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Journal articles on the topic 'Antiestrogenic resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

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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2

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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3

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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4

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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6

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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7

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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8

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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9

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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10

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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11

Frogne, T., J. S. Jepsen, S. S. Larsen, C. K. Fog, B. L. Brockdorff, and A. E. Lykkesfeldt. "Antiestrogen-resistant human breast cancer cells require activated Protein Kinase B/Akt for growth." Endocrine-Related Cancer 12, no. 3 (2005): 599–614. http://dx.doi.org/10.1677/erc.1.00946.

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Development of acquired resistance to antiestrogens is a major clinical problem in endocrine treatment of breast cancer patients. The IGF system plays a profound role in many cancer types, including breast cancer. Thus, overexpression and/or constitutive activation of the IGF-I receptor (IGF-IR) or different components of the IGF-IR signaling pathway have been reported to render breast cancer cells less estrogen dependent and capable of sustaining cell proliferation in the presence of antiestrogens. In this study, growth of the antiestrogen-sensitive human breast cancer cell line MCF-7 was inh

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12

Fan, Ping, Wei Yue, Ji-Ping Wang, et al. "Mechanisms of Resistance to Structurally Diverse Antiestrogens Differ under Premenopausal and Postmenopausal Conditions: Evidence from in Vitro Breast Cancer Cell Models." Endocrinology 150, no. 5 (2009): 2036–45. http://dx.doi.org/10.1210/en.2008-1195.

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This study questioned whether the mechanisms of resistance to antiestrogens differ when acquired under premenopausal (Pre-M) vs. postmenopausal (PM) conditions and whether structurally diverse antiestrogens induce adaptation of differing signaling pathways. To address this issue, we conducted systematic studies under Pre-M vs. PM culture conditions with long-term exposure to different antiestrogens and examined the resultant “specific biologic signatures” of the various resistant cells. Estradiol stimulated growth and inhibited apoptosis of “pre-menopausal” antiestrogen-resistant cells but exe

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13

Hu, Rong, Anni Warri, Lu Jin та ін. "NF-κB Signaling Is Required for XBP1 (Unspliced and Spliced)-Mediated Effects on Antiestrogen Responsiveness and Cell Fate Decisions in Breast Cancer". Molecular and Cellular Biology 35, № 2 (2014): 379–90. http://dx.doi.org/10.1128/mcb.00847-14.

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Antiestrogen therapy induces the unfolded protein response (UPR) in estrogen receptor-positive (ER+) breast cancer. X-box binding protein 1 (XBP1), which exists in the transcriptionally inactive unspliced form [XBP1(U)] and the spliced active form [XBP1(S)], is a key UPR component mediating antiestrogen resistance. We now show a direct link between the XBP1 and NF-κB survival pathways in driving the cell fate decisions in response to antiestrogens in ER+breast cancer cells, bothin vitroand in a xenograft mouse model. Using novel spliced and nonspliceable forms of XBP1, we show that XBP1(U) fun

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14

Bogush, Tatiana, Evgeny Dudko, Elena Bogush, Boris Polotsky, Sergei Tjulandin, and Mikhail Davydov. "Tamoxifen non-estrogen receptor mediated molecular targets." Oncology Reviews 6, no. 2 (2012): 15. http://dx.doi.org/10.4081/oncol.2012.e15.

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Recent experimental studies revealing new biological effects of tamoxifen on tumor cells both expressing and not expressing different types of estrogen receptors (ERα and ERβ) show new aspects of a seemingly well known agent. This review describes tamoxifen targets, the blocking of which leads to inhibition of tumor cell growth and angiogenesis, stimulation of programmed cell death (apoptosis, autophagia and necrosis), inhibition of multidrug resistance, invasion and metastasis. Since outcomes of tamoxifen action on cells are prognostically good from the point of view of both tumor growth/meta

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15

Ma, Yongxian, York Tomita, Anju Preet та ін. "Small-Molecule “BRCA1-Mimetics” Are Antagonists of Estrogen Receptor-α". Molecular Endocrinology 28, № 12 (2014): 1971–86. http://dx.doi.org/10.1210/me.2014-1146.

