We are analyzing https://link.springer.com/article/10.1007/s10555-023-10163-6.

Title:
Glucocorticoid receptor: a harmonizer of cellular plasticity in breast cancer—directs the road towards therapy resistance, metastatic progression and recurrence | Cancer and Metastasis Reviews
Description:
Recent therapeutic advances have significantly uplifted the quality of life in breast cancer patients, yet several impediments block the road to disease-free survival. This involves unresponsiveness towards administered therapy, epithelial to mesenchymal transition, and metastatic progression with the eventual appearance of recurrent disease. Attainment of such characteristics is a huge adaptive challenge to which tumour cells respond by acquiring diverse phenotypically plastic states. Several signalling networks and mediators are involved in such a process. Glucocorticoid receptor being a mediator of stress response imparts prognostic significance in the context of breast carcinoma. Involvement of the glucocorticoid receptor in the signalling cascade of breast cancer phenotypic plasticity needs further elucidation. This review attempted to shed light on the inter-regulatory interactions of the glucocorticoid receptor with the mediators of the plasticity program in breast cancer; which may provide a hint for strategizing therapeutics against the glucocorticoid/glucocorticoid receptor axis so as to modulate phenotypic plasticity in breast carcinoma.
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Keywords {🔍}

pubmed, article, cancer, google, scholar, cas, breast, central, journal, cell, receptor, glucocorticoid, httpsdoiorgs, research, cells, zhang, nature, metastasis, clinical, liu, wang, resistance, therapy, signaling, chen, expression, molecular, plasticity, oncology, biology, cellular, progression, promotes, pathway, metastatic, role, cancers, stem, international, sciences, therapeutic, epithelial, transition, glucocorticoids, httpsdoiorg, communications, activation, tumor, reviews, recurrence,

Topics {✒️}

month download article/chapter pelp1-mediated stress signaling mitogen-activated protein kinases hormone-naïve prostate carcinoma akt-gsk3-snail pathway wnt/beta-catenin signaling triple-negative breast cancer akt/mtor/rhoa pathway cancerous epithelial-mesenchymal transdifferentiation enhanced tumor-cell growth glucocorticoid/glucocorticoid receptor axis er-negative breast cancer m6a methylation-mediated col3a1 hypoxia inducible factor-1 hybrid epithelial/mesenchymal state tamoxifen-resistant breast cancer nanoparticle albumin-bound paclitaxel estrogen receptor signaling activating β-adrenergic signaling breast cancer-specific mortality hypoxia controls metastasis cisplatin-mediated activation data mining-based study genome-wide binding potential salini das & sutapa mukherjee regulates nf-kappab activity full article pdf leukemia inhibitory factor induced tamoxifen resistance stat3/hif-α signaling positive prognostic marker regulates epithelial plasticity dna damage/repair system breast cancer dormancy glucocorticoids promote transition fibroblast activation protein protein kinase cε brca1-deficient mammary tumors triple-negative subtype promotes tumor progression mettl3 promotes metastasis tgf-β type epithelial-mesenchymal transition human breast cancer stress-related disorders inos mediated pathway therapy resistant access high-risk clinical cisplatin resistance partially cancer drug resistance

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         description:Recent therapeutic advances have significantly uplifted the quality of life in breast cancer patients, yet several impediments block the road to disease-free survival. This involves unresponsiveness towards administered therapy, epithelial to mesenchymal transition, and metastatic progression with the eventual appearance of recurrent disease. Attainment of such characteristics is a huge adaptive challenge to which tumour cells respond by acquiring diverse phenotypically plastic states. Several signalling networks and mediators are involved in such a process. Glucocorticoid receptor being a mediator of stress response imparts prognostic significance in the context of breast carcinoma. Involvement of the glucocorticoid receptor in the signalling cascade of breast cancer phenotypic plasticity needs further elucidation. This review attempted to shed light on the inter-regulatory interactions of the glucocorticoid receptor with the mediators of the plasticity program in breast cancer; which may provide a hint for strategizing therapeutics against the glucocorticoid/glucocorticoid receptor axis so as to modulate phenotypic plasticity in breast carcinoma.
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      description:Recent therapeutic advances have significantly uplifted the quality of life in breast cancer patients, yet several impediments block the road to disease-free survival. This involves unresponsiveness towards administered therapy, epithelial to mesenchymal transition, and metastatic progression with the eventual appearance of recurrent disease. Attainment of such characteristics is a huge adaptive challenge to which tumour cells respond by acquiring diverse phenotypically plastic states. Several signalling networks and mediators are involved in such a process. Glucocorticoid receptor being a mediator of stress response imparts prognostic significance in the context of breast carcinoma. Involvement of the glucocorticoid receptor in the signalling cascade of breast cancer phenotypic plasticity needs further elucidation. This review attempted to shed light on the inter-regulatory interactions of the glucocorticoid receptor with the mediators of the plasticity program in breast cancer; which may provide a hint for strategizing therapeutics against the glucocorticoid/glucocorticoid receptor axis so as to modulate phenotypic plasticity in breast carcinoma.
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         Cellular plasticity
         Glucocorticoid receptor
         EMT
         Cancer dormancy
         Reawakening
         Cancer Research
         Oncology
         Biomedicine
         general
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