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Journal articles on the topic 'Endocrine resistance'

To see the other types of publications on this topic, follow the link: Endocrine resistance.

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Pinto, Ana Catarina, and Martine J. Piccart-Gebhart. "IN5 ADVANCES IN ENDOCRINE THERAPY AND ENDOCRINE RESISTANCE." Breast 22 (November 2013): S19—S20. http://dx.doi.org/10.1016/s0960-9776(13)70020-1.

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2

Zheng, L. H., Y. H. Zhao, H. L. Feng, and Y. J. Liu. "Endocrine resistance in breast cancer." Climacteric 17, no. 5 (December 19, 2013): 522–28. http://dx.doi.org/10.3109/13697137.2013.864268.

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3

Lei, Jonathan T., Meenakshi Anurag, Svasti Haricharan, Xuxu Gou, and Matthew J. Ellis. "Endocrine therapy resistance: new insights." Breast 48 (November 2019): S26—S30. http://dx.doi.org/10.1016/s0960-9776(19)31118-x.

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4

KRAEMER, WILLIAM J. "Endocrine responses to resistance exercise." Medicine & Science in Sports & Exercise 20, Sup 1 (October 1988): S152—S157. http://dx.doi.org/10.1249/00005768-198810001-00011.

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5

Johnston, Stephen R. D. "Molecular insights into endocrine resistance." European Journal of Cancer Supplements 3, no. 3 (October 2005): 225–36. http://dx.doi.org/10.1016/s1359-6349(05)80279-4.

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6

Dixon, J. M. "Endocrine Resistance in Breast Cancer." New Journal of Science 2014 (September 17, 2014): 1–27. http://dx.doi.org/10.1155/2014/390618.

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Around 70% of all breast cancers are estrogen receptor alpha positive and hence their development is highly dependent on estradiol. While the invention of endocrine therapies has revolusioned the treatment of the disease, resistance to therapy eventually occurs in a large number of patients. This paper seeks to illustrate and discuss the complexity and heterogeneity of the mechanisms which underlie resistance and the approaches proposed to combat them. It will also focus on the use and development of methods for predicting which patients are likely to develop resistance.

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7

Nicholson, Robert I., Iain R. Hutcheson, Janice M. Knowlden, Helen E. Jones, Maureen E. Harper, Nicola Jordan, Steve E. Hiscox, Denise Barrow, and Julia M. W. Gee. "Nonendocrine Pathways and Endocrine Resistance." Clinical Cancer Research 10, no. 1 (January 1, 2004): 346s—354s. http://dx.doi.org/10.1158/1078-0432.ccr-031206.

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8

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 evidence indicates that oncogenic signaling pathways underlie endocrine resistance, including growth factor receptor tyrosine kinases (HER2, epidermal growth factor receptor [EGFR], fibroblast growth factor receptor 1/2 [FGFR], insulin-like growth factor-1 receptor [IGF-1R]/ insulin receptor [InsR]), PI3K/AKT/ mTOR, MAPK/ERK, Src, CDK4/CDK6, and ER itself. Combined targeting of ER and such pathways may be the most effective means to combat antiestrogen resistance, and clinical trials testing such strategies show promising results. Herein, we discuss pathways associated with endocrine resistance, biomarkers that may be useful to predict response to targeted agents, and avenues for further exploration to identify strategies for the treatment of patients with endocrine-resistant disease.

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9

Dzhelyalova, M. A. Dzhelyalova, and V. F. Semiglazov Semiglazov. "Endocrine resistance in breast cancer treatment." Pharmateca 11_2020 (October 23, 2020): 21–29. http://dx.doi.org/10.18565/pharmateca.2020.11.21-29.

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10

Madaio, R. A., G. Spalletta, L. Cravello, M. Ceci, L. Repetto, and G. Naso. "Overcoming Endocrine Resistance in Breast Cancer." Current Cancer Drug Targets 10, no. 5 (August 1, 2010): 519–28. http://dx.doi.org/10.2174/156800910791517226.

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11

Dowsett, Mitchell. "Endocrine Resistance in Advanced Breast Cancer." Acta Oncologica 35, sup5 (January 1996): 91–95. http://dx.doi.org/10.3109/02841869609083979.

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12

Damodaran, Senthil, Sarmila Majumder, and Bhuvaneswari Ramaswamy. "Endocrine resistance: mechanisms and therapeutic targets." Clinical Investigation 3, no. 7 (July 2013): 681–90. http://dx.doi.org/10.4155/cli.13.49.

