Relevant bibliographies by topics / Antiestrogenic resistance

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'Antiestrogenic resistance'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Antiestrogenic resistance"

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Direito, Inês, Liliana Monteiro, Tânia Melo, et al. "Protein Aggregation Patterns Inform about Breast Cancer Response to Antiestrogens and Reveal the RNA Ligase RTCB as Mediator of Acquired Tamoxifen Resistance." Cancers 13, no. 13 (2021): 3195. http://dx.doi.org/10.3390/cancers13133195.

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The protein quality control network, including autophagy, the proteasome and the unfolded protein response (UPR), is triggered by stress and is overactive in acquired antiestrogen therapy resistance. We show for the first time that the aggresome load correlates with apoptosis and is increased in antiestrogen-sensitive cells compared to endocrine-resistant variants. LC-MS/MS analysis of the aggregated proteins obtained after 4OH-tamoxifen and Fulvestrant treatment identified proteins with essential function in protein quality control in antiestrogen-sensitive cells, but not in resistant variant
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Osborne, C. K., V. J. Wiebe, W. L. McGuire, D. R. Ciocca, and M. W. DeGregorio. "Tamoxifen and the isomers of 4-hydroxytamoxifen in tamoxifen-resistant tumors from breast cancer patients." Journal of Clinical Oncology 10, no. 2 (1992): 304–10. http://dx.doi.org/10.1200/jco.1992.10.2.304.

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PURPOSE The antiestrogen tamoxifen is effective in therapy for breast cancer. However, its use is limited by the eventual development of acquired tamoxifen resistance in many patients. The mechanisms responsible for tamoxifen resistance remain unknown; loss of estrogen receptor (ER), selection of hormone-independent breast cancer clones, or alterations in serum tamoxifen levels after long-term use do not explain acquired resistance in most patients. Using an experimental model in which human breast cancer cells develop resistance in athymic mice treated with tamoxifen, we have recently shown t
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Donnez, Jacques, Christina Anna Stratopoulou, and Marie-Madeleine Dolmans. "Uterine Adenomyosis: From Disease Pathogenesis to a New Medical Approach Using GnRH Antagonists." International Journal of Environmental Research and Public Health 18, no. 19 (2021): 9941. http://dx.doi.org/10.3390/ijerph18199941.

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Uterine adenomyosis is a common chronic disorder frequently encountered in reproductive-age women, causing heavy menstrual bleeding, intense pelvic pain, and infertility. Despite its high prevalence, its etiopathogenesis is not yet fully understood, so there are currently no specific drugs to treat the disease. A number of dysregulated mechanisms are believed to contribute to adenomyosis development and symptoms, including sex steroid signaling, endometrial proliferation and invasiveness, and aberrant immune response. Abnormal sex steroid signaling, particularly hyperestrogenism and subsequent
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Levenson, Anait S., Douglas M. Wolf, William H. Catherino, Hiroyuki Takei, and V. Craig Jordan. "Understanding the antiestrogenic actions of raloxifene and a mechanism of drug resistance to tamoxifen." Breast Cancer 5, no. 2 (1998): 99–106. http://dx.doi.org/10.1007/bf02966681.

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Antoon, James W., Martin D. White, William D. Meacham, et al. "Antiestrogenic Effects of the Novel Sphingosine Kinase-2 Inhibitor ABC294640." Endocrinology 151, no. 11 (2010): 5124–35. http://dx.doi.org/10.1210/en.2010-0420.

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Alterations in sphingolipid metabolism have been shown to contribute to the development of endocrine resistance and breast cancer tumor survival. Sphingosine kinase (SK), in particular, is overexpressed in breast cancer and is a promising target for breast cancer drug development. In this study, we used the novel SK inhibitor ABC294640 as a tool to explore the relationship between SK and estrogen (E2) receptor (ER) signaling in breast cancer cells. Treatment with ABC294640 decreased E2-stimulated ERE-luciferase activity in both MCF-7 and ER-transfected HEK293 cells. Furthermore, the inhibitor
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Jordan, V. Craig. "The 38th David A. Karnofsky Lecture: The Paradoxical Actions of Estrogen in Breast Cancer—Survival or Death?" Journal of Clinical Oncology 26, no. 18 (2008): 3073–82. http://dx.doi.org/10.1200/jco.2008.17.5190.