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Context: Resistance to conventional antiestrogens is a major cause of treatment failure and, ultimately, death in breast cancer. Objective: The objective of the study was to identify small-molecule estrogen receptor (ER)-α antagonists that work differently from tamoxifen and other selective estrogen receptor modulators. Design: Based on in silico screening of a pharmacophore database using a computed model of the BRCA1-ER-α complex (with ER-α liganded to 17β-estradiol), we identified a candidate group of small-molecule compounds predicted to bind to a BRCA1-binding interface separate from the

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16

Miller, Todd W. "Endocrine Resistance: What Do We Know?" American Society of Clinical Oncology Educational Book, no. 33 (May 2013): e37-e42. http://dx.doi.org/10.14694/edbook_am.2013.33.e37.

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Adjuvant therapy with antiestrogens targeting estrogen receptor α (ER) signaling prevents disease recurrence in many patients with early-stage ER+ breast cancer. However, a significant number of cases exhibit de novo or acquired endocrine resistance. While other clinical subtypes of breast cancer (HER2+, triple-negative) have disproportionately higher rates of mortality, ER+ breast cancer is responsible for at least as many deaths because it is the most common subtype. Therefore, identifying mechanisms that drive endocrine resistance is a high clinical priority. A large body of experimental ev

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17

González González, Alicia, Noemi Rueda Revilla, and Emilio J, Sánchez-Barceló. "Clinical uses of melatonin: evaluation of human trials on cancer treatment." Melatonin Research 2, no. 2 (2019): 47–69. http://dx.doi.org/10.32794/mr11250021.

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Melatonin is a molecule with numerous properties, which are applicable to the treatment of different types of cancers. Experimental in vitro and in vivo studies conducted with human cancer cells or animal models of carcinogenesis, have shown that melatonin enhances apoptosis and inhibits cell proliferation of several human cancer cells, reduces tumor growth rate and its metastases, reduces the side effects of chemotherapy and radiotherapy, decreases the resistance to standard cancer treatments, and potentiates the therapeutic effects of other conventional therapies. These satisfactory results

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18

Clusan, Léa, Pascale Le Goff, Gilles Flouriot, and Farzad Pakdel. "A Closer Look at Estrogen Receptor Mutations in Breast Cancer and Their Implications for Estrogen and Antiestrogen Responses." International Journal of Molecular Sciences 22, no. 2 (2021): 756. http://dx.doi.org/10.3390/ijms22020756.

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Breast cancer (BC) is the most common cancer among women worldwide. More than 70% of BC cases express estrogen receptor alpha (ERα), a central transcription factor that stimulates the proliferation of breast cancer cells, usually in the presence of estrogen. While most cases of ER-positive BC initially respond to antiestrogen therapies, a high percentage of cases develop resistance to treatment over time. The recent discovery of mutated forms of ERα that result in constitutively active forms of the receptor in the metastatic-resistance stage of BC has provided a strong rationale for the develo

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19

O'Leary, Kathleen A., Fatou Jallow, Debra E. Rugowski та ін. "Prolactin Activates ERα in the Absence of Ligand in Female Mammary Development and Carcinogenesis in Vivo". Endocrinology 154, № 12 (2013): 4483–92. http://dx.doi.org/10.1210/en.2013-1533.

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Resistance of estrogen receptor positive (ERα+) breast cancers to antiestrogens is a major factor in the mortality of this disease. Although activation of ERα in the absence of ligand is hypothesized to contribute to this resistance, the potency of this mechanism in vivo is not clear. Epidemiologic studies have strongly linked prolactin (PRL) to both development of ERα+ breast cancer and resistance to endocrine therapies. Here we employed genetically modified mouse models to examine the ability of PRL and cross talk with TGFα to activate ERα, using a mutated ERα, ERα(G525L), which is refractor

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20

Louie, Maggie C., June X. Zou, Alina Rabinovich, and Hong-Wu Chen. "ACTR/AIB1 Functions as an E2F1 Coactivator To Promote Breast Cancer Cell Proliferation and Antiestrogen Resistance." Molecular and Cellular Biology 24, no. 12 (2004): 5157–71. http://dx.doi.org/10.1128/mcb.24.12.5157-5171.2004.