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13

Miller, Todd W. "Endocrine Resistance: What Do We Know?" American Society of Clinical Oncology Educational Book 33 (2013): e37-e42. http://dx.doi.org/10.1200/edbook_am.2013.33.e37.

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14

Saji, Shigehira. "Introduction: Strategies to overcome endocrine resistance." Annals of Oncology 27 (November 2016): vii27. http://dx.doi.org/10.1093/annonc/mdw473.

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15

Hanker, Ariella B., Dhivya R. Sudhan, and Carlos L. Arteaga. "Overcoming Endocrine Resistance in Breast Cancer." Cancer Cell 37, no. 4 (April 2020): 496–513. http://dx.doi.org/10.1016/j.ccell.2020.03.009.

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16

Murray, Jill I., Nathan R. West, Leigh C. Murphy, and Peter H. Watson. "Intratumoural inflammation and endocrine resistance in breast cancer." Endocrine-Related Cancer 22, no. 1 (November 17, 2014): R51—R67. http://dx.doi.org/10.1530/erc-14-0096.

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It is becoming clear that inflammation-associated mechanisms can affect progression of breast cancer and modulate responses to treatment. Estrogen receptor alpha (ERα (ESR1)) is the principal biomarker and therapeutic target for endocrine therapies in breast cancer. Over 70% of patients are ESR1-positive at diagnosis and are candidates for endocrine therapy. However, ESR1-positive tumours can become resistant to endocrine therapy. Multiple mechanisms of endocrine resistance have been proposed, including suppression of ESR1. This review discusses the relationship between intratumoural inflammation and endocrine resistance with a particular focus on inflammation-mediated suppression of ESR1.

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17

Jackisch, Christian. "Overcoming endocrine resistance in neoadjuvant endocrine therapy for early breast cancer." Lancet Oncology 20, no. 9 (September 2019): 1185–87. http://dx.doi.org/10.1016/s1470-2045(19)30500-5.

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18

Hartkopf, Andreas D., Eva-Maria Grischke, and Sara Y. Brucker. "Endocrine-Resistant Breast Cancer: Mechanisms and Treatment." Breast Care 15, no. 4 (2020): 347–54. http://dx.doi.org/10.1159/000508675.

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Background: Endocrine treatment is one of the most effective therapies for estrogen receptor-positive breast cancer. However, most tumors will develop resistance to endocrine therapy as the cancer progresses. This review focuses on the mechanisms and markers of endocrine-resistant breast cancer. In addition, current and future strategies to overcome endocrine resistance are discussed. Summary: Several molecular mechanisms of endocrine resistance have been identified, including alterations in the ESR1 gene or in the PIK3CA/mTOR pathway. Meanwhile, CDK4/6, mTOR, and PI3K inhibition have shown to improve the efficacy of endocrine treatment and new promising approaches are being developed. Key Message: Overcoming primary or acquired resistance to endocrine treatment remains a major challenge. Since the molecular mechanisms of endocrine resistance are manifold, optimal combination and sequencing strategies will have to be developed in the future.

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19

Cook, Katherine L., Ayesha N. Shajahan, and Robert Clarke. "Autophagy and endocrine resistance in breast cancer." Expert Review of Anticancer Therapy 11, no. 8 (August 2011): 1283–94. http://dx.doi.org/10.1586/era.11.111.

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20

Biganzoli, L., E. Zafarana, N. Turner, and L. Malorni. "Overcoming endocrine resistance in breast cancer patients." Journal of Geriatric Oncology 3 (October 2012): S12—S13. http://dx.doi.org/10.1016/j.jgo.2012.10.141.

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21

Bansal, Naresh, Narendra Kotwal, and Sandeep Kumar. "Aerobic vs Resistance Exercise—An Endocrine Perspective." Journal of Medical Academics 3, no. 1 (2020): 7–10. http://dx.doi.org/10.5005/jp-journals-10070-0057.

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22

Osborne, C. Kent, and Rachel Schiff. "Mechanisms of Endocrine Resistance in Breast Cancer." Annual Review of Medicine 62, no. 1 (February 18, 2011): 233–47. http://dx.doi.org/10.1146/annurev-med-070909-182917.

