Glucocorticoid receptor (GR) is a key homeostatic regulator involved in governing immune response, neuro-integration, metabolism and lung function. In conjunction with its pivotal role in human biology, GR action is critically linked to the pathology of various disease types, including cancer. While pharmacological activation of GR has been used for the treatment of various liquid cancers, its role in solid cancers is less clearly defined and seems to be cancer-type dependent. This review focuses on the molecular aspects of GR biology, spanning the structural and functional basis of response to glucocorticoids, as well as how this transcription factor operates in cancer, including the implications in disease development, progression and drug resistance.
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ORIC-101, a Glucocorticoid Receptor Antagonist, in Combination with Nab-Paclitaxel in Patients with Advanced Solid Tumors.
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University of California San Francisco Helen Diller Family Comprehensive Cancer Center, San Francisco, California.
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Patients And Methods: The ability of ORIC-101 to reverse taxane resistance was assessed in cell lines and xenograft models, and a phase 1 study (NCT03928314) was conducted in patients with advanced solid tumors to determine the dose, safety, and antitumor activity of ORIC-101 with nab-paclitaxel.
Intermittent Fasting-Improved Glucose Homeostasis Is Not Entirely Dependent on Caloric Restriction in db/db Male Mice.
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Department of Endocrinology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Intermittent fasting (IF), which involves prolonged fasting intervals accompanied by caloric restriction (CR), is an effective dietary treatment for obesity and diabetes. Although IF offers many benefits, it is difficult to determine whether these benefits are the consequences of CR. Every-other-day feeding (EODF) is a commonly used IF research model.
View Article and Find Full Text PDFResistance exercise alleviates dexamethasone-induced muscle atrophy via Sestrin2/MSTN pathway in C57BL/6J mice.
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Department of Rehabilitation, School of Medical Technology, Tianjin Medical University, Tianjin, 300070, China; Department of Physiology and Pathophysiology, School of Basic Medical Science, Tianjin Medical University, Tianjin, 300070, China. Electronic address:
Aim: It has long been recognized that resistance exercise can substantially increase skeletal muscle mass and strength, but whether it can protect against glucocorticoid-induced muscle atrophy and its potential mechanism is yet to be determined. This study aimed to investigate the protective effects of resistance exercise in dexamethasone-induced muscle atrophy and elucidate the possible function of exercise-induced protein Sestrin2 in this process.
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Article Synopsis
- The study aimed to examine the link between genetic risk for type 2 diabetes (T2D) and hyperglycemia development in patients treated with glucocorticoids.
- A retrospective analysis was conducted on 546 individuals who received glucocorticoids; results showed that 210 developed hyperglycemia, with a significant correlation found between hyperglycemia and T2D genetic risk scored on a polygenic scale.
- The findings suggest that those with a higher genetic risk for T2D are more likely to experience hyperglycemia following glucocorticoid treatment, which could help in personalizing medical treatment strategies.
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