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Therapy: Endocrine Therapy

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Total 38 results found since Jan 2013.

Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential
Conclusions: Our study shows that TNBC cells have profound metabolic alterations characterized by decreased mitochondrial respiration and increased glycolysis. Due to their impaired mitochondrial function, TNBC cells are highly sensitive to glycolytic inhibition, suggesting that such metabolic intervention may be an effective therapeutic strategy for this subtype of breast cancer cells.
Source: Breast Cancer Research - September 11, 2014 Category: Cancer & Oncology Authors: Hélène PelicanoWan ZhangJinyun LiuNaima HammoudiJiale DaiRui-hua XuLajos PusztaiPeng Huang Source Type: research

Abstract 2739: Specific interaction of human MGMT with ER-{alpha} in breast cancer cells: Co-degradation of MGMT and ER- {alpha} proteins by either fulvestrant or O6-benzylguanine and its therapeutic significance
This study investigated whether i) MGMT is modulated by endocrine therapies, ii) MGMT interacts with ER-signaling components and iii) if such findings are exploitable for improved breast cancer treatment. The ER-α positive cell lines MCF-7, T47D and ER- α negative MDAMB 468 cells, all MGMT-proficient, were treated with Fulvestrant (Faslodex, ICI 182, 780) or O6-benzylguanine (BG) in various experiments. Fulvestrant is a pure antiestrogen that binds to ER without eliciting any transcriptional effects, but leads to the receptor degradation through the ubiquitin-proteasome (ub-P) pathway. BG is a specific pseudosubstrate fo...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Srivenugopal, K. S., Paranjpe, A. Tags: Experimental and Molecular Therapeutics 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

Abstract P3-04-05: Invasive lobular carcinoma cell lines utilize WNT4 signaling to mediate estrogen-induced growth
Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer representing 10-15% of newly diagnosed breast tumors. Over 90% of ILC 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 similar invasive ductal carcinoma (IDC) patients, and that ILC patients may not benefit from adjuvant tamoxifen. Additionally, we recently identified ILC-specific ER-target genes and de novo tamoxifen resistance driven by ER in ILC model systems. Based on these observations, we ...
Source: Cancer Research - April 30, 2015 Category: Cancer & Oncology Authors: Sikora, M. J., Bahreini, A., Alexander, C. M., Oesterreich, S. Tags: Poster Session Abstracts Source Type: research

Protein Kinase A-induced tamoxifen resistance is mediated by anchoring protein AKAP13
Conclusions: We show that the PKA-anchoring protein AKAP13 is essential for the phosphorylation of ERαS305, which leads to tamoxifen resistance both in cell lines and tamoxifen-treated breast cancer patients.
Source: BMC Cancer - August 14, 2015 Category: Cancer & Oncology Authors: Cristiane Bentin ToaldoXanthippi AlexiKarin BeelenMarleen KokMichael HauptmannMaurice JansenEls BernsJacques NeefjesSabine LinnRob MichalidesWilbert Zwart Source Type: research

Abstract C150: High expression of SNAI2 is associated with the emergence of a highly motile fulvestrant-resistant phenotype and is an indicator of poor response to endocrine treatment in estrogen receptor-positive metastatic breast cancer
Endocrine resistance is a major clinical problem and is associated with the acquisition of aggressive tumor spread and invasion. To investigate the association between endocrine resistance and tumor cell migration and invasion, we evaluated a panel of MCF7-based cell line models resistant to either tamoxifen, aromatase inhibitors or fulvestrant. Fulvestrant-resistant cell lines showed a significantly higher migration capacity than the parental fulvestrant-sensitive cell line. Gene expression profiling and data analysis using Ingenuity Pathway Analysis (IPA) of these fulvestrant-resistant/fulvestrant-sensitive cell lines id...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Alves, C. L., Elias, D., Lyng, M., Bak, M., Lykkesfeldt, A. E., Ditzel, H. J. Tags: Target Identification and Validation: Poster Presentations - Proffered Abstracts Source Type: research

Abstract P3-04-02: Invasive lobular carcinoma cell lines utilize WNT4 signaling to mediate estrogen-induced growth
Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer representing 10-15% of newly diagnosed breast tumors. Over 90% of ILC are estrogen receptor (ER)-positive, however, endocrine response and estrogen signaling are not well understood in ILC. Retrospective analyses suggest that ILC patients treated with endocrine therapy have poorer outcomes than invasive ductal carcinoma (IDC) patients, and that ILC patients may not benefit from adjuvant tamoxifen. Based on these observations, we hypothesize that ER regulates unique signaling pathways in ILC cells that control growth and endocrine response.To identi...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Sikora, M., Oesterreich, S. Tags: Poster Session Abstracts Source Type: research