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23

Miller, William R., Alexey Larionov, Thomas J. Anderson, John R. Walker, Andreas Krause, Dean B. Evans, and J. Michael Dixon. "Predicting response and resistance to endocrine therapy." Cancer 112, S3 (2008): 689–94. http://dx.doi.org/10.1002/cncr.23187.

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24

Macedo, Luciana F., Gauri Sabnis, and Angela Brodie. "Preclinical modeling of endocrine response and resistance." Cancer 112, S3 (2008): 679–88. http://dx.doi.org/10.1002/cncr.23191.

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25

Kim, Tae Hyun. "Overcoming Endocrine Therapy Resistance in Breast Caner." Korean Journal of Clinical Oncology 5, no. 2 (December 30, 2009): 25–31. http://dx.doi.org/10.14216/kjco.09011.

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26

Falk, Bareket, and Alon Eliakim. "Endocrine Response to Resistance Training in Children." Pediatric Exercise Science 26, no. 4 (November 2014): 404–22. http://dx.doi.org/10.1123/pes.2014-0161.

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27

Peppa, Melpomeni, Chrysi Koliaki, Panagiotis Nikolopoulos, and Sotirios A. Raptis. "Skeletal Muscle Insulin Resistance in Endocrine Disease." Journal of Biomedicine and Biotechnology 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/527850.

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We summarize the existing literature data concerning the involvement of skeletal muscle (SM) in whole body glucose homeostasis and the contribution of SM insulin resistance (IR) to the metabolic derangements observed in several endocrine disorders, including polycystic ovary syndrome (PCOS), adrenal disorders and thyroid function abnormalities. IR in PCOS is associated with a unique postbinding defect in insulin receptor signaling in general and in SM in particular, due to a complex interaction between genetic and environmental factors. Adrenal hormone excess is also associated with disrupted insulin action in peripheral tissues, such as SM. Furthermore, both hyper- and hypothyroidism are thought to be insulin resistant states, due to insulin receptor and postreceptor defects. Further studies are definitely needed in order to unravel the underlying pathogenetic mechanisms. In summary, the principal mechanisms involved in muscle IR in the endocrine diseases reviewed herein include abnormal phosphorylation of insulin signaling proteins, altered muscle fiber composition, reduced transcapillary insulin delivery, decreased glycogen synthesis, and impaired mitochondrial oxidative metabolism.

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28

McGuire, William L., Marc E. Lippman, C. Kent Osborne, and E. Brad Thompson. "Resistance to endocrine therapy A panel discussion." Breast Cancer Research and Treatment 9, no. 3 (October 1987): 165–73. http://dx.doi.org/10.1007/bf01806377.

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29

Trivedi, Dipali, Sujatha Murali, and Ruth M. O’Regan. "Endocrine Therapy for Metastatic Disease: Reversing Resistance." Current Breast Cancer Reports 2, no. 2 (April 17, 2010): 114–19. http://dx.doi.org/10.1007/s12609-010-0002-8.

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30

Kurebayashi, Junichi. "Resistance to endocrine therapy in breast cancer." Cancer Chemotherapy and Pharmacology 56, S1 (November 2005): 39–46. http://dx.doi.org/10.1007/s00280-005-0099-z.

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31

Chia, KeeMing, Heloisa Milioli, Neil Portman, Geraldine Laven-Law, Rhiannon Coulson, Aliza Yong, Davendra Segara, et al. "Non-canonical AR activity facilitates endocrine resistance in breast cancer." Endocrine-Related Cancer 26, no. 2 (February 2019): 251–64. http://dx.doi.org/10.1530/erc-18-0333.

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The role of androgen receptor (AR) in endocrine-resistant breast cancer is controversial and clinical trials targeting AR with an AR antagonist (e.g., enzalutamide) have been initiated. Here, we investigated the consequence of AR antagonism using in vitro and in vivo models of endocrine resistance. AR antagonism in MCF7-derived tamoxifen-resistant (TamR) and long-term estrogen-deprived breast cancer cell lines were achieved using siRNA-mediated knockdown or pharmacological inhibition with enzalutamide. The efficacy of enzalutamide was further assessed in vivo in an estrogen-independent endocrine-resistant patient-derived xenograft (PDX) model. Knockdown of AR inhibited the growth of the endocrine-resistant cell line models. Microarray gene expression profiling of the TamR cells following AR knockdown revealed perturbations in proliferative signaling pathways upregulated in endocrine resistance. AR loss also increased some canonical ER signaling events and restored sensitivity of TamR cells to tamoxifen. In contrast, enzalutamide did not recapitulate the effect of AR knockdown in vitro, even though it inhibited canonical AR signaling, which suggests that it is the non-canonical AR activity that facilitated endocrine resistance. Enzalutamide had demonstrable efficacy in inhibiting AR activity in vivo but did not affect the growth of the endocrine-resistant PDX model. Our findings implicate non-canonical AR activity in facilitating an endocrine-resistant phenotype in breast cancer. Unlike canonical AR signaling which is inhibited by enzalutamide, non-canonical AR activity is not effectively antagonized by enzalutamide, and this has important implications in the design of future AR-targeted clinical trials in endocrine-resistant breast cancer.

