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Drug: Tamoxifen

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Total 2054 results found since Jan 2013.

4-Hydroxytamoxifen-stimulated processing of cyclin E is mediated via G protein-coupled receptor 30 (GPR30) and accompanied by enhanced migration in MCF-7 breast cancer cells.
Abstract Over-expression of cleaved cyclin E in breast tumors is closely associated with tumor progression and resistance to antiestrogens. 17β-Estradiol (E2) has been recently shown to induce cyclin E processing in breast cancer cells. Tamoxifen has been used in patients with estrogen-sensitive breast cancer, yet resistance to antiestrogens and recurrence will appear in some of the patients after its continued use. We therefore addressed possible effects of tamoxifen on the generation of cleaved cyclin E and its signal mechanism(s) in estrogen-responsive MCF-7 breast cancer cells that express both G protein-coup...
Source: Toxicology - April 25, 2013 Category: Toxicology Authors: Li Y, Chen Y, Zhu ZX, Liu XH, Yang L, Wan L, Lei TW, Wang XD Tags: Toxicology Source Type: research

Tamoxifen inhibits macrophage FABP4 expression through the combined effects of GR and PPAR{gamma} pathways
In this study, we determined if the anti-atherogenic property of tamoxifen was related to its inhibition of macrophage FABP4 expression. We initially observed that tamoxifen inhibited macrophage/foam cell formation but the inhibition was attenuated when FABP4 expression was selectively inhibited by siRNA. We then observed that tamoxifen and 4-hydroxytamoxifen inhibited FABP4 protein expression in primary macrophages isolated from both the male and female wild type mice suggesting the inhibition is sex-independent. Tamoxifen and 4-hydroxytamoxifen inhibited macrophage FABP4 protein expression induced either by activation of...
Source: BJ Signal - June 28, 2013 Category: Biochemistry Authors: M Jiang, L Zhang, X Ma, W Hu, Y Chen, M Yu, Q Wang, X Li, Z Yin, Y Zhu, X Gao, D P Hajjar, Y Duan, J Han Tags: BJ Metabolism Source Type: research

Epidermal growth factor receptor signalling in human breast cancer cells operates parallel to estrogen receptor alpha signalling and results in tamoxifen insensitive proliferation
Conclusions: Our data indicate that enhanced EGFR-driven signalling is sufficient to overrule the TAM- mediated inhibition of E2-driven cell proliferation. This may have profound implications for the anti-estrogen treatment of ER-positive breast cancers that have increased levels of EGFR.
Source: BMC Cancer - April 23, 2014 Category: Cancer & Oncology Authors: Marja MoerkensYinghui ZhangLynn WesterBob van de WaterJohn Meerman Source Type: research

A Tamoxifen Derivative, N,N-Diethyl-2-4-(phenylmethyl) phenoxy Ethanamine, Selectively Targets P-glycoprotein-Positive Multidrug Resistant Chinese Hamster Cells.
In this study we examined the effects of DPPE alone on the growth of drug sensitive and P-gp positive CHO cell line. Our results demonstrate DPPE is selectively toxic to P-gp positive cells and the sensitivity to DPPE alone correlated with the levels of P-gp expression. Moreover, in MDR cells, DPPE-induced apoptosis was significantly reduced with Bcl2 overexpression and in the presence of P-gp ATPase inhibitor, PSC833. Furthermore, knockdown of P-gp expression in MDR cells with P-gp-siRNA reversed DPPE sensitivity and increased their sensitivity to doxorubicin and taxol but not to cisplatin. The addition of DPPE to membran...
Source: Biochemical Pharmacology - May 9, 2014 Category: Drugs & Pharmacology Authors: Georges E, Lian J, Laberge R Tags: Biochem Pharmacol Source Type: research

Tamoxifen induces apoptosis through cancerous inhibitor of protein phosphatase 2A dependent phospho-Akt inactivation in estrogen-receptor negative human breast cancer cells
Conclusions: Inhibition of CIP2A determines the effects of tamoxifen-induced apoptosis in ER-negative breast cancer cells. Our data suggest a novel ?off-target? mechanism of tamoxifen and suggest that CIP2A/PP2A/p-Akt signaling as a feasible anti-cancer pathway.
Source: Breast Cancer Research - September 17, 2014 Category: Cancer & Oncology Authors: Chun-Yu LiuMan-Hsin HungDuen-Shian WangPei-Yi ChuJung-Chen SuTsung-Han TengChun-Teng HuangTing-Ting ChaoCheng-Yi WangChung-Wai ShiauLing-Ming TsengKuen-Feng Chen Source Type: research