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ABSTRACT Overexpression or amplification of ACTR (also named AIB1, RAC3, p/CIP, TRAM-1, and SRC-3), a member of the p160 family of coactivators for nuclear hormone receptors, has been frequently detected in multiple types of human tumors, including breast cancer. However, its role in cancer cell proliferation and the underlying mechanism are unclear. Here, we show that overexpression of ACTR not only enhances estrogen-stimulated cell proliferation but also, more strikingly, completely negates the cell cycle arrest effect by tamoxifen and pure antiestrogens. Unexpectedly, we found that ACTR dir

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21

Clarke, R., and N. Brunner. "Cross-resistance and molecular mechanisms in antiestrogen resistance." Endocrine Related Cancer 2, no. 1 (1995): 59–72. http://dx.doi.org/10.1677/erc.0.0020059.

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22

Miller, Todd W., Justin M. Balko, and Carlos L. Arteaga. "Phosphatidylinositol 3-Kinase and Antiestrogen Resistance in Breast Cancer." Journal of Clinical Oncology 29, no. 33 (2011): 4452–61. http://dx.doi.org/10.1200/jco.2010.34.4879.

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Although antiestrogen therapies targeting estrogen receptor (ER) α signaling prevent disease recurrence in the majority of patients with hormone-dependent breast cancer, a significant fraction of patients exhibit de novo or acquired resistance. Currently, the only accepted mechanism linked with endocrine resistance is amplification or overexpression of the ERBB2 (human epidermal growth factor receptor 2 [HER2]) proto-oncogene. Experimental and clinical evidence suggests that hyperactivation of the phosphatidylinositol 3-kinase (PI3K) pathway, the most frequently mutated pathway in breast cance

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23

Clarke, Robert, Todd C. Skaar, Kerrie B. Bouker, et al. "Molecular and pharmacological aspects of antiestrogen resistance." Journal of Steroid Biochemistry and Molecular Biology 76, no. 1-5 (2001): 71–84. http://dx.doi.org/10.1016/s0960-0760(00)00193-x.

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Mayer, Ingrid A., Vandana Gupta Abramson, Justin M. Balko, et al. "SU2C phase Ib study of pan-PI3K inhibitor BKM120 with letrozole in ER+/HER2- metastatic breast cancer (MBC)." Journal of Clinical Oncology 30, no. 15_suppl (2012): 510. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.510.

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510 Background: Mutations in PIK3CA, the gene encoding the p110a subunit of PI3K, have been associated with antiestrogen resistance in ER+ BC. In general, antiestrogen-resistant cancers retain ER and responsiveness to estradiol. This suggests that treatment of ER+/PI3K mutant BC should include PI3K inhibitors plus antiestrogens. Methods: We conducted a phase Ib trial of letrozole (2.5 mg/d) with the pan-PI3K inhibitor BKM120 in post-menopausal patients (pts) with ER+/HER2 MBC. BKM120 (100 mg/d) was given continuously (Arm A) or intermittently (5 on/2 off days; Arm B). Upon toxicity, BKM120 was

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Cook, Katherine L., Pamela AG Clarke, and Robert Clarke. "Targeting GRP78 and antiestrogen resistance in breast cancer." Future Medicinal Chemistry 5, no. 9 (2013): 1047–57. http://dx.doi.org/10.4155/fmc.13.77.

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Bouker, Kerrie B., Yue Wang, Jianhua Xuan, and Robert Clarke. "Antiestrogen resistance and the application of systems biology." Drug Discovery Today: Disease Mechanisms 9, no. 1-2 (2012): e11-e17. http://dx.doi.org/10.1016/j.ddmec.2012.10.003.

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27

Paik, Soonmyoung, Dan Paul Hartmann, Robert B. Dickson, and Marc E. Lippman. "Antiestrogen resistance in ER positive breast cancer cells." Breast Cancer Research and Treatment 31, no. 2-3 (1994): 301–7. http://dx.doi.org/10.1007/bf00666162.

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28

Wallez, Yann, Stefan J. Riedl, and Elena B. Pasquale. "Association of the Breast Cancer Antiestrogen Resistance Protein 1 (BCAR1) and BCAR3 Scaffolding Proteins in Cell Signaling and Antiestrogen Resistance." Journal of Biological Chemistry 289, no. 15 (2014): 10431–44. http://dx.doi.org/10.1074/jbc.m113.541839.