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32

Johnston, Stephen R. D., and Gaia Schiavon. "Treatment Algorithms for Hormone Receptor–Positive Advanced Breast Cancer: Going Forward in Endocrine Therapy—Overcoming Resistance and Introducing New Agents." American Society of Clinical Oncology Educational Book, no. 33 (May 2013): e28-e36. http://dx.doi.org/10.14694/edbook_am.2013.33.e28.

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Overcoming de novo or acquired endocrine resistance remains critical to further enhancing the benefit of existing endocrine therapies. Recent progress has been made in understanding the molecular biology associated with acquired endocrine resistance, including adaptive “cross-talk” between ER and various growth factor receptor and cell-signaling pathways. Strategies that combine endocrine therapy with targeted inhibitors of growth factor receptors or cell-survival pathways to further enhance first-line response have largely been disappointing, suggesting that any attempts to prevent endocrine resistance by blocking specific pathways from the outset will be futile. In contrast, success has been seen by selecting patients with acquired endocrine resistance and enhancing response to further endocrine therapy by the addition of mTOR antagonists. Numerous other therapeutics are being evaluated in combination with endocrine therapies based on varying levels of preclinical science to support their use, including inhibitors of PI3K, HDAC, Src, IGFR-1, and CDK4/6. Enriching trial recruitment by molecular profiling of different ER+ subtypes will become increasingly important to maximize any additional benefit that these new agents may bring to current endocrine therapies for breast cancer.

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33

Rodriguez, David, Marc Ramkairsingh, Xiaozeng Lin, Anil Kapoor, Pierre Major, and Damu Tang. "The Central Contributions of Breast Cancer Stem Cells in Developing Resistance to Endocrine Therapy in Estrogen Receptor (ER)-Positive Breast Cancer." Cancers 11, no. 7 (July 22, 2019): 1028. http://dx.doi.org/10.3390/cancers11071028.

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Breast cancer stem cells (BCSC) play critical roles in the acquisition of resistance to endocrine therapy in estrogen receptor (ER)-positive (ER + ve) breast cancer (BC). The resistance results from complex alterations involving ER, growth factor receptors, NOTCH, Wnt/β-catenin, hedgehog, YAP/TAZ, and the tumor microenvironment. These mechanisms are likely converged on regulating BCSCs, which then drive the development of endocrine therapy resistance. In this regard, hormone therapies enrich BCSCs in ER + ve BCs under both pre-clinical and clinical settings along with upregulation of the core components of “stemness” transcriptional factors including SOX2, NANOG, and OCT4. SOX2 initiates a set of reactions involving SOX9, Wnt, FXY3D, and Src tyrosine kinase; these reactions stimulate BCSCs and contribute to endocrine resistance. The central contributions of BCSCs to endocrine resistance regulated by complex mechanisms offer a unified strategy to counter the resistance. ER + ve BCs constitute approximately 75% of BCs to which hormone therapy is the major therapeutic approach. Likewise, resistance to endocrine therapy remains the major challenge in the management of patients with ER + ve BC. In this review we will discuss evidence supporting a central role of BCSCs in developing endocrine resistance and outline the strategy of targeting BCSCs to reduce hormone therapy resistance.

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34

Bullock, M. "FOXO factors and breast cancer: outfoxing endocrine resistance." Endocrine-Related Cancer 23, no. 2 (November 26, 2015): R113—R130. http://dx.doi.org/10.1530/erc-15-0461.