151pd * arid1a role in cell cycle regulation and proliferation in mouse and human gynaecological tissues reveals potential therapeutic targets
Conclusions: A core ARID1A-driven transcriptional programme, conserved accross normal tissues and species appears to exist, centred around regulation of genes involved in the G2/M checkpoint. ARID1A loss promotes proliferation in normal tissues, providing important clues as to the mechanisms of ARID1A-driven carcinogenesis. Mitotic kinases emerge as potential therapeutic targets in ARID1A mutant tumours, an observation that is not evident from studies in cancer cell lines.Disclosure: All authors have declared no conflicts of interest.
Source: Annals of Oncology - September 24, 2014 Category: Cancer & Oncology Authors: Gounaris, I., Brenton, J. Tags: basic science Source Type: research

Abstract 620: Evidence for combination tamoxifen and betulinic acid to treat hormone responsive- and unresponsive breast cancer by attenuation of Pygopus expression
The presence of the estrogen and progesterone hormone receptors (ER and PR) in advanced breast cancer tumour nuclei is predictive for response to hormone disruptive therapy. However, the accuracy of ER and PR testing can be variable and although patients receive significant benefit from hormone therapy, they ultimately become refractory to treatment. The chromatin remodeling protein: human Pygopus2 (hPygo2), is important for oncogenic growth and cell cycle progression and may serve as a diagnostic or targetable biomarker for breast cancer. Here we demonstrate that ER-alpha (Erα)−Sp1 transcription factor (Sp1) complexes ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Tzenov, Y., Andrews, P., Popadiuk, C., Kao, K. R. Tags: Endocrinology Source Type: research

Abstract 1969: Overexpression of specific CD44 variants mediate endocrine insensitivity and invasion in breast cancer cells
The majority of breast cancers express the oestrogen receptor and are potentially amenable to antihormone therapy; however the clinical effectiveness of these agents is limited by the phenomenon of acquired resistance which is associated with disease relapse and poor prognosis. In vitro evidence suggests that acquired resistance to tamoxifen and fulvestrant results in a significant gain to the migratory and invasive nature of breast cancer cells which may augment their metastatic potential in vivo. We have previously demonstrated that the CD44 receptor is overexpressed in acquired endocrine resistance and contributes to a ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Bellerby, R. L., Smith, C., Gee, J., Martin, T., Barrett-Lee, P., Hiscox, S. Tags: Tumor Biology Source Type: research

Abstract 4048: GFR{alpha}1 is required for GDNF-induced viability, migration, and signaling through RET in breast cancer cells
In this study we tested the functional consequences of silencing GFRα1 in ERα + MCF7 cells on tumor cell migration, invasion, and RET signaling. We showed that targeted reduction of GFRα1 significantly inhibited GDNF-induced migration in both a transwell (p=
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Ferrante, C. A., DeAngelis, N., Verona, R. Tags: Tumor Biology Source Type: research

Abstract 4227: The ribonucleotide reductase inhibitor Didox reverses tamoxifen resistance in breast cancer cells
In this study, we report that the inhibition of RRM2 by the small molecule inhibitor of ribonucleotide reductase activity Didox (3, 4-dihydroxybenzohydroxamic acid), significantly reduced tamoxifen induced cell proliferation in AKT overexpressing cells and tamoxifen resistant tumors generated by these cells. As well, Didox in combination with tamoxifen also inhibited cell proliferation in acquired tamoxifen resistant breast cancer cell lines. Employing comprehensive cell culture and in vivo models, we demonstrate that combining tamoxifen with Didox may reverse tamoxifen resistance in AKT expressing breast cancer cells. Cit...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Shah, K. N., Elford, H. L., Faridi, J. S. Tags: Molecular and Cellular Biology Source Type: research

