We are analyzing https://link.springer.com/article/10.1007/s10555-022-10047-1.

Title:
Mechanisms behind context-dependent role of glucocorticoids in breast cancer progression | Cancer and Metastasis Reviews
Description:
Glucocorticoids (GCs), mostly dexamethasone (dex), are routinely administered as adjuvant therapy to manage side effects in breast cancer. However, recently, it has been revealed that dex triggers different effects and correlates with opposite outcomes depending on the breast cancer molecular subtype. This has raised new concerns regarding the generalized use of GC and suggested that the context-dependent effects of GCs can be taken into potential consideration during treatment design. Based on this, attention has recently been drawn to the role of the glucocorticoid receptor (GR) in development and progression of breast cancer. Therefore, in this comprehensive review, we aimed to summarize the different mechanisms behind different context-dependent GC actions in breast cancer by applying a multilevel examination, starting from the association of variants of the GR-encoding gene to expression at the mRNA and protein level of the receptor, and its interactions with other factors influencing GC action in breast cancer. The role of GCs in chemosensitivity and chemoresistance observed during breast cancer therapy is discussed. In addition, experiences using GC targeting therapeutic options (already used and investigated in preclinical and clinical trials), such as classic GC dexamethasone, selective glucocorticoid receptor agonists and modulators, the GC antagonist mifepristone, and GR coregulators, are also summarized. Evidence presented can aid a better understanding of the biology of context-dependent GC action that can lead to further advances in the personalized therapy of breast cancer by the evaluation of GR along with the conventional estrogen receptor (ER) and progesterone receptor (PR) in the routine diagnostic procedure.
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Keywords {🔍}

cancer, breast, article, google, scholar, cas, receptor, glucocorticoid, expression, cell, gcs, journal, effects, tumor, molecular, gene, role, research, activity, cells, clinical, response, patients, binding, survival, protein, genes, signaling, activation, tumors, action, effect, therapy, transcriptional, treatment, transcription, grβ, cancers, human, chromatin, resistance, nuclear, mechanisms, glucocorticoids, suggested, httpsdoiorgs, addition, estrogen, receptors, development,

Topics {✒️}

dimethyl-alpha-benzanthracene-induced mammary tumors membrane-bound g-protein-coupled receptor tnf-alpha-induced cell death e2-induced pro-proliferative genes anti-apoptotic protein c-iapi gc-induced drug-resistant phenotype c-jun n-terminal kinase tnf-α-mediated cell death article download pdf triple-negative tumors responded atp-dependent switch/sucrose serum/glucocorticoid-inducible protein kinase triple-negative breast cancer triple-negative breast cancer swi/snf chromatin-remodeling complex glucocorticoid-induced leucine zipper pro-proliferative signaling networks g-protein-coupled receptors [42 antagonized gr-induced sgk1 hormone-positive breast cancer pr − /gr + breast cancer cells subsequent rap1b-mediated signaling swi/snf-dependent fashion mda-mb-231 agonist-liganded glucocorticoid receptor akt/mtor/rhoa pathway gc-induced cell death paclitaxel-induced cell death preventing chemotherapy-induced nausea longer breast cancer–specific serine/arginine-rich proteins phosphatidylinositol 3-kinase/akt signaling ar + /er + /pr + breast tumors steroid-free glucocorticoid receptor c3h/hej mammary tumors pro-oncogenic wnt signaling swi/snf subunits smarce1 membrane-bound glucocorticoid receptors glucocorticoid receptor pre-mrna cell-type specific manner nanoparticle albumin-bound paclitaxel er-positive tumor cells hormone-dependent breast cancers brca-mutated ovarian cancers improved relapse-free survival glucocorticoid receptor-mediated activation glucocorticoid receptor-mediated protection caspase-3/parp cleavage er-negative breast cancer er-positive breast cancer

Questions {❓}

A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: Tumor growth promotion or suppression?
Duality of glucocorticoid action in cancer: Tumor-suppressor or oncogene?
Improved glucocorticoid receptor ligands: Fantastic beasts, but how to find them?
Molecular mechanisms of glucocorticoid action: What is important?

Schema {🗺️}

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         description:Glucocorticoids (GCs), mostly dexamethasone (dex), are routinely administered as adjuvant therapy to manage side effects in breast cancer. However, recently, it has been revealed that dex triggers different effects and correlates with opposite outcomes depending on the breast cancer molecular subtype. This has raised new concerns regarding the generalized use of GC and suggested that the context-dependent effects of GCs can be taken into potential consideration during treatment design. Based on this, attention has recently been drawn to the role of the glucocorticoid receptor (GR) in development and progression of breast cancer. Therefore, in this comprehensive review, we aimed to summarize the different mechanisms behind different context-dependent GC actions in breast cancer by applying a multilevel examination, starting from the association of variants of the GR-encoding gene to expression at the mRNA and protein level of the receptor, and its interactions with other factors influencing GC action in breast cancer. The role of GCs in chemosensitivity and chemoresistance observed during breast cancer therapy is discussed. In addition, experiences using GC targeting therapeutic options (already used and investigated in preclinical and clinical trials), such as classic GC dexamethasone, selective glucocorticoid receptor agonists and modulators, the GC antagonist mifepristone, and GR coregulators, are also summarized. Evidence presented can aid a better understanding of the biology of context-dependent GC action that can lead to further advances in the personalized therapy of breast cancer by the evaluation of GR along with the conventional estrogen receptor (ER) and progesterone receptor (PR) in the routine diagnostic procedure.
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      headline:Mechanisms behind context-dependent role of glucocorticoids in breast cancer progression
      description:Glucocorticoids (GCs), mostly dexamethasone (dex), are routinely administered as adjuvant therapy to manage side effects in breast cancer. However, recently, it has been revealed that dex triggers different effects and correlates with opposite outcomes depending on the breast cancer molecular subtype. This has raised new concerns regarding the generalized use of GC and suggested that the context-dependent effects of GCs can be taken into potential consideration during treatment design. Based on this, attention has recently been drawn to the role of the glucocorticoid receptor (GR) in development and progression of breast cancer. Therefore, in this comprehensive review, we aimed to summarize the different mechanisms behind different context-dependent GC actions in breast cancer by applying a multilevel examination, starting from the association of variants of the GR-encoding gene to expression at the mRNA and protein level of the receptor, and its interactions with other factors influencing GC action in breast cancer. The role of GCs in chemosensitivity and chemoresistance observed during breast cancer therapy is discussed. In addition, experiences using GC targeting therapeutic options (already used and investigated in preclinical and clinical trials), such as classic GC dexamethasone, selective glucocorticoid receptor agonists and modulators, the GC antagonist mifepristone, and GR coregulators, are also summarized. Evidence presented can aid a better understanding of the biology of context-dependent GC action that can lead to further advances in the personalized therapy of breast cancer by the evaluation of GR along with the conventional estrogen receptor (ER) and progesterone receptor (PR) in the routine diagnostic procedure.
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         Oncology
         Biomedicine
         general
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      name:Hereditary Tumours Research Group, Hungarian Academy of Sciences-Semmelweis University, Budapest, Hungary
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