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During the first David A. Karnofsky Award lecture entitled “Thoughts on Chemical Therapy” in 1970, Sir Alexander Haddow commented about the dramatic regressions observed with estrogen in some breast cancers in postmenopausal women, but regrettably the mechanism was unknown. He was concerned that a cancer-specific target would remain elusive, without tests to predict response to therapy. At that time, I was conducting research for my PhD on an obscure group of estrogen derivatives called nonsteroidal antiestrogens. Antiestrogens had failed to fulfill their promise as postcoital contraceptives a
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ARTENE, Diana Violeta, Cristian Ioan BORDEA, and Alexandru BLIDARU. "A moderately high protein diet and 4’ isometric exercises efficacy in breast cancer patients treated with antiestrogenic medication." Romanian Journal of Medical Practice 12, no. 2 (2017): 83–90. http://dx.doi.org/10.37897/rjmp.2017.2.5.

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Many breast cancer patients gain weight during treatment increasing recurrence, oncology specific mortality and general mortality risks. Breast cancer diagnosis and treatment overthrow patients’ lifestyle aggravating sedentariness and any preexisting weight gain causes like insulin and leptin resistance, dysbiosys and dyslipidemia. The aim of this study is to evaluate the efficiency of a moderately high protein diet – based on foods naturally high in proteins, omega-3 fatty acids, calcium, probiotics and prebiotics – and of an isometric exercise protocol to generate fat loss without muscle los
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Castellaro, Andrés M., María C. Rodriguez-Baili, Cecilia E. Di Tada, and Germán A. Gil. "Tumor-Associated Macrophages Induce Endocrine Therapy Resistance in ER+ Breast Cancer Cells." Cancers 11, no. 2 (2019): 189. http://dx.doi.org/10.3390/cancers11020189.

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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 microenvir
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Silveira, Maruhen AD, Christophe Tav, Félix-Antoine Bérube-Simard та ін. "Modulating HSF1 levels impacts expression of the estrogen receptor α and antiestrogen response". Life Science Alliance 4, № 5 (2021): e202000811. http://dx.doi.org/10.26508/lsa.202000811.

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Master transcription factors control the transcriptional program and are essential to maintain cellular functions. Among them, steroid nuclear receptors, such as the estrogen receptor α (ERα), are central to the etiology of hormone-dependent cancers which are accordingly treated with corresponding endocrine therapies. However, resistance invariably arises. Here, we show that high levels of the stress response master regulator, the heat shock factor 1 (HSF1), are associated with antiestrogen resistance in breast cancer cells. Indeed, overexpression of HSF1 leads to ERα degradation, decreased ex
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Zwart, Wilbert, Mariska Rondaij, Kees Jalink, et al. "Resistance to Antiestrogen Arzoxifene Is Mediated by Overexpression of Cyclin D1." Endocrine Reviews 30, no. 5 (2009): 540. http://dx.doi.org/10.1210/edrv.30.5.9990.

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ABSTRACT Resistance to tamoxifen treatment occurs in approximately 50% of the estrogen receptor (ER)α-positive breast cancer patients. Resistant patients would benefit from treatment with other available antiestrogens. Arzoxifene is an effective growth inhibitor of ERα-positive breast cancer cells, including tamoxifen-resistant tumors. In this study, we show that overexpression of a regular component of the ERα transcription factor complex, cyclin D1, which occurs in approximately 40% of breast cancer patients, renders cells resistant to a new promising antiestrogen, arzoxifene. Overexpression
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Dissertations / Theses on the topic "Antiestrogenic resistance"

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Long, Xinghua. "Novel mechanisms underlying antiestrogen activity and antiestrogen resistance in breast cancer." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3307565.

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Thesis (Ph.D.)--Indiana University, Dept. of Biology, 2008.<br>Title from dissertation home page (viewed Dec. 9, 2008). Source: Dissertation Abstracts International, Volume: 69-05, Section: B, page: 2835. Adviser: Kenneth P. Nephew.
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Crawford, Anatasha Carissa. "BCL-2 family function in antiestrogen-resistant breast cancer cells." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/463256217/viewonline.

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Nehra, Ruchi. "The nuclear factor kappa b (NFkb) plays a critical role in the development of antiestrogen resistance." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/642829667/viewonline.

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Penney, Rosalind B. "Thioredoxin and Jab1 Control Estrogen- and Antiestrogen-Mediated Progression of the Cell Cycle Through p27 Interactions." FIU Digital Commons, 2011. http://digitalcommons.fiu.edu/etd/380.

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A major problem with breast cancer treatment is the prevalence of antiestrogen resistance, be it de novo or acquired after continued use. Many of the underlying mechanisms of antiestrogen resistance are not clear, although estrogen receptor-mediated actions have been identified as a pathway that is blocked by antiestrogens. Selective estrogen receptor modulators (SERMs), such as tamoxifen, are capable of producing reactive oxygen species (ROS) through metabolic activation, and these ROS, at high levels, can induce irreversible growth arrest that is similar to the growth arrest incurred by SERM
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Parkes, Alicia Teresa. "The role of estrogen receptors and their co-regulators in the development of antiestrogen resistance in breast cancer." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406884.

