Depression and glioblastoma, complicated concomitant diseases: a systemic review of published literature

Mugge, Luke; Mansour, Tarek R; Crippen, Megan; Alam, Yasaman; Schroeder, Jason

doi:10.1007/s10143-018-1017-2

Cited by 32 publications

(29 citation statements)

References 136 publications

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“…It has been reported that mental disorders, especially depression and anxiety disorders, could affect the inflammation level [16], cytokines [17] and chemokines [18], neurotransmitter metabolism [19,20], neuroendocrine function [21], and so forth, which are also recognized as possible causes for the development and heterogeneity of GBM [22]. And research have also discovered that compared with other form of cancers, glioblastoma could be concomitant with depression/anxiety [23,24]. However, until now, there are not yet any research focusing on the possible shared molecule mechanisms between depression/anxiety and GBM.…”

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confidence: 99%

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Zhang

Song

et al. 2020

J Transl Med

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Background Glioblastoma multiforme (GBM) is the most malignant tumor in human brain. Diagnosis and treatment of GBM may lead to psychological disorders such as depressive and anxiety disorders. There was no research focusing on the correlation between depressive/anxiety disorder and the outcome of GBM. Thus, the aim of this study was to investigate the possibility of depressive/anxiety disorder correlated with the outcome of GBM patients, as well as the overlapped mechanism bridge which could link depressive/anxiety disorders and GBM. Methods Patient Health Questionnaire (PHQ-9) and Generalized Anxiety Disorder (GAD-7) were used to investigate the psychological condition of GBM patients in our department. To further explore the potential mechanism, bioinformatic methods were used to screen out genes that could be indicators of outcome in GBM, followed by gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and protein–protein interaction (PPI) analysis. Further, cellular experiments were conducted to evaluate the proliferation, migration capacity of primary GBM cells from the patients. Results It was revealed that patients with higher PHQ-9 and GAD-7 scores had significantly worse prognosis than their lower-scored counterparts. Bioinformatic mining revealed that LTBP1 could be a potential genetic mechanism in both depressive/anxiety disorder and GBM. Primary GBM cells with different expression level of LTBP1 should significantly different proliferation and migration capacity. GO, KEGG analysis confirmed that extracellular matrix (ECM) was the most enriched function of LTBP1. PPI network showed the interaction of proteins altered by LTBP1. Hub genes COL1A2, COL5A1 and COL10A1, as well as mesenchymal marker CD44 and Vimentin were statistically higher expressed in LTBP1 high group; while proneural marker E-cadherin was significantly higher expressed in low LTBP1 group. Conclusion There is closely correlation between depressive/anxiety disorders and GBM. LTBP1 could be a potential bridge linking the two diseases through the regulation of ECM.

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confidence: 99%

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Zhang

Song

et al. 2020

J Transl Med

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“…Globally, >300 million people suffer from depression, which is listed by the World Health Organization (WHO) as the single largest factor contributing to global disability (25). Depressive disorder has adverse effects on the occurrence, development and prognosis of malignant tumors (26). In patients with malignant tumors, depression affects immune function, thus altering the occurrence, development and outcomes of malignant tumors (12,27,28).…”

Section: Discussionmentioning

confidence: 99%

“…Mice were randomly divided into 6 groups of 10 mice: i) Cancer model group (CA), mice grafted with CT-26 cells (5x10 5 in 200 µl DMEM) through subcutaneous injection to the right armpit; ii) cancer depression model group (CD), in which following CT-26 cell engraftment, depression was established by chronic mild stress from day 1; iii) cancer depression with paroxetine group (CDP), CD model mice were intraperitoneally injected with 10 mg/kg/day paroxetine for 28 days from the 14th day of chronic mild stress; iv) cancer depression with fluorouracil group (CDF), CD mice intraperitoneally injected with 20 mg/kg/day fluorouracil for 10 days from the 14th day of chronic stress; v) cancer depression with paroxetine and fluorouracil group (CDP+F), CD mice intraperitoneally injected with both 10 mg/kg/day paroxetine and 20 mg/kg/day fluorouracil; and vi) control group (CON), mice given equal amounts of saline. Tumor volumes were measured at 0, 7,14,17,20,23,26,29,32,35,38 and 42 days and inhibition rate and behavioral changes were calculated. A tumor diameter of 1.5 cm was set as the humane endpoint.…”

