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Latest perspectives on glucocorticoid-induced apoptosis and resistance in lymphoid malignancies

Dorien Clarisse (UGent) , Fritz Offner (UGent) and Karolien De Bosscher (UGent)
Author
Organization
Abstract
Glucocorticoids are essential drugs in the treatment protocols of lymphoid malignancies. These steroidal hormones trigger apoptosis of the malignant cells by binding to the glucocorticoid receptor (GR), which is a member of the nuclear receptor superfamily. Long term glucocorticoid treatment is limited by two major problems: the development of glucocorticoid-related side effects, which hampers patient quality of life, and the emergence of glucocorticoid resistance, which is a gradual process that is inevitable in many patients. This emphasizes the need to reevaluate and optimize the widespread use of glucocorticoids in lymphoid malignancies. To achieve this goal, a deep understanding of the mechanisms governing glucocorticoid responsiveness is required, yet, a recent comprehensive overview is currently lacking. In this review, we examine how glucocorticoids mediate apoptosis by detailing GR’s genomic and non-genomic action mechanisms in lymphoid malignancies. We continue with a discussion of the glucocorticoid-related problems and how these are intertwined with one another. We further zoom in on glucocorticoid resistance by critically analyzing the plethora of proposed mechanisms and highlighting therapeutic opportunities that emerge from these studies. In conclusion, early detection of glucocorticoid resistance in patients remains an important challenge as this would result in a timelier treatment reorientation and reduced glucocorticoid-instigated side effects.
Keywords
Genetics, Cancer Research, Oncology, Glucocorticoids, Apoptosis, Glucocorticoid receptor, Glucocorticoid resistance, Side effects, Lymphoid malignancies, ACUTE LYMPHOBLASTIC-LEUKEMIA, DEXAMETHASONE-INDUCED APOPTOSIS, MULTIPLE-MYELOMA CELLS, GLYCOGEN-SYNTHASE KINASE-3-BETA, MESSENGER-RNA EXPRESSION, INDUCED LEUCINE-ZIPPER, BCL-2 FAMILY PROTEINS, FACTOR-KAPPA-B, RECEPTOR GENE, MOLECULAR-MECHANISMS

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MLA
Clarisse, Dorien, et al. “Latest Perspectives on Glucocorticoid-Induced Apoptosis and Resistance in Lymphoid Malignancies.” BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, vol. 1874, no. 2, 2020, doi:10.1016/j.bbcan.2020.188430.
APA
Clarisse, D., Offner, F., & De Bosscher, K. (2020). Latest perspectives on glucocorticoid-induced apoptosis and resistance in lymphoid malignancies. BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1874(2). https://doi.org/10.1016/j.bbcan.2020.188430
Chicago author-date
Clarisse, Dorien, Fritz Offner, and Karolien De Bosscher. 2020. “Latest Perspectives on Glucocorticoid-Induced Apoptosis and Resistance in Lymphoid Malignancies.” BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER 1874 (2). https://doi.org/10.1016/j.bbcan.2020.188430.
Chicago author-date (all authors)
Clarisse, Dorien, Fritz Offner, and Karolien De Bosscher. 2020. “Latest Perspectives on Glucocorticoid-Induced Apoptosis and Resistance in Lymphoid Malignancies.” BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER 1874 (2). doi:10.1016/j.bbcan.2020.188430.
Vancouver
1.
Clarisse D, Offner F, De Bosscher K. Latest perspectives on glucocorticoid-induced apoptosis and resistance in lymphoid malignancies. BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER. 2020;1874(2).
IEEE
[1]
D. Clarisse, F. Offner, and K. De Bosscher, “Latest perspectives on glucocorticoid-induced apoptosis and resistance in lymphoid malignancies,” BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, vol. 1874, no. 2, 2020.
@article{8677630,
  abstract     = {{Glucocorticoids are essential drugs in the treatment protocols of lymphoid malignancies. These steroidal hormones trigger apoptosis of the malignant cells by binding to the glucocorticoid receptor (GR), which is a member of the nuclear receptor superfamily. Long term glucocorticoid treatment is limited by two major problems: the development of glucocorticoid-related side effects, which hampers patient quality of life, and the emergence of glucocorticoid resistance, which is a gradual process that is inevitable in many patients. This emphasizes the need to reevaluate and optimize the widespread use of glucocorticoids in lymphoid malignancies. To achieve this goal, a deep understanding of the mechanisms governing glucocorticoid responsiveness is required, yet, a recent comprehensive overview is currently lacking. In this review, we examine how glucocorticoids mediate apoptosis by detailing GR’s genomic and non-genomic action mechanisms in lymphoid malignancies. We continue with a discussion of the glucocorticoid-related problems and how these are intertwined with one another. We further zoom in on glucocorticoid resistance by critically analyzing the plethora of proposed mechanisms and highlighting therapeutic opportunities that emerge from these studies. In conclusion, early detection of glucocorticoid resistance in patients remains an important challenge as this would result in a timelier treatment reorientation and reduced glucocorticoid-instigated side effects.}},
  articleno    = {{188430}},
  author       = {{Clarisse, Dorien and Offner, Fritz and De Bosscher, Karolien}},
  issn         = {{0304-419X}},
  journal      = {{BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER}},
  keywords     = {{Genetics,Cancer Research,Oncology,Glucocorticoids,Apoptosis,Glucocorticoid receptor,Glucocorticoid resistance,Side effects,Lymphoid malignancies,ACUTE LYMPHOBLASTIC-LEUKEMIA,DEXAMETHASONE-INDUCED APOPTOSIS,MULTIPLE-MYELOMA CELLS,GLYCOGEN-SYNTHASE KINASE-3-BETA,MESSENGER-RNA EXPRESSION,INDUCED LEUCINE-ZIPPER,BCL-2 FAMILY PROTEINS,FACTOR-KAPPA-B,RECEPTOR GENE,MOLECULAR-MECHANISMS}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{20}},
  title        = {{Latest perspectives on glucocorticoid-induced apoptosis and resistance in lymphoid malignancies}},
  url          = {{http://doi.org/10.1016/j.bbcan.2020.188430}},
  volume       = {{1874}},
  year         = {{2020}},
}

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