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29

Katzenellenbogen, Benita S., Monica M. Montano, Kirk Ekena, Mary E. Herman, and Eileen M. McInerney. "Antiestrogens: Mechanisms of action and resistance in breast cancer." Breast Cancer Research and Treatment 44, no. 1 (1997): 23–38. http://dx.doi.org/10.1023/a:1005835428423.

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30

Guo, Shangqin, and Gail E. Sonenshein. "Forkhead Box Transcription Factor FOXO3a Regulates Estrogen Receptor Alpha Expression and Is Repressed by the Her-2/neu/Phosphatidylinositol 3-Kinase/Akt Signaling Pathway." Molecular and Cellular Biology 24, no. 19 (2004): 8681–90. http://dx.doi.org/10.1128/mcb.24.19.8681-8690.2004.

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ABSTRACT The expression status of the estrogen receptor alpha (ERα) and that of the epidermal growth factor receptor Her-2/neu frequently correlate inversely in breast cancers. While ERα-dependent cancers respond to antiestrogen therapy, Her-2/neu-overexpressing cancers typically display resistance to antiestrogens and poor prognosis. In this report we have explored the mechanism linking the loss of expression of ERα in breast cancer cells with overexpression of Her-2/neu, which signals constitutively via a phosphatidylinositol 3-kinase (PI3K)/Akt kinase pathway. We identify for the first time

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31

Clarke, Robert, and Nils Brunner. "Acquired estrogen independence and antiestrogen resistance in breast cancer." Trends in Endocrinology & Metabolism 7, no. 8 (1996): 291–301. http://dx.doi.org/10.1016/s1043-2760(96)00127-0.

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Suparwitri, Sri, Pinandi Sri Pudyani, Sofia Mubarika Haryana, and Dewi Agustina. "Effects of soy isoflavone genistein on orthodontic tooth movement in guinea pigs." Dental Journal (Majalah Kedokteran Gigi) 49, no. 3 (2016): 168. http://dx.doi.org/10.20473/j.djmkg.v49.i3.p168-174.

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Background: Osteoblast and osteoclast are the important factor in periodontal tissue remodeling for the orthodontic treatment success. Resorption process takes place in compression area by osteoclast and apposition in the tension area by osteoblast. In general hormone condition and age affect remodeling process. Estrogen has a high contribution in remodelling process and decreased in elderly individual such as menopausal women. Soybean contains isoflavone genistein which has similar structure and activity to estrogen. Many researchers indicate that isoflavone genistein not only has an inhibito

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Li, Ye, Katherine L. Cook, Wei Yu, et al. "Inhibition of Antiestrogen-Promoted Pro-Survival Autophagy and Tamoxifen Resistance in Breast Cancer through Vitamin D Receptor." Nutrients 13, no. 5 (2021): 1715. http://dx.doi.org/10.3390/nu13051715.

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We determined how vitamin D receptor (VDR) is linked to disease outcome in estrogen receptor-positive (ER+) breast cancer patients treated with tamoxifen (TAM). Breast cancer patients (n = 581) in four different datasets were divided into those expressing higher (above median) and lower levels of VDR in pretreatment ER+ tumors. Across all datasets, TAM-treated patients with higher pretreatment tumor VDR expression exhibited significantly longer recurrence-free survival. Ingenuity pathway analysis identified autophagy and unfolded protein response (UPR) as top differentially expressed pathways

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Semina, Svetlana, Alexander Scherbakov, Anna Vnukova, et al. "Exosome-Mediated Transfer of Cancer Cell Resistance to Antiestrogen Drugs." Molecules 23, no. 4 (2018): 829. http://dx.doi.org/10.3390/molecules23040829.

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Dowsett, Mitch, Robert I. Nicholson, and Richard J. Pietras. "Biological characteristics of the pure antiestrogen fulvestrant: overcoming endocrine resistance." Breast Cancer Research and Treatment 93, S1 (2005): 11–18. http://dx.doi.org/10.1007/s10549-005-9037-3.

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Giltnane, Jennifer M., Katherine E. Hutchinson, Thomas P. Stricker, et al. "Genomic profiling of ER+ breast cancers after short-term estrogen suppression reveals alterations associated with endocrine resistance." Science Translational Medicine 9, no. 402 (2017): eaai7993. http://dx.doi.org/10.1126/scitranslmed.aai7993.