Section: Animals and Groupingmentioning

confidence: 99%

Paroxetine combined with fluorouracil plays a therapeutic role in mouse models of colorectal cancer with depression through inhibiting IL‑22 expression to regulate the MAPK signaling pathway

et al. 2020

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The objective of the present study was to observe the therapeutic effect of paroxetine combined with fluorouracil on mice with colorectal cancer (CRC) complicated with depression and to explore its mechanism of action. Using chronic mild stress and xenograft tumor methods to model CRC complicated with depression, 60 BALB/c mice were randomly divided into control, tumor model, tumor depression model, tumor depression antidepressant, tumor depression chemotherapy and tumor depression antidepressant plus chemotherapeutic drug groups. Changes in mouse sucrose preference and forced swimming tests were tracked. Changes in tumor volume and weight were compared, the tumor inhibition rate was calculated, Ki-67 expression in tumor tissues was detected using immunohistochemistry and IL-22 levels in peripheral blood were detected using ELISAs. Additionally, protein expression levels of IL-22, Bcl-2, Bax, caspase-3, p38, phosphorylated (p)-p38, ERK, pERK , JNK and p-JNK in tumor tissue were detected using western blotting. Following treatment with paroxetine and chemotherapy drugs, the sucrose preference index was increased, autonomic behavior dysfunction was alleviated and tumor growth was significantly inhibited. Furthermore, the expression levels of Ki-67 and apoptosis-related proteins, Bax and caspase-3, increased in tumor tissues, anti-apoptosis protein Bcl2 expression levels decreased significantly, IL-22 levels in the blood and tumor tissues were reduced and p-p38, pERK and p-JNK proteins were significantly reduced. It was concluded that paroxetine combined with chemotherapy drugs improved depressive behavior and promoted the survival state in a mouse model of CRC and depression, possibly through inhibiting IL-22 expression to regulate the activity of the MAPK signaling pathway.

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“…Given the poor prognosis of glioblastoma, depression stands to worsen outcomes when it develops concomitantly [26]. Despite this common interaction, relatively little research has been performed on the development of depression associated with glioblastoma.…”

Section: Discussionmentioning

confidence: 99%

Association of miR-34a Expression with Quality of Life of Glioblastoma Patients: A Prospective Study

Vaitkienė

Pranckevičienė

Stakaitis

et al. 2019

Cancers

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MiR-34a acts as tumor-suppressor by targeting many oncogenes related to proliferation, apoptosis, and invasion of gliomas. We studied the relationships between health-related quality of life (HRQOL), depression, and miR-34a expression status in patients with newly diagnosed glioblastoma (GBM). A comprehensive HRQOL assessment was completed by 38 patients with glioblastoma prior to surgical resection and included the European Organization for Research and Treatment of Cancer (EORTC) questionnaire for cancer patients (QLQ-C30) and the Brain Cancer-Specific Quality of Life Questionnaire (QLQ-BN20), the Patient Health Questionnaire-9 (PHQ-9), the Karnofsky performance index (KPS), and The Glasgow Outcome Scale (GOS). The miR-34a expression in glioblastoma tissue was measured using quantitative reverse transcription PCR. Our findings show that lower miR-34a expression is significantly associated with higher tumor volume, worse physical functioning, lower KPS, and greater depressive symptom severity of GBM patients. Moreover, analysis reveals that miR-34a effects might be gender specific, as stronger relationships between miR-34a and patient functioning measures were observed in males when compared to females. Despite the fact that, due to small sample size, our results should be considered as preliminary, our study suggests that miR-34a is associated with tumor burden and can be important for health-related quality of life, functional status, and mood symptoms of glioblastoma patients.

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Depression and glioblastoma, complicated concomitant diseases: a systemic review of published literature

Cited by 32 publications

References 136 publications

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

LTBP1 plays a potential bridge between depressive disorder and glioblastoma

Paroxetine combined with fluorouracil plays a therapeutic role in mouse models of colorectal cancer with depression through inhibiting IL‑22 expression to regulate the MAPK signaling pathway

Association of miR-34a Expression with Quality of Life of Glioblastoma Patients: A Prospective Study

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