Abstract 4755: Estrogen receptor mediates novel mechanisms of estrogen-induced growth and tamoxifen resistance in invasive lobular carcinoma
Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer representing ∼10% of newly diagnosed breast tumors. Over 90% of ILC cases are ER-positive, however, endocrine response and estrogen signaling are not well described in ILC. Retrospective analyses suggest that ILC patients treated with endocrine therapy have poorer outcomes than invasive ductal carcinoma (IDC) patients with similar biomarkers, and that ILC patients may not benefit from adjuvant tamoxifen. Additionally, we have recently identified ILC-specific ER-target genes and de novo tamoxifen resistance driven by ER in ILC model systems. Based...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Sikora, M. J., Bahreini, A., Oesterreich, S. Tags: Endocrinology Source Type: research

O2-15-2 * y-box binding protein-1 activation may modify the responses to endocrine and her2-targeted therapeutics in breast cancer
Conclusion and Discussion: Based on our basic and clinical study, YB-1 activation plays an essential role in expression of HER2/ErbB2, depending upon the absence or presence of ERα in breast cancer. The cross-talk of ERα and HER2 through activated YB-1 may thus specify biological characteristics in breast cancers luminal A, luminal B (HER2+), luminal B (HER2-), HER2 disease and triple negative. This study may propose an idea how endocrine and HER2-targeted therapeutics are mutually optimized against breast cancer.
Source: Annals of Oncology - October 19, 2014 Category: Cancer & Oncology Authors: Kuwano, M., Shibata, T., Kawahara, A., Hattori, S., Takahashi, R., Watari, K., Murakami, Y., Izumi, H., Kage, M., Ono, M. Tags: Oral Session (Oral presentations categorized by each organ) Source Type: research

O2-15-2 * y-box binding protein-1 activation may modify the responses to endocrine and her2-targeted therapeutics in breast cancer
Conclusion and Discussion: Based on our basic and clinical study, YB-1 activation plays an essential role in expression of HER2/ErbB2, depending upon the absence or presence of ERα in breast cancer. The cross-talk of ERα and HER2 through activated YB-1 may thus specify biological characteristics in breast cancers luminal A, luminal B (HER2+), luminal B (HER2-), HER2 disease and triple negative. This study may propose an idea how endocrine and HER2-targeted therapeutics are mutually optimized against breast cancer.
Source: Annals of Oncology - October 19, 2014 Category: Cancer & Oncology Authors: Kuwano, M., Shibata, T., Kawahara, A., Hattori, S., Takahashi, R., Watari, K., Murakami, Y., Izumi, H., Kage, M., Ono, M. Tags: Oral Session (Oral presentations categorized by each organ) Source Type: research

Secretory prostate apoptosis response (Par)-4 sensitizes multicellular spheroids (MCS) of glioblastoma multiforme cells to tamoxifen-induced cell death
Publication date: Available online 21 November 2014 Source:FEBS Open Bio Author(s): Jayashree C. Jagtap , Parveen D , Reecha D. Shah , Aarti Desai , Dipali Bhosale , Ashish Chugh , Deepak Ranade , Swapnil Karnik , Bhushan Khedkar , Aaishwarya Mathur , Kumar Natesh , Goparaju Chandrika , Padma Shastry Glioblastoma multiforme (GBM) is the most malignant form of brain tumor and is associated with resistance to conventional therapy and poor patient survival. Prostate apoptosis response (Par)-4, a tumor suppressor, is expressed as both an intracellular and secretory/extracellular protein. Though secretory Par-4 induces apopto...
Source: FEBS Open Bio - November 22, 2014 Category: Molecular Biology Source Type: research

A precisely substituted benzopyran targets androgen refractory prostate cancer cells through selective modulation of estrogen receptors.
Abstract Dietary consumption of phytoestrogens like genistein has been linked with lower incidence of prostate cancer. The estradiol-like benzopyran core of genistein confers estrogen receptor-β (ER-β) selectivity that imparts weak anti-proliferative activity against prostate cancer cells. DL-2-[4-(2-piperidinoethoxy)phenyl]-3-phenyl-2H-1-benzopyran (BP), a SERM designed with benzopyran core, targeted androgen independent prostate cancer (PC-3) cells 14-times more potently than genistein, ~25% more efficiently than tamoxifen and 6.5-times more actively than ICI-182780, without forfeiting significant specificity ...
Source: Toxicology and Applied Pharmacology - February 2, 2015 Category: Toxicology Authors: Kumar R, Verma V, Sharma V, Jain A, Singh V, Sarswat A, Maikhuri JP, Sharma VL, Gupta G Tags: Toxicol Appl Pharmacol Source Type: research