Present Role of Corticosteroids as Antiemetics

Aapro, Matti

doi:10.1007/978-3-642-84138-5_11

Cited by 22 publications

(6 citation statements)

References 58 publications

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“…Dexamethasone alone did not affect cell viability. [1,3], and as discussed recently [22], dexamethasone concentrations used in vitro correspond to those achieved in vivo. It is, therefore, our concern that the widespread administration of corticosteroids to patients undergoing irradiation and chemotherapy with DNA damaging agents might negatively affect treatment outcome in some of the patients.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone-Induced Enhancement of Resistance to Ionizing Radiation and Chemotherapeutic Agents in Human Tumor Cells

Mariotta

Perewusnnyk

Koechli

et al. 1999

Strahlentherapie und Onkologie

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In agreement with previous reports, we found that dexamethasone may induce radioresistance in human carcinoma cells. Including the published data from the literature, dexamethasone induced enhancement in radioresistance in 4 of 12 carcinoma cell lines (33%), but not in 3 glioblastoma cell lines, nor in 3 fibroblast strains. Dexamethasone also induced enhanced resistance to carboplatin with a similar probability in fresh samples of ovarian cancer evaluated prospectively (in 4 of 13 samples; 31%). We worry that induction of resistance by corticosteroids given to patients undergoing either radiotherapy or chemotherapy with agents causing DNA damage might be associated with a reduced clinical responsiveness in a significant fraction of patients with a carcinoma.

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Section: Discussionmentioning

confidence: 99%

Dexamethasone-Induced Enhancement of Resistance to Ionizing Radiation and Chemotherapeutic Agents in Human Tumor Cells

Mariotta

Perewusnnyk

Koechli

et al. 1999

Strahlentherapie und Onkologie

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“…Steroids such as dexamethasone are often used with chemotherapy and radiation treatments of patients to combat nausea and vomiting [102,103]. The therapeutic outcome of many solid tumors and cancers may be negatively impacted by glucocorticoid treatment depending on the type of cancer.…”

Section: Anti-apoptotic Effects Of Glucocorticoid Signalingmentioning

confidence: 99%

Tissue-Specific Actions of Glucocorticoids on Apoptosis: A Double-Edged Sword

Gruver-Yates

Cidlowski

2013

Cells

129

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First described for their metabolic and immunosuppressive effects, glucocorticoids are widely prescribed in clinical settings of inflammation. However, glucocorticoids are also potent inducers of apoptosis in many cell types and tissues. This review will focus on the established mechanisms of glucocorticoid-induced apoptosis and outline what is known about the apoptotic response in cells and tissues of the body after exposure to glucocorticoids. Glucocorticoid-induced apoptosis affects the skeletal system, muscular system, circulatory system, nervous system, endocrine system, reproductive system, and the immune system. Interestingly, several cell types have an anti-apoptotic response to glucocorticoids that is cytoprotective. Lastly, we will discuss the pro- and anti-apoptotic effects of glucocorticoids in cancers and their clinical implications.

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“…immunosuppressant, mainly due to its capacity to inhibit the production of pro-inflammatory cytokines (6,7). DEX is also clinically used in the treatment of human malignancies, especially leukemia and myelomas.…”

Section: Dexamethasone As a Chemosensitizer For Breast Cancer Chemothmentioning

confidence: 99%

Dexamethasone as a chemosensitizer for breast cancer chemotherapy: Potentiation of the antitumor activity of adriamycin, modulation of cytokine expression, and pharmacokinetics

Wang¹,

Wang²,

Rayburn³

et al. 2007

Int J Oncol

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Dexamethasone (DEX) is mainly used as an antiemetic agent in cancer therapy. We have recently demonstrated that DEX pretreatment increases the antitumor activity of the cancer chemotherapeutic agents carboplatin and gemcitabine, and decreases host toxicity in nude mouse xenograft models of human cancer. However, the underlying mechanisms are not fully understood. The present study was designed to determine the effects of DEX pretreatment on the anticancer activity of adriamycin (ADR) in a syngeneic model of breast cancer (4T1), emphasizing the effects of DEX on cytokine expression and modulation of ADR pharmacokinetics. We have demonstrated five major new findings about DEX pretreatment: a) it enhances the therapeutic effect of ADR, inducing almost complete inhibition of tumor growth; b) it increases tumor ADR accumulation; c) it modulates the expression of cytokines produced by the tumor, increasing TNF• and decreasing IL-1ß and VEGF expression; d) it enhances the effects of ADR on induction of apoptosis and inhibition of cell proliferation; and e) it suppresses nuclear NFκB activation and inhibits ADR-induced NFκB activation, possibly via IκB up-regulation. These findings suggest that DEX can be used as a chemosensitizer and chemoprotectant. These results provide a rationale for the expanded clinical use of DEX for cancer therapy.

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Present Role of Corticosteroids as Antiemetics

Cited by 22 publications

References 58 publications

Dexamethasone-Induced Enhancement of Resistance to Ionizing Radiation and Chemotherapeutic Agents in Human Tumor Cells

Dexamethasone-Induced Enhancement of Resistance to Ionizing Radiation and Chemotherapeutic Agents in Human Tumor Cells

Tissue-Specific Actions of Glucocorticoids on Apoptosis: A Double-Edged Sword

Dexamethasone as a chemosensitizer for breast cancer chemotherapy: Potentiation of the antitumor activity of adriamycin, modulation of cytokine expression, and pharmacokinetics

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