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Artykuły w czasopismach na temat „Endocrine resistance”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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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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Arneth, Borros. "Insulin Resistance and Glucose Metabolism during Infection." Endocrines 4, no. 4 (2023): 685–95. http://dx.doi.org/10.3390/endocrines4040049.

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Specific critical functions of endocrine and immune cells ensure that an individual remains healthy and free from infection. This study aimed to explore immune–endocrine associations involved in disease. Methods: The PsycINFO, PubMed, Web of Science, and CINAHL databases were searched for relevant articles using the following search terms and phrases: “hormones”, “hormonal responses”, “immune system”, “endocrine system”, “infection”, “immune cells”, “endocrine cells”, “infection”, “immune”, “endocrine”, and “interactions”. The search was limited to articles published between 2009 and 2023. Res

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

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

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Nicholson, Robert I., Iain R. Hutcheson, Janice M. Knowlden, et al. "Nonendocrine Pathways and Endocrine Resistance." Clinical Cancer Research 10, no. 1 (2004): 346s—354s. http://dx.doi.org/10.1158/1078-0432.ccr-031206.

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

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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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Carey, Lisa A. "IN23 RE-DEFINING ENDOCRINE RESISTANCE." Breast 71 (October 2023): S22. http://dx.doi.org/10.1016/s0960-9776(23)00598-2.

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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

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11

Lu, Qianyi, Fei Xu, Shusen Wang, Na Wang, Yang Shao, and Yuming Ouyang. "Tumor copy number alterations were associated with primary endocrine resistance in ER+ breast cancer." Journal of Clinical Oncology 40, no. 16_suppl (2022): e12567-e12567. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e12567.

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e12567 Background: Several studies has showed alterations in genes were associated with endocrine resistance in breast cancer. Nevertheless, genomic landscape in primary endocrine-resistant breast cancer has not been thoroughly reported. Whether the genomic landscape of primary endocrine-resistant breast cancer is different from that of secondary endocrine-resistant breast cancer is unknown. Methods: We analyzed the genomic landscape of primary tumor of consecutive patients with estrogen-receptor positive (ER+) breast cancer in real-world clinical practice in our center between September, 2019

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12

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 (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 inflammat

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13

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

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14

Khan, Asiya, Sandeep Sisodiya, Mehreen Aftab, Pranay Tanwar, Showket Hussain, and Vivek Gupta. "Mechanisms and Therapeutic Strategies for Endocrine Resistance in Breast Cancer: A Comprehensive Review and Meta-Analysis." Cancers 17, no. 10 (2025): 1653. https://doi.org/10.3390/cancers17101653.

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Background: As per recent scenarios, drug resistance is a significant challenge in treating breast cancer for several reasons, such as genetic mutations, altered signaling pathways, and tumor microenvironment. Endocrine resistance is one of the biggest significant barriers to treatment, particularly in hormone receptor-positive (HR+) breast cancers, which depends on estrogen or progesterone signaling for growth. While therapies such as tamoxifen, aromatase inhibitors, and selective estrogen receptor degraders (SERDs) have effectively targeted these pathways, many patients develop resistance, r

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15

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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16

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 (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

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17

Sun, Hong, Congting Hu, Xiaohan Zheng, Jie Zhuang, Xiaoxia Wei, and Jiaqin Cai. "Correlation between serum lipid levels and endocrine resistance in patients with ER-positive breast cancer." Medicine 102, no. 41 (2023): e35048. http://dx.doi.org/10.1097/md.0000000000035048.

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Lipid metabolism may be involved in the development of endocrine drug resistance in ER-positive (ER+) breast cancer (BC). This study aimed to investigate the relationship between serum lipid levels, risk stratification of dyslipidemia, and endocrine resistance. We collected the data from 166 ER + breast cancer patients who received endocrine therapy (ET). 73 of 166 patients (44.0%)developed endocrine resistance. Univariate and multivariate COX regression were conducted to explore the potential factors affecting endocrine resistance in BC. The clinical T stage, mean serum lipid levels in ET pro

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18

Udden, SM Nashir, Asal Rahimi, Dong W. Nathan Kim, and Prasanna Alluri. "Abstract P4-02-08: Towards Precision Radiation Oncology: Endocrine Therapy Resistance as a Biomarker for Radiation Resistance in ER-Positive Breast Cancer." Cancer Research 83, no. 5_Supplement (2023): P4–02–08—P4–02–08. http://dx.doi.org/10.1158/1538-7445.sabcs22-p4-02-08.