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The majority of metastatic breast cancers cannot be cured and present a major public health problem worldwide. Approximately 70% of breast cancers express the estrogen receptor, and endocrine-based therapies have significantly improved patient outcomes. However, the development of endocrine resistance is extremely common. Understanding the molecular pathways that regulate the hormone sensitivity of breast cancer cells is important to improving the efficacy of endocrine therapy. It is becoming clearer that the PI3K–AKT–forkhead box O (FOXO) signaling axis is a key player in the hormone-independent growth of many breast cancers. Constitutive PI3K–AKT pathway activation, a driver of breast cancer growth, causes down-regulation of FOXO tumor suppressor functions. This review will summarize what is currently known about the role of FOXOs in endocrine-resistance mechanisms. It will also suggest potential therapeutic strategies for the restoration of normal FOXO transcriptional activity.

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35

Roßwag, Sven, Cristina L. Cotarelo, Klaus Pantel, Sabine Riethdorf, Jonathan P. Sleeman, Marcus Schmidt, and Sonja Thaler. "Functional Characterization of Circulating Tumor Cells (CTCs) from Metastatic ER+/HER2− Breast Cancer Reveals Dependence on HER2 and FOXM1 for Endocrine Therapy Resistance and Tumor Cell Survival: Implications for Treatment of ER+/HER2− Breast Cancer." Cancers 13, no. 8 (April 10, 2021): 1810. http://dx.doi.org/10.3390/cancers13081810.

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Mechanisms of acquired endocrine resistance and late recurrence in patients with ER+/HER2− breast cancer are complex and not fully understood. Here, we evaluated mechanisms of acquired resistance in circulating tumor cells (CTCs) from an ER+/HER2− breast cancer patient who initially responded but later progressed under endocrine treatment. We found a switch from ERα-dependent to HER2-dependent and ERα-independent expression of FOXM1, which may enable disseminated ER+/HER2− cells to re-initiate tumor cell growth and metastasis formation in the presence of endocrine treatment. Our results also suggest a role for HER2 in resistance, even in ER+ breast cancer cells that have neither HER2 amplification nor activating HER2 mutations. We found that NFkB signaling sustains HER2 and FOXM1 expression in CTCs in the presence of ERα inhibitors. Inhibition of NFkB signaling blocked expression of HER2 and FOXM1 in the CTCs, and induced apoptosis. Thus, targeting of NFkB and FOXM1 might be an efficient therapeutic approach to prevent late recurrence and to treat endocrine resistance. Collectively our data show that CTCs from patients with endocrine resistance allow mechanisms of acquired endocrine resistance to be delineated, and can be used to test potential drug regimens for combatting resistance.

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36

AlFakeeh, A., and C. Brezden-Masley. "Overcoming endocrine resistance in hormone receptor–positive breast cancer." Current Oncology 25 (June 14, 2018): 18. http://dx.doi.org/10.3747/co.25.3752.

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Endocrine therapy, a major modality in the treatment of hormone receptor (hr)–positive breast cancer (bca), has improved outcomes in metastatic and nonmetastatic disease. However, a limiting factor to the use of endocrine therapy in bca is resistance resulting from the development of escape pathways that promote the survival of cancer cells despite estrogen receptor (er)–targeted therapy. The resistance pathways involve extensive cross-talk between er and receptor tyrosine kinase growth factors [epidermal growth factor receptor, human epidermal growth factor receptor 2 (her2), and insulin-like growth factor 1 receptor] and their downstream signalling pathways—most notably pi3k/akt/mtor and mapk. In some cases, resistance develops as a result of genetic or epigenetic alterations in various components of the signalling pathways, such as overexpression of her2 and erα co-activators, aberrant expression of cell-cycle regulators, and PIK3CA mutations. By combining endocrine therapy with various molecularly targeted agents and signal transduction inhibitors, some success has been achieved in overcoming and modulating endocrine resistance in hr-positive bca. Established strategies include selective er downregulators, anti-her2 agents, mtor (mechanistic target of rapamycin) inhibitors, and inhibitors of cyclin-dependent kinases 4 and 6. Inhibitors of pi3ka are not currently a treatment option for women with hr-positive bca outside the context of clinical trial. Ongoing clinical trials are exploring more agents that could be combined with endocrine therapy, and biomarkers that would help to guide decision-making and maximize clinical efficacy. In this review article, we address current treatment strategies for endocrine resistance, and we highlight future therapeutic targets in the endocrine pathway of bca.

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37

Muluhngwi, Penn, and Carolyn M. Klinge. "Roles for miRNAs in endocrine resistance in breast cancer." Endocrine-Related Cancer 22, no. 5 (October 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 implicated as disruptors of antiestrogen therapies, theirbona fidegene targets and associated pathways promoting endocrine resistance.