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Inhibition of proliferation in estrogen receptor–positive (ER+) breast cancers after short-term antiestrogen therapy correlates with long-term patient outcome. We profiled 155 ER+/human epidermal growth factor receptor 2–negative (HER2−) early breast cancers from 143 patients treated with the aromatase inhibitor letrozole for 10 to 21 days before surgery. Twenty-one percent of tumors remained highly proliferative, suggesting that these tumors harbor alterations associated with intrinsic endocrine therapy resistance. Whole-exome sequencing revealed a correlation between 8p11-12 and 11q13 gene a

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Muluhngwi, Penn, and Carolyn M. Klinge. "Roles for miRNAs in endocrine resistance in breast cancer." Endocrine-Related Cancer 22, no. 5 (2015): R279—R300. http://dx.doi.org/10.1530/erc-15-0355.

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Therapies targeting estrogen receptor alpha (ERα), including selective ER modulators such as tamoxifen, selective ER downregulators such as fulvestrant (ICI 182 780), and aromatase inhibitors such as letrozole, are successfully used in treating breast cancer patients whose initial tumor expresses ERα. Unfortunately, the effectiveness of endocrine therapies is limited by acquired resistance. The role of microRNAs (miRNAs) in the progression of endocrine-resistant breast cancer is of keen interest in developing biomarkers and therapies to counter metastatic disease. This review focuses on miRNAs

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38

Ratajczak, T. "Protein coregulators that mediate estrogen receptor function." Reproduction, Fertility and Development 13, no. 4 (2001): 221. http://dx.doi.org/10.1071/rd01023.

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The recent discovery of estrogen receptor β as a biological partner with estrogen receptor β in mediating the estrogen response has come at precisely the same time as intensive research is revealing the role played by downstream coregulator proteins in linking nuclear hormone receptor activity to general transcription machinery involved in gene transcriptional activation. In what is a rapidly evolving area of research, findings to date have led to a proposed model of hormonal action, in which a receptor activated by estrogen or cell-membrane-derived phosphorylation-dependent signaling pathways

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van Agthoven, Ton, Anieta M. Sieuwerts, Marion E. Meijer-van Gelder, et al. "Relevance of Breast Cancer Antiestrogen Resistance Genes in Human Breast Cancer Progression and Tamoxifen Resistance." Journal of Clinical Oncology 27, no. 4 (2009): 542–49. http://dx.doi.org/10.1200/jco.2008.17.1462.

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Purpose We have previously identified a set of breast cancer antiestrogen resistance (BCAR) genes causing estrogen independence and tamoxifen resistance in vitro using a functional genetic screen. Here, we explored whether these BCAR genes provide predictive value for tamoxifen resistance and prognostic information for tumor aggressiveness in breast cancer patients. Patients and Methods mRNA levels of 10 BCAR genes (AKT1, AKT2, BCAR1, BCAR3, EGFR, ERBB2, GRB7, SRC, TLE3, and TRERF1) were measured in estrogen receptor–positive breast tumors using quantitative reverse-transcriptase polymerase ch

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Zwart, Wilbert, Mariska Rondaij, Kees Jalink, et al. "Resistance to Antiestrogen Arzoxifene Is Mediated by Overexpression of Cyclin D1." Molecular Endocrinology 23, no. 9 (2009): 1335–45. http://dx.doi.org/10.1210/me.2008-0268.

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Kang, J., P. X. Qian, V. Pandey, et al. "Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma." Oncogene 29, no. 22 (2010): 3228–40. http://dx.doi.org/10.1038/onc.2010.71.

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42

Zwart, Wilbert, Mariska Rondaij, Kees Jalink, et al. "Resistance to Antiestrogen Arzoxifene Is Mediated by Overexpression of Cyclin D1." Journal of Clinical Endocrinology & Metabolism 94, no. 8 (2009): 3101. http://dx.doi.org/10.1210/jcem.94.8.9994.

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Morotti, Matteo, Esther Bridges, Alessandro Valli, et al. "Hypoxia-induced switch in SNAT2/SLC38A2 regulation generates endocrine resistance in breast cancer." Proceedings of the National Academy of Sciences 116, no. 25 (2019): 12452–61. http://dx.doi.org/10.1073/pnas.1818521116.