Abstract A35: WNT4 signaling mediates endocrine response and resistance in invasive lobular carcinoma cells
Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer, affecting ~30,000 U.S. women annually. Over 90% of ILC are estrogen receptor (ER)-positive, however, endocrine therapy may have poorer efficacy in a subset of ILC patients compared to invasive ductal carcinoma (IDC) patients. Based on these observations, we assessed genome-wide ER-mediated gene expression and ER genomic binding in ILC cell lines MDA MB 134VI (MM134) and SUM44PE (44PE), to identify novel mediators of ER signaling and putative therapeutic targets specifically in ILC.Among ILC-specific estrogen-regulated genes, the most strongly indu...
Source: Molecular Cancer Research - February 29, 2016 Category: Cancer & Oncology Authors: Sikora, M. J., Bahreini, A., Alexander, C. M., Oesterreich, S. Tags: Luminal Breast Cancer: Poster Presentations - Proffered Abstracts Source Type: research

Combined blockade of activating ERBB2 mutations and ER results in synthetic lethality of ER+/HER2 mutant breast cancer.
CONCLUSIONS: ERBB2 mutations hyperactivate the HER3/PI3K/AKT/mTOR axis, leading to antiestrogen resistance in ER+ breast cancer. Dual blockade of the HER2 and ER pathways is required for the treatment of ER+/HER2 mutant breast cancers. PMID: 30314968 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - October 12, 2018 Category: Cancer & Oncology Authors: Croessmann S, Formisano L, Kinch L, Gonzalez-Ericsson PI, Sudhan DR, Nagy RJ, Mathew A, Bernicker EH, Cristofanilli M, He J, Cutler RE, Lalani AS, Miller VA, Lanman RB, Grishin N, Arteaga CL Tags: Clin Cancer Res Source Type: research

Cancers, Vol. 11, Pages 189: Tumor-Associated Macrophages Induce Endocrine Therapy Resistance in ER+ Breast Cancer Cells
a Gil Antiestrogenic adjuvant treatments are first-line therapies in patients with breast cancer positive for estrogen receptor (ER+). Improvement of their treatment strategies is needed because most patients eventually acquire endocrine resistance and many others are initially refractory to anti-estrogen treatments. The tumor microenvironment plays essential roles in cancer development and progress; however, the molecular mechanisms underlying such effects remain poorly understood. Breast cancer cell lines co-cultured with TNF-α-conditioned macrophages were used as pro-inflammatory tumor microenvironm...
Source: Cancers - February 6, 2019 Category: Cancer & Oncology Authors: Castellaro Rodriguez-Baili Di Tada Gil Tags: Article Source Type: research

Contrasting activities of estrogen receptor beta isoforms in triple negative breast cancer
ConclusionsER β2/ERβ5 and ERβ1 exhibit sharply contrasting activities in TNBC cells. Our findings imply that delineating the absolute amounts and relative ratios of the different ERβ isoforms might have prognostic and therapeutic relevance, and could enable better selection of optimal approaches for treatment of this often aggressive form of breast cancer.
Source: Breast Cancer Research and Treatment - September 30, 2020 Category: Cancer & Oncology Source Type: research

PELP-1 regulates adverse responses to endocrine therapy in Estrogen Receptor (ER) positive breast cancer.
CONCLUSIONS: Our data confirms previous reports that anti-estrogens induce an adverse cell phenotype in ER+ breast cancer, particularly in the absence of homotypic cell contact. These results implicate E-cadherin and PELP-1 as potential biomarkers when deciding upon optimum adjuvant endocrine therapy, whereby tumours with high PELP-1/low E-cadherin expression may benefit from estrogen withdrawal therapy via aromatase inhibition, as opposed to ER modulation/antagonism. PMID: 33473257 [PubMed]
Source: Oncotarget - January 23, 2021 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Overexpression of TMEM47 Induces Tamoxifen Resistance in Human Breast Cancer Cells
CONCLUSIONS: Our results suggest that overexpression of TMEM47 in MCF-7 cells acquired TAM resistance to those cells, and knockdown of TMEM47 in TAMR/MCF-7 cells reversed their resistance to TAM. TMEM47 might confer TAM resistance on MCF-7 cells through the inhibition of apoptosis.PMID:33745390 | DOI:10.1177/15330338211004916
Source: Technology in Cancer Research and Treatment - March 22, 2021 Category: Cancer & Oncology Authors: Xin Men Mengyang Su Jun Ma Yueyang Mou Penggao Dai Chao Chen Xi An Cheng Source Type: research