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38

Johnston, Stephen R. D. "Mechanisms of Resistance to Endocrine and Biological Agents." Breast 36 (November 2017): S23. http://dx.doi.org/10.1016/s0960-9776(17)30632-x.

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39

Musgrove, Elizabeth A., and Robert L. Sutherland. "Biological determinants of endocrine resistance in breast cancer." Nature Reviews Cancer 9, no. 9 (September 2009): 631–43. http://dx.doi.org/10.1038/nrc2713.

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40

Lord, Christopher J., Elizabeth Iorns, and Alan Ashworth. "Dissecting resistance to endocrine therapy in breast cancer." Cell Cycle 7, no. 13 (July 2008): 1895–98. http://dx.doi.org/10.4161/cc.7.13.6118.

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41

Ellis, Matthew. "Overcoming Endocrine Therapy Resistance by Signal Transduction Inhibition." Oncologist 9, S3 (June 3, 2004): 20–26. http://dx.doi.org/10.1634/theoncologist.9-suppl_3-20.

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42

Samdariya, Saurabh, PuneetKumar Bagri, Puneet Pareek, and Ruchi Kumawat. "Palbociclib: Will the race against endocrine resistance end?" Clinical Cancer Investigation Journal 4, no. 6 (2015): 775. http://dx.doi.org/10.4103/2278-0513.167861.

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43

Dawood, S., and M. Cristofanilli. "Endocrine resistance in breast cancer: what really matters?" Annals of Oncology 18, no. 8 (August 2007): 1289–91. http://dx.doi.org/10.1093/annonc/mdm359.

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44

Hurvitz, Sara A., and Richard J. Pietras. "Rational management of endocrine resistance in breast cancer." Cancer 113, no. 9 (November 1, 2008): 2385–97. http://dx.doi.org/10.1002/cncr.23875.

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45

Stenz, Ludwig, Rita Rahban, Julien Prados, Serge Nef, and Ariane Paoloni-Giacobino. "Genetic resistance to DEHP-induced transgenerational endocrine disruption." PLOS ONE 14, no. 6 (June 10, 2019): e0208371. http://dx.doi.org/10.1371/journal.pone.0208371.

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46

Fry, A. C., R. S. Staron, F. C. Hagerman, R. S. Hikida, W. J. Kraemer, G. E. R. Campos, M. A. Starks, and J. C. Melton. "ENDOCRINE RESPONSES TO THREE DIFFERENT RESISTANCE EXERCISE REGIMENS." Medicine & Science in Sports & Exercise 31, Supplement (May 1999): S269. http://dx.doi.org/10.1097/00005768-199905001-01307.

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47

Rotondo, Eleonora, and Francesco Chiarelli. "Endocrine-Disrupting Chemicals and Insulin Resistance in Children." Biomedicines 8, no. 6 (May 28, 2020): 137. http://dx.doi.org/10.3390/biomedicines8060137.

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The purpose of this article is to review the evidence linking background exposure to endocrine-disrupting chemicals (EDCs) with insulin resistance in children. Although evidence in children is scarce since very few prospective studies exist even in adults, evidence that EDCs might be involved in the development of insulin resistance and related diseases such as obesity and diabetes is accumulating. We reviewed the literature on both cross-sectional and prospective studies in humans and experimental studies. Epidemiological studies show a statistical link between exposure to pesticides, polychlorinated bisphenyls, bisphenol A, phthalates, aromatic polycyclic hydrocarbides, or dioxins and insulin resistance.

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48

Nardone, Agostina, Carmine De Angelis, Meghana V. Trivedi, C. Kent Osborne, and Rachel Schiff. "The changing role of ER in endocrine resistance." Breast 24 (November 2015): S60—S66. http://dx.doi.org/10.1016/j.breast.2015.07.015.

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49

Maurer, Christian, Samuel Martel, Dimitrios Zardavas, and Michail Ignatiadis. "New agents for endocrine resistance in breast cancer." Breast 34 (August 2017): 1–11. http://dx.doi.org/10.1016/j.breast.2017.04.007.

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50

Rasha, Fahmida, Monica Sharma, and Kevin Pruitt. "Mechanisms of endocrine therapy resistance in breast cancer." Molecular and Cellular Endocrinology 532 (July 2021): 111322. http://dx.doi.org/10.1016/j.mce.2021.111322.

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