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Abstract Pre-operative endocrine therapy use in post-menopausal women with localized, ER-positive breast cancer affords comparable rates of response and breast preservation, but lower toxicity relative to chemotherapy. Pre-operative endocrine therapy exerts selective pressure on cancer cells and promote evolution and/or enrichment of pathogenic alternations such as ESR1 mutations and other cellular adaptations. How such endocrine therapy-induced adaptations alter response to radiation therapy remains poorly defined. In this study, we show that diverse mechanisms that confer endocrine therapy r

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19

Roßwag, Sven, Cristina L. Cotarelo, Klaus Pantel, et al. "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 (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 s

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20

Ottenbourgs, Tine, and Els Van Nieuwenhuysen. "Novel Endocrine Therapeutic Opportunities for Estrogen Receptor-Positive Ovarian Cancer—What Can We Learn from Breast Cancer?" Cancers 16, no. 10 (2024): 1862. http://dx.doi.org/10.3390/cancers16101862.

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Low-grade serous ovarian cancer (LGSOC) is a rare ovarian malignancy primarily affecting younger women and is characterized by an indolent growth pattern. It exhibits indolent growth and high estrogen/progesterone receptor expression, suggesting potential responsiveness to endocrine therapy. However, treatment efficacy remains limited due to the development of endocrine resistance. The mechanisms of resistance, whether primary or acquired, are still largely unknown and present a significant hurdle in achieving favorable treatment outcomes with endocrine therapy in these patients. In estrogen r

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21

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

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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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23

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

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24

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 (2010): 519–28. http://dx.doi.org/10.2174/156800910791517226.

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25

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

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Halim, Freda, Yohana Azhar, Suwarman Suwarman, and Bethy Hernowo. "p53 Mutation as Plausible Predictor for Endocrine Resistance Therapy in Luminal Breast Cancer." F1000Research 11 (March 18, 2022): 330. http://dx.doi.org/10.12688/f1000research.108628.1.

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Endocrine therapy resistance in Luminal Breast Cancer is a significant issue to be tackled, but currently no specific biomarker could be used to anticipate this event. p53 mutation is widely known as one of Breast Cancer’s most prominent genetic alterations. Its mutation could generate various effects in Estrogen Receptor and Progesteron Receptor molecular works, tangled in events leading to the aggravation of endocrine therapy resistance. Hence the possibility of p53 mutation utilization as an endocrine therapy resistance predictive biomarker is plausible. The purpose of this review is to exp

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Halim, Freda, Yohana Azhar, Suwarman Suwarman, and Bethy Hernowo. "p53 Mutation as Plausible Predictor for Endocrine Resistance Therapy in Luminal Breast Cancer." F1000Research 11 (November 30, 2022): 330. http://dx.doi.org/10.12688/f1000research.108628.2.

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Endocrine therapy resistance in Luminal Breast Cancer is a significant issue to be tackled, but currently, no specific biomarker could be used to anticipate this event. p53 mutation is widely known as one of Breast Cancer’s most prominent genetic alterations. Its mutation could generate various effects in Estrogen Receptor and Progesterone Receptor molecular works, tangled in events leading to the aggravation of endocrine therapy resistance. Hence the possibility of p53 mutation utilization as an endocrine therapy resistance predictive biomarker is plausible. The purpose of this review is to e

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30

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

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Raheem, Farah, Suganya Arunachalam Karikalan, Felipe Batalini, Aya El Masry, and Lida Mina. "Metastatic ER+ Breast Cancer: Mechanisms of Resistance and Future Therapeutic Approaches." International Journal of Molecular Sciences 24, no. 22 (2023): 16198. http://dx.doi.org/10.3390/ijms242216198.

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Endocrine therapy is the main treatment for hormone receptor-positive (HR+) breast cancer. However, advanced tumors develop resistance to endocrine therapy, rendering it ineffective as the disease progresses. There are several molecular mechanisms of primary and secondary endocrine resistance. Resistance can develop due to either alteration of the estrogen receptor pathway (e.g., ESR1 mutations) or upstream growth factors signaling pathways (e.g., PI3K/Akt/mTOR pathway). Despite progress in the development of molecularly targeted anticancer therapies, the emergence of resistance remains a majo

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Chia, KeeMing, Heloisa Milioli, Neil Portman, et al. "Non-canonical AR activity facilitates endocrine resistance in breast cancer." Endocrine-Related Cancer 26, no. 2 (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 endocri

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Li, Kang, Dan Shu, and Han Li. "Abstract PO2-23-11: SMAD4 depletion contributes to endocrine therapy resistance by ERBB signaling in HR+HER2- breast cancer." Cancer Research 84, no. 9_Supplement (2024): PO2–23–11—PO2–23–11. http://dx.doi.org/10.1158/1538-7445.sabcs23-po2-23-11.