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Ruddy, Samantha. "Preferential Estrogen Receptor β Ligands Inhibit Proliferation and Reduce Bcl-2 Expression in Fulvestrant-resistant Breast Cancer Cells". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23669.

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Endocrine resistance is a significant clinical problem in the treatment of estrogen (E2) receptor positive breast cancers. There are two ER subtypes, ERα and ERβ, which promote and inhibit breast cancer cell proliferation respectively. While ER positive breast cancers typically express a high ratio of ERα to ERβ, the acquisition of antiestrogen resistance in vitro and in vivo is associated with increased relative expression of the ERβ. On some gene enhancers ERβ has been shown to function in opposition to the ERα in the presence of E2. Here we demonstrate that exposure to two different ERβ ag
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Johnson, Neil. "Investigation into the therapeutic potential of novel cyclin dependent kinase (CDK) inhibitors in the treatment of antiestrogen sensitive and resistant breast cancer." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427304.

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McCarrick, Jessica Anne. "Differential Regulation of Steroid Receptors in Breast Cancer by the Rho GEF Vav3." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/124.

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Recently reported data demonstrate that Vav3, a Rho Guanine Nucleotide Exchange Factor (Rho GEF) is overexpressed in breast tumors, coexpressed with ER, necessary for proliferation in breast cancer cells, and predictive of response to neoadjuvant endocrine therapies in patients with ER+ tumors. Such data beg the question as to what roles Vav3 plays in modulation of steroid receptor activity in breast cancer and in resistance to current hormonal therapies. Using reporter assays, I provide novel evidence that Vav3 potentiates Estrogen Receptor activity and represses Androgen Receptor activity in
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Dreaden, Erik Christopher. "Chemistry, photophysics, and biomedical applications of gold nanotechnologies." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/51320.

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Gold nanoparticles exhibit a combination of physical, chemical, optical, and electronic properties unique from all other nanotechnologies. These structures can provide a highly multifunctional platform with which to diagnose and treat diseases and can dramatically enhance a variety of photonic and electronic processes and devices. The work herein highlights some newly emerging applications of these phenomena as they relate to the targeted diagnosis and treatment of cancer, improved charge carrier generation in photovoltaic device materials, and strategies for enhanced spectrochemical analysis
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Dibus, Michal. "Propojení signalizace PKN3 a p130Cas/BCAR1." Master's thesis, 2016. http://www.nusl.cz/ntk/nusl-351484.

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Both p130Cas and PKN3 are important regulators of cellular signaling deregulation of which leads to malignant behavior of cancer cells. Recently we have found that SH3 domain of p130Cas mediates interaction with proline rich region of PKN3 suggesting their possible cooperation in regulation of these processes. In this work we have focused on the phosphorylation of p130Cas by PKN3 and identified serine 498 (S498) within the serine rich domain of p130Cas to be phosphorylated by PKN3 in vitro. Given that S498 is localized within the 14-3-3 binding motif and its phosphorylation is required for int
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Book chapters on the topic "Antiestrogenic resistance"

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O’Regan, Ruth M., Anait S. Levenson, Gale M. England, et al. "Drug Resistance to Antiestrogens." In Hormone Therapy in Breast and Prostate Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59259-152-7_3.

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Nakshatri, Hariktishna. "Breast Cancer Antiestrogen Resistance." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6676-2.

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Nakshatri, Hariktishna. "Breast Cancer Antiestrogen Resistance." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6676.

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Pavlik, Edward J., Katherine Nelson, Suseela Srinivasan, Paul D. Depriest, and Daniel E. Kenady. "Antiestrogen Resistance in Human Breast Cancer." In Estrogens, Progestins, and Their Antagonists. Birkhäuser Boston, 1997. http://dx.doi.org/10.1007/978-1-4612-2306-1_5.

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Pavlik, Edward J., Katherine Nelson, Suseela Srinivasan, Paul D. Depriest, and Daniel E. Kenady. "Antiestrogen Resistance in Human Breast Cancer." In Estrogens, Progestins, and Their Antagonists. Birkhäuser Boston, 1997. http://dx.doi.org/10.1007/978-1-4612-4096-9_5.

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Clarke, Robert, Todd Skaar, Fabio Leonessa, et al. "Acquisition of an Antiestrogen-Resistant Phenotype in Breast Cancer: Role of Cellular and Molecular Mechanisms." In Drug Resistance. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_11.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "Breast Cancer Antiestrogen Resistance Protein 1 (BCAR1)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100135.

