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Cancer: HER2
Drug: Tamoxifen

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Total 7 results found since Jan 2013.

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Williams syndrome transcription factor (WSTF) acts as an activator of estrogen receptor signaling in breast cancer cells and the effect can be abrogated by 1 α,25-dihydroxyvitamin D3
This study reports a novel transcription factor critical to 1α,25-dihydroxyvitamin D3-mediated regulation of estrogenic signaling in MCF-7 breast cancer cells. We have investigated the molecular mechanisms for the 1α,25-dihydroxyvitamin D3-mediated down-regulation of CYP19A1 and ERα gene expression in human MCF-7 breast cancer cells and found that Williams syndrome transcription factor (WSTF) plays a key role by binding to the promoters of CYP19A1 and ERα. Although sometimes reported as an inhibitor of gene expression, we found that WSTF acts as an activator of the promoter activity of both CYP19A1 and ERα. Silencing ...
Source: The Journal of Steroid Biochemistry and Molecular Biology - June 11, 2017 Category: Biochemistry Source Type: research

Abstract P5-04-17: From transcriptome meta-analysis to targeted therapies in triple negative breast cancer
Triple-Negative Breast Cancer (TNBC) is a subtype of breast cancer that urgently requires the identification and approval of novel targeted therapies. Even for breast cancer subtypes that have approved targeted therapies such as tamoxifen in ER+ and herceptin in HER2+ patients, there are a proportion of patients that do not respond to these therapies or develop resistance and succumb to metastatic recurrence. Thus, there is a clinical need to identify patients who do not benefit from current standard therapies and developing new strategies for therapy for non-responsive patients across all breast cancer subtypes.We hypothe...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Rozali, E., Al-Ejeh, F. Tags: Poster Session Abstracts Source Type: research

Anti-cancer effect of metformin by suppressing signaling pathway of HER2 and HER3 in tamoxifen-resistant breast cancer cells
Abstract Development of new therapeutic strategies is becoming increasingly important to overcome tamoxifen resistance. Recently, much interest has been focused on anti-tumor effects of metformin commonly used to treat type II diabetes. Increased protein expression and signaling of epidermal growth factor receptor (EGFR) family is a possible mechanism involved in tamoxifen resistance. Since HER2/HER3 heterodimers are able to induce strong downstream signaling and activate various biological responses such as cellular proliferation and growth, we investigated the anti-cancer effect of metformin by inhibition of sig...
Source: Tumor Biology - November 18, 2015 Category: Cancer & Oncology 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

Inhibition of vacuolar H+ ATPase enhances sensitivity to tamoxifen via up-regulation of CHOP in breast cancer cells.
Abstract Resistance of estrogen receptor-positive breast cancer cells to tamoxifen represents a major barrier to the successful treatment of breast cancer. In the present study, we found that vacuolar H+ ATPase (vATPase) inhibitors, bafilomycin A1 and concanamycin A, sensitize tamoxifen-induced cell death. siRNA targeting ATP6V0C, a 16-kDa hydrophobic proteolipid subunit of vATPase that plays a central role in H+ transport, markedly increased cell death induced by tamoxifen. Interestingly, bafilomycin A1 induced up-regulation of DR4/DR5 and CHOP. Knock-down of CHOP by siRNA suppressed the cell death induced by baf...
Source: Biochemical and Biophysical Research communications - July 6, 2013 Category: Biochemistry Authors: Jin HO, Lee YH, Kim HA, Kim EK, Noh WC, Kim YS, Hwang CS, Kim JI, Chang YH, Hong SI, Hong YJ, Park IC, Lee JK Tags: Biochem Biophys Res Commun Source Type: research