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Abstract Objectives: Endocrine therapy resistance is a significant clinical challenge for patients with estrogen receptor (ER)-positive breast cancer. Dysregulation of the ER and ERBB signaling pathways plays a key role in endocrine therapy resistance. However, it is unclear how these pathways are integrated during resistance development. SMAD4 is involved in multiple stages of tumorigenesis, but its role in endocrine resistance development remains elusive. Here, we aimed to investigate the role of SMAD4 in the development of acquired endocrine therapy resistance in ER-positive breast cancer.

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Sanjay Kalra, Saptarshi Bhattacharya, Atul Dhingra, Jaideep Khare, and Sushil Jindal. "Endocrine Fever." Journal of the Pakistan Medical Association 74, no. 5 (2024): 998–99. http://dx.doi.org/10.47391/jpma.24-36.

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Fever is usually thought to be of an infectious orinflammatory etiology. In this brief communication, weexplore the multifaceted connections between fever andendocrine dysfunction. Impaired resistance to infectionoften leads to fever in conditions like diabetes andCushing's syndrome. Additionally, several endocrinedisorders, including hyperthyroidism, subacute thyroiditis,carcinoid syndrome, and pheochromocytoma, canmanifest as fever. Furthermore, fever can be an adverseeffect of various endocrine treatments, such asbisphosphonates and antithyroid drugs. We refer to thesescenarios as 'endocrin

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Bullock, M. "FOXO factors and breast cancer: outfoxing endocrine resistance." Endocrine-Related Cancer 23, no. 2 (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-independ

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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

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Zhang, Rui, Wen-Jing Jiang, Shuai Zhao, Li-Juan Kang, Qing-Shan Wang, and Yu-Mei Feng. "Abstract 1312: FOXF2 expression triggered by endocrine therapy orchestrates therapeutic resistance through reorganization of chromatin architecture in breast cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 1312. https://doi.org/10.1158/1538-7445.am2025-1312.

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Estrogen receptor-positive (ER+) breast cancer accounts for 80% breast cancer cases. The estrogen-ERα signaling pathway plays a pivotal role in driving the progression of ER+ breast cancer cells. Thus, endocrine therapy targeting the estrogen-ERα signaling pathway is a predominant treatment for ER+ breast cancer. Most patients with ER+ breast cancer require long-term treatment with endocrine agents. Although endocrine therapy effectively improves the survival of patients with ER+ breast cancer, bone metastasis frequently occurs in patients receiving long-term endocrine therapy due to acquired

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Poulard, Coralie, Julien Jacquemetton, Olivier Trédan, et al. "Oestrogen Non-Genomic Signalling is Activated in Tamoxifen-Resistant Breast Cancer." International Journal of Molecular Sciences 20, no. 11 (2019): 2773. http://dx.doi.org/10.3390/ijms20112773.

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Endocrine therapies targeting oestrogen signalling have significantly improved breast cancer management. However, their efficacy is limited by intrinsic and acquired resistance to treatment, which remains a major challenge for oestrogen receptor α (ERα)-positive tumours. Though many studies using in vitro models of endocrine resistance have identified putative actors of resistance, no consensus has been reached. We demonstrated previously that oestrogen non-genomic signalling, characterized by the formation of the ERα/Src/PI3K complex, is activated in aggressive breast cancers (BC). We wondere

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Li, Qing-xia, Dong-jian Shi, Li-xia Zhang, et al. "Association of body mass and systemic immune-inflammation indices with endocrine therapy resistance in luminal breast cancers." Journal of International Medical Research 47, no. 5 (2019): 1936–47. http://dx.doi.org/10.1177/0300060519831570.

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Objective To explore correlations between body mass index (BMI), preoperative systemic immune-inflammation index (SII) and endocrine therapy resistance, and evaluate BMI and SII as predictors of resistance, in patients with luminal breast cancer. Methods This retrospective study included patients with luminal breast cancer who underwent endocrine therapy at Hebei General Hospital. Relationships between BMI and SII subgroups, and clinicopathological parameters were analysed using χ2-tests. Disease-free survival was assessed using Log-rank statistics. Multivariate analysis of factors related to

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40

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

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

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

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

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

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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

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

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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 (1987): 165–73. http://dx.doi.org/10.1007/bf01806377.

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Miller, William R., Alexey Larionov, Thomas J. Anderson, et al. "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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