Selective Serotonin Reuptake Inhibitors, Glioblastoma Multiforme, and Impact on Toxicities and Overall Survival

Caudill, Jonathan S.; Brown, Paul D.; Cerhan, Jane H.; Rummans, Teresa A.

doi:10.1097/coc.0b013e3181e8461a

Cited by 83 publications

(44 citation statements)

References 7 publications

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“…Previous clinical trials indicated that paroxetine and citalopram markedly improved cancer patients' quality of life [37, 38]. Additionally, a retrospective review suggested that using SSRI antidepressants, including citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline, for glioma treatment did not adversely affect survival rates [39]. Based on those studies, we attempted to identify which SSRI antidepressants could be potentially used for treating glioma cells and studied the underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis

et al. 2014

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The efficacy of glioblastoma chemotherapy is not satisfactory; therefore, a new medication is expected to improve outcomes. As much evidence shows that antidepressants decrease cancer incidence and improve patients' quality of life, we therefore attempted to explore the potential for fluoxetine to be used to treat GBM and its possible underlying mechanism. The expression level of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) was determined using immunohistochemical staining and PCR analysis. The mechanism of fluoxetine-induced apoptosis of gliomas was elucidated. Computer modeling and a binding assay were conducted to investigate the interaction of fluoxetine with the AMPAR. The therapeutic effect of fluoxetine was evaluated using an animal model. We found that fluoxetine directly bound to AMPAR, thus inducing transmembrane Ca2+ influx. The rise in the intracellular calcium concentration ([Ca2+]i) causes mitochondrial Ca2+ overload, thereby triggering apoptosis. AMPARs are excessively expressed in glioma tissues, suggesting that fluoxetine specifically executes glioma cells. Our in vivo study revealed that fluoxetine suppressed the growth of glioblastomas in brains of Nu/Nu mice, an effect similar to that produced by temozolomide. Our preclinical studies suggest fluoxetine, a commonly used antidepressant, might be selectively toxic to gliomas and could provide a new approach for managing this disease.

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Section: Discussionmentioning

confidence: 99%

Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis

et al. 2014

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“…Retrospective data further suggest that selective serotonin reuptake inhibitor (SSRI) antidepressants may be safe in glioma. In one large case notes review (n=160), there was no evidence of increased toxicity among patients with glioblastoma multiforme taking an SSRI 64. These and other retrospective studies are reassuring,52 65 but the potential risks of prescribing antidepressants in glioma justify prospective studies 66…”

Section: Unanswered Questionsmentioning

confidence: 95%

“…However, a subsequent case–control retrospective study by the same group found no association between tricyclic antidepressant (TCA) prescription and all-cause mortality following glioma diagnosis 73. A retrospective case-note review suggested, by contrast, that GBM patients who received an SSRI had a reduced risk of death in the first 2 years postoperatively 64. Prospective case–control studies are warranted to explore these interesting but contradictory findings.…”

Section: Unanswered Questionsmentioning

confidence: 99%

Depression in glioma: a primer for clinicians and researchers

Rooney

Brown

Reijneveld

et al. 2013

Journal of Neurology, Neurosurgery & Psychiatry

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Depression is one of the leading causes of global disability, and a considerable hidden morbidity among patients with glioma. In this narrative review, we summarise what is currently known about depression in glioma, the main unanswered questions and the types of studies that should be prioritised in order to find out. We conclude by calling for a prospective Phase II study of antidepressants in depressed glioma patients, to test methodologies for a multicentre randomised controlled trial.

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“…However, there are little data on the use of antidepressants in this patient population. In order to investigate selective serotonin reuptake inhibitors (SSRIs) and their impact on toxicities and survival in patients with GBM, a review was performed on data from 160 patients from 1999 to 2008 [50]. A majority of the patients received temozolomide and radiation, and 21.8% of patients overall received SSRIs during initial therapy.…”

Section: Seizure Control -Implications For the Pharmacistmentioning

confidence: 99%

Pharmacists Perspective on Management of GBM

Ellinger¹

2016

CTOIJ

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Selective Serotonin Reuptake Inhibitors, Glioblastoma Multiforme, and Impact on Toxicities and Overall Survival

Abstract: This retrospective review suggests that concomitant use of an SSRI during treatment does not adversely affect survival. There was no increased toxicity with the use of SSRI concurrent with treatment of newly-diagnosed GBM.

Cited by 83 publications

References 7 publications

Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis

Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis

Depression in glioma: a primer for clinicians and researchers

Pharmacists Perspective on Management of GBM

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