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Tumor hypoxia is associated with poor patient outcomes in estrogen receptor-α–positive (ERα+) breast cancer. Hypoxia is known to affect tumor growth by reprogramming metabolism and regulating amino acid (AA) uptake. Here, we show that the glutamine transporter, SNAT2, is the AA transporter most frequently induced by hypoxia in breast cancer, and is regulated by hypoxia both in vitro and in vivo in xenografts. SNAT2 induction in MCF7 cells was also regulated by ERα, but it became predominantly a hypoxia-inducible factor 1α (HIF-1α)–dependent gene under hypoxia. Relevant to this, binding sites f

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Traboulsi, T., M. El Ezzy, J. L. Gleason, and S. Mader. "Antiestrogens: structure-activity relationships and use in breast cancer treatment." Journal of Molecular Endocrinology 58, no. 1 (2017): R15—R31. http://dx.doi.org/10.1530/jme-16-0024.

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About 70% of breast tumors express estrogen receptor alpha (ERα), which mediates the proliferative effects of estrogens on breast epithelial cells, and are candidates for treatment with antiestrogens, steroidal or non-steroidal molecules designed to compete with estrogens and antagonize ERs. The variable patterns of activity of antiestrogens (AEs) in estrogen target tissues and the lack of systematic cross-resistance between different types of molecules have provided evidence for different mechanisms of action. AEs are typically classified as selective estrogen receptor modulators (SERMs), whi

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Pietras, R. J., D. C. Marquez, H. Chen, M. X. Sliwkowski, and D. J. Slamon. "Improved antitumor therapy by dual targeting of estrogen and growth factor receptor signaling in human breast cancer cells." Journal of Clinical Oncology 24, no. 18_suppl (2006): 637. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.637.

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637 Background: Breast cancer growth is tightly regulated by interactions between growth factor and estrogen receptors. Dimerization is crucial for activation of HER receptors (EGFR, HER2, HER3, HER4) that contribute to modulation of tumor progression and the failure of antiestrogen therapy. HER2 is the preferred dimerization partner in a process stimulated by the several HER receptor ligands. HER2 antibody (trastuzumab) shows antitumor efficacy in HER2-overexpressing cancers. New antibodies that disrupt HER2 dimerization (pertuzumab) may be useful in treating cancers with normal HER2 levels.

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Schwarz, Luis J., Emily M. Fox, Justin M. Balko, et al. "LYN-activating mutations mediate antiestrogen resistance in estrogen receptor–positive breast cancer." Journal of Clinical Investigation 124, no. 12 (2014): 5490–502. http://dx.doi.org/10.1172/jci72573.

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Kang, J., P. X. Qian, V. Pandey, et al. "Erratum: Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma." Oncogene 31, no. 3 (2012): 402. http://dx.doi.org/10.1038/onc.2011.553.

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Clarke, Robert, Minetta C. Liu, Kerrie B. Bouker, et al. "Antiestrogen resistance in breast cancer and the role of estrogen receptor signaling." Oncogene 22, no. 47 (2003): 7316–39. http://dx.doi.org/10.1038/sj.onc.1206937.

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Nabha, Sanaa M., Selina Glaros, Meng Hong та ін. "Upregulation of PKC-δ contributes to antiestrogen resistance in mammary tumor cells". Oncogene 24, № 19 (2005): 3166–76. http://dx.doi.org/10.1038/sj.onc.1208502.

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Sorokin, D. V., O. E. Andreeva, E. I. Mikhaevich, et al. "Effect of the exosome-mediated suppression of the estrogen signaling: the role in the progression of the hormonal resistance of breast cancer cells." Advances in Molecular Oncology 7, no. 3 (2020): 58–62. http://dx.doi.org/10.17650/2313-805x-2020-7-3-58-62.

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The most effective treatment of the hormone-dependent breast cancer is based on the antiestrogens SERM and aromatase inhibitor treatment, however its efficiency is limited by the acquired resistance to the drugs.Previously we have revealed the effect of the transferring of the hormonal resistance from the resistant to the sensitive cells under in vitro cell co-cultivation, and demonstrated exosomes involvement in this process. Here we have shown that the exosomes of the resistant cells caused the marked inhibition of the estrogen signaling in the recipient cells, and identified microRNAs – ERα

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