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Clarke, Robert, and Marc E. Lippman. "Mechanisms of Resistance to Antiestrogens and Their Implications for Crossresistance." In Tamoxifen. Birkhäuser Boston, 1996. http://dx.doi.org/10.1007/978-1-4612-4092-1_5.

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Bronzert, D. A., N. Davidson, and M. Lippman. "Estrogen and Antiestrogen Resistance in Human Breast Cancer Cell Lines." In Advances in Experimental Medicine and Biology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5101-6_22.

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"Breast Cancer Antiestrogen Resistance Protein 1 (BCAR1)." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100439.

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Conference papers on the topic "Antiestrogenic resistance"

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Berg, P., G. Uzturk, S. Awate, H. Stevenson, and A. Schwartz. "Role of BP1, a Novel Transcription Factor, in Antiestrogen Resistance." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5144.

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Conger, Jason, Matthew Manning, Kingsley Anosike, et al. "Abstract 4672: Targeting MEK/MAPK1/2in vivoto eradicate antiestrogen resistance." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4672.

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Shajahan, Ayesha N., Katherine L. Cook, Jessica L. Schwartz-Roberts, et al. "Abstract 5397: MYC-driven glutamine metabolism promotes antiestrogen resistance in breast cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5397.

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Gutgesell, Lauren M., Rui Xiong, Jiong Zhao, Debra A. Tonetti, and Gregory R. Thatcher. "Abstract 3603: Optimizing combination therapy against antiestrogen-resistance in estrogen receptor positive breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3603.

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Shajahan, Ayesha N., Rebecca B. Riggins, Alan Zwart, F. Edward Hickman, and Robert Clarke. "Abstract 2919: XBP1 and the unfolded protein response in antiestrogen resistance in breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2919.

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Toy, W., KE Carlson, TA Martin, et al. "Abstract P5-04-11: Non-canonical, clinical ESR1 mutations promote resistance to antiestrogen therapies." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-04-11.

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Hu, Rong, Alan Zwart, Anni Warri, and Robert Clarke. "Abstract LB-254: XBP1-NFkappaB signaling promotes antiestrogen resistance in breast cancer animal model." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-254.

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Hu, Rong, Ahreej Eltayeb, Ayesha Shajahan, Rebecca Riggins, and Robert Clarke. "Abstract LB-148: XBP1 regulates NFkappaB signaling in antiestrogen resistant breast cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-148.

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McDaniel, Lauren M., Ayesha N. Shajahan, and Robert Clarke. "Abstract 4601: XBP1 regulated function of c-MYC and BCL2 in antiestrogen resistance in breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4601.

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Manning, Mathew, Suchreet Takhar, Sudharsan Periyasamy-Thandavan, et al. "Abstract 1005: Dual targeting of MEK/MAPK1/2 and pro-survival autophagy to optimize antiestrogen treatment toward the eradication of antiestrogen resistant breast cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1005.

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Reports on the topic "Antiestrogenic resistance"

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Clarke, Robert. Molecular Mechanisms of Estrogen and Antiestrogen Resistance. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada395408.

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Clarke, Robert R. Molecular Mechanisms of Estrogen and Antiestrogen Resistance. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada418636.

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Clarke, Robert R. Molecular Mechanisms of Estrogen and Antiestrogen Resistance. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada403335.

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Wang, Zhaoyi, Hao Deng, and MingXi Guo. Breast Cancer Stem Cells in Antiestrogen Resistance. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada586468.

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Wang, Zhaoyi, Hao Deng, XinTian Zhang, and GuanGuan Li. Breast Cancer Stem Cells in Antiestrogen Resistance. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada566767.

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Urbauer, Jeffrey L., Ramona J. Bieber Urbauer, and Carrie E. Jolly. Mechanistic Basis Of Calmodulin Mediated Estrogen Receptor Alpha Activation and Antiestrogen Resistance. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada536000.

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Urbauer, Jeffrey L., Ramona J. Bieber-Urbauer, and Carrie E. Jolly. Mechanistic Basis of Calmodulin Mediated Estrogen Receptor Alpha Activation and Antiestrogen Resistance. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada510053.

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Arteaga, Carlos L. Blockade of Tumor Cell TGF-Betas: A Strategy to Reverse Antiestrogen Resistance in Human Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada404918.

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Roy, Deodutta. Identification of the Mechanisms Underlying Antiestrogen Resistance: Breast Cancer Research Partnership between FIU-UM Braman Family Breast Cancer Institute. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada488031.

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Roy, Deodutta. Identification of the Mechanisms Underlying Antiestrogen Resistance: Breast Cancer Research Partnership between FIU-UM Braman Family Breast Cancer Institute. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada566229.

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