Vivo

Cremer

Delattin

Brucker

et al. 2014

Antimicrob Agents Chemother

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“…Despite the progress in combined modality therapies, the long-term outcome of patients with breast cancer is far from satisfactory [2]. This outcome is mainly attributed to the induction and progression of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

C-terminal binding protein-2 promotes cell proliferation and migration in breast cancer via suppression of p16INK4A

Yang

Sun

et al. 2017

Oncotarget

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C-terminal binding protein-2 (CtBP2) enhances cancer proliferation and metastasis. The role and mechanism of CtBP2 in breast cancer remains to be elucidated. Western blot and immunochemistry were employed to evaluate the level of CtBP2 and p16INK4A in breast cancer. Genetic manipulation was used to study the expression of p16INK4A and its downstream genes regulated by CtBP2. Functional assays, including colony formation, wound healing, transwell invasion, anchorage-independent growth assay and a xenograft tumor model were used to determine the oncogenic role of CtBP2 in breast cancer progression. The expression of CtBP2 was increased in breast cancer tissues and cell lines. The expression of p16INK4A were inversely correlated CtBP2 (r2 = 0.43, P < 0.01). The expression of both CtBP2 and p16INK4A were significantly related to histological differentiation (P < 0.01 and P = 0.004, respectively) and metastasis (P = 0.046 and 0.047, respectively). The overall survival rate was lower in patients with increased CtBP2 expression and lower p16INK4A expression. Knockdown of CtBP2 resulted in the activation of p16INK4A and down–regulation of cell cycle regulators cyclin D, cyclin E and cyclin-dependent kinase 2 and 4. This down-regulation also led to a decreased transition of the G1-S phase in breast cancer cells. Moreover, gain-of-function experiments showed that CtBP2 suppressed p16INK4A and matrix metalloproteinase-2, subsequently enhancing the migration in breast cancer. However, the silence of CtBP2 abrogated this effect. Collectively, these findings provide insight into the role CtBP2 plays in promoting proliferation and migration in breast cancer by the inhibition of p16INK4A.

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“…Toremifene ( Figure 1B) is similar to TAM in clinical activity, efficacy and tolerability, and is cross-resistant to TAM. It causes less vascular and endometrial adverse effects than TAM, but has less favorable actions on bone and lipids levels [30] . Also in patients with metastatic BC, the results of TAM and toremifene therapy did not differ significantly, and the latter represents a reliable alternative to TAM in menopausal women [31] .…”

Section: Down-regulatorsmentioning

confidence: 99%

Current medical treatment of estrogen receptor-positive breast cancer

Lumachi

Santeufemia

Basso

2015

WJBC

168

126

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Approximately 80% of breast cancers (BC) are estrogen receptor (ER)-positive and thus endocrine therapy (ET) should be considered complementary to surgery in the majority of patients. The advantages of oophorectomy, adrenalectomy and hypophysectomy in women with advanced BC have been demonstrated many years ago, and currently ET consist of (1) ovarian function suppression (OFS), usually obtained using gonadotropinreleasing hormone agonists (GnRHa); (2) selective estrogen receptor modulators or down-regulators (SERMs or SERDs); and (3) aromatase inhibitors (AIs), or a combination of two or more drugs. For patients aged less than 50 years and ER+ BC, there is no conclusive evidence that the combination of OFS and SERMs (i.e. , tamoxifen) or chemotherapy is superior to OFS alone. Tamoxifen users exhibit a reduced risk of BC, both invasive and in situ , especially during the first 5 years of therapy, and extending the treatment to 10 years further reduced the risk of recurrences. SERDs (i.e. , fulvestrant) are especially useful in the neoadjuvant treatment of advanced BC, alone or in combination with either cytotoxic agents or AIs. There are two types of AIs: type Ⅰ are permanent steroidal inhibitors of aromatase, while type Ⅱ are reversible nonsteroidal inhibitors. Several studies demonstrated the superiority of the third-generation AIs (i.e. , anastrozole and letrozole) compared with tamoxifen, and adjuvant therapy with AIs reduces the recurrence risk especially in patients with advanced BC. Unfortunately, some cancers are or became ET-resistant, and thus other drugs have been suggested in combination with SERMs or AIs, including cyclin-dependent kinase 4/6 inhibitors (palbociclib) and mammalian target of rapamycin (mTOR) inhibitors, such as everolimus. Further studies are required to confirm their real usefulness.

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Toremifene in the treatment of breast cancer

Cited by 32 publications

References 61 publications

Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm Formation In Vivo

Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm Formation In Vivo

C-terminal binding protein-2 promotes cell proliferation and migration in breast cancer via suppression of p16INK4A

Current medical treatment of estrogen receptor-positive breast cancer

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