Environmental risk factors of primary brain tumors: A review

Vienne-Jumeau, A.; Tafani, C.; Ricard, D.

doi:10.1016/j.neurol.2019.08.004

Cited by 75 publications

(28 citation statements)

References 94 publications

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“…[434,436] -PCBs [436] Cx43 upregulation in rodent striatum [437] GJIC inhibition and decreased expression of Cx43 among astrocytes (Mn exposure) [438] Alzheimer disease -Air pollution [439,440] Cx43 HC activation [441][442][443][444] Cancer Glioma -Pesticides (?) [445][446][447][448] GJIC inhibition and decreased Cx43 expression in neuronal stem cells [449] Emerging evidence suggested that alterations in normal astrocyte function contributes to the etiology and progression of varied neurological disorders including migraine with aura, neurodegenerative disorders, schizophrenia, epilepsy, and ASD. Therefore, targeting astrocyte dysfunction may lead to new therapeutic strategies for these disorders [450,451].…”

Section: Pathologiesmentioning

confidence: 99%

“…Several environmental exposures have been investigated as potential risk factors, but for most, scientific evidence is still lacking. The role of pesticides in CNS tumor risk, especially gliomas and meningiomas, was first investigated by studies of mortality rates in farmers in the USA or Europe but results do not all converge [445]. Previous reviews have concluded that there was a weak-positive association between brain cancers and farming [446].…”

Section: Gliomamentioning

confidence: 99%

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Brain Disorders and Chemical Pollutants: A Gap Junction Link?

et al. 2020

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The incidence of brain pathologies has increased during last decades. Better diagnosis (autism spectrum disorders) and longer life expectancy (Parkinson’s disease, Alzheimer’s disease) partly explain this increase, while emerging data suggest pollutant exposures as a possible but still underestimated cause of major brain disorders. Taking into account that the brain parenchyma is rich in gap junctions and that most pollutants inhibit their function; brain disorders might be the consequence of gap-junctional alterations due to long-term exposures to pollutants. In this article, this hypothesis is addressed through three complementary aspects: (1) the gap-junctional organization and connexin expression in brain parenchyma and their function; (2) the effect of major pollutants (pesticides, bisphenol A, phthalates, heavy metals, airborne particles, etc.) on gap-junctional and connexin functions; (3) a description of the major brain disorders categorized as neurodevelopmental (autism spectrum disorders, attention deficit hyperactivity disorders, epilepsy), neurobehavioral (migraines, major depressive disorders), neurodegenerative (Parkinson’s and Alzheimer’s diseases) and cancers (glioma), in which both connexin dysfunction and pollutant involvement have been described. Based on these different aspects, the possible involvement of pollutant-inhibited gap junctions in brain disorders is discussed for prenatal and postnatal exposures.

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Section: Pathologiesmentioning

confidence: 99%

Section: Gliomamentioning

confidence: 99%

Brain Disorders and Chemical Pollutants: A Gap Junction Link?

et al. 2020

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“…Some chemicals in the environment, such as heavy metals and various drugs, easily cause damage to children, especially to the nervous system and immune system, and can even cause tumors 198,199 . The inflammatory response plays an important role in this damage.…”

Section: Role Of Hmgb1 In Pediatric Diseasesmentioning

confidence: 99%

The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic

Peng

et al. 2020

Immunity Inflam & Disease

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Introduction The ubiquitously expressed nonhistone nuclear protein high‐mobility group box protein 1 (HMGB1) has different functions related to posttranslational modifications and cellular localization. In the nucleus, HMGB1 modulates gene transcription, replication and DNA repair as well as determines chromosomal architecture. When the post‐transcriptional modified HMGB1 is released into the extracellular space, it triggers several physiological and pathological responses and initiates innate immunity through interacting with its reciprocal receptors (i.e., TLR4/2 and RAGE). The effect of HMGB1‐mediated inflammatory activation on different systems has received increasing attention. HMGB1 is now considered to be an alarmin and participates in multiple inflammation‐related diseases. In addition, HMGB1 also affects the occurrence and progression of tumors. However, most studies involving HMGB1 have been focused on adults or mature animals. Due to differences in disease characteristics between children and adults, it is necessary to clarify the role of HMGB1 in pediatric diseases. Methods and Results Through systematic database retrieval, this review aimed to first elaborate the characteristics of HMGB1 under physiological and pathological conditions and then discuss the clinical significance of HMGB1 in the pediatric diseases according to different systems. Conclusions HMGB1 plays an important role in a variety of pediatric diseases and may be used as a diagnostic biomarker and therapeutic target for new strategies for the prevention and treatment of pediatric diseases.

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“…8 Exposure to high dose ionizing radiation is the most firmly established environmental risk factor for CNS tumor. [9][10][11] Other factors such as cellular phones, tobacco uses, and allergies/atopic disease have been extensively investigated for CNS tumor risk. 12,13 However, such relationships remain inconclusive.…”

Section: Introductionmentioning

confidence: 99%

No Association Between FTO Gene Polymorphisms and Central Nervous System Tumor Susceptibility in Chinese Children

Liao¹,

Li²,

Zhang³

et al. 2021

PGPM

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Background: Central nervous system (CNS) tumor is a malignancy commonly seen occurring in childhood, worldwide. Fat mass and obesity-associated (FTO) enzyme, initially identified as an obesity-related protein, also functions as a susceptibility gene for cancers. However, predisposing effect of FTO gene single nucleotide polymorphisms (SNPs) on CNS tumor risk remains unknown. Methods: Herein, we genotyped 314 CNS tumor patients and 380 healthy controls samples from three hospitals to explore whether FTO gene SNPs impact CNS tumor risk. TaqMan SNP genotyping assay was applied for the genotyping. Odds ratios (ORs) and 95% confidence intervals (CIs), generated from multinomial logistic regression, were applied to determine the associations of SNPs (rs1477196 G>A, rs9939609 T>A, rs7206790 C>G, and rs8047395 A>G) in FTO gene with risk of CNS tumor. Results: We failed to detect significant associations between FTO gene SNPs and CNS tumor risk, either in single-locus or combined analysis. A significantly increased ependymoma risk was found for carriers with 3-4 risk genotypes in comparison to 0-2 risk genotypes (adjusted OR=1.94, 95% CI=1.11-3.37, P=0.020). Conclusion:Our data indicated that FTO gene SNPs are unlikely to have large effects on CNS tumor risk but may have weaker effects.

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Environmental risk factors of primary brain tumors: A review

Cited by 75 publications

References 94 publications

Brain Disorders and Chemical Pollutants: A Gap Junction Link?

Brain Disorders and Chemical Pollutants: A Gap Junction Link?

The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic

No Association Between FTO Gene Polymorphisms and Central Nervous System Tumor Susceptibility in Chinese Children

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