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Corresponding author: Georgios Sioutas ( sioutasgiorgos@gmail.com ) © 2022 Georgios Sioutas, Alexandrina Nikova, Theodossios Birbilis.
This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Citation:
Sioutas G, Nikova A, Birbilis T (2022) Risk factors for pediatric glioma. Folia Medica 64(4): 566-571. https://doi.org/10.3897/folmed..e64431
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Brain tumours are a heterogenic group, a subtype of which is arising from glial cells. Pediatric low-grade gliomas are the most common primary CNS tumour group in childhood, representing 25% to over 30% of pediatric CNS tumours. Pediatric high-grade gliomas are relatively rare and have a poor prognosis. Epidemiological studies have reported various potential risk factors, such as demographics, ionizing and nonionizing radiation, allergic conditions, and infections, immunologic, parental, genetic, and developmental risk factors. These risk factors are relatively unclear and understudied; thus, this narrative review aims to summarize all studies connecting risk factors and pediatric gliomas.
epidemiology, glioma, high-grade glioma, low-grade glioma, pediatric, risk factors
Primary malignant central nervous system (CNS) tumours are the most common pediatric solid organ tumours and the second most common pediatric malignancies after hematologic malignancies.[
Gliomas originate from glial cells.[
Pediatric low-grade gliomas are a group of entities that is highly histologically and molecularly heterogeneous.[
On the contrary, pediatric high-grade gliomas (HGGs) are relatively rare and represent 8%–12% of all primary pediatric CNS tumours.[
Various epidemiological studies have reported potential risk factors for developing pediatric glioma. This narrative review aims to summarize all connections between risk factors and pediatric gliomas.
The overall incidence of brain and CNS tumours is higher among females, concerning all age groups in the USA.[
Animal models have shown that ionizing radiation induces double-strand breaks, leading to HGGs.[
According to several studies, prenatal X-ray abdominal exposures are only associated with an about 2-fold increased risk for primitive neuroectodermal tumours (PNET), while neonatal diagnostic X-ray exposure is probably not associated with childhood brain cancer.[
Nonionizing radiation includes radiofrequency/microwave (cellular phones, radio) and extremely low-frequency magnetic fields (electrical wiring and power lines). They are characterized as possibly carcinogenic; however, studies have found no significant associations with childhood CNS tumours.[
After the 1980s, there has been a significant increase in the use of cellular phones. However, the overall incidence rates of glioma have not been significantly increased.[
Allergic conditions, such as asthma, allergies, and eczema, have been investigated for a role in glioma etiology. Adult gliomas are inversely associated with allergic conditions.[
Various studies tried to correlate infectious exposures with childhood brain cancer.[
Maternal exposure to medications containing amides or amines such as antiepileptics, barbiturates, and antihistamines was examined for connections with offspring’s pediatric brain tumours.[
Maternal alcohol consumption is not related to offspring childhood brain tumours.[
There is evidence that prenatal vitamins have a protective effect on offspring’s brain cancer risk. Although some studies found no association between childhood brain cancer and maternal vitamin, folate, or iron supplementation, a study reported protective effects of maternal folic acid and multivitamin supplementation.[
Several studies have reported that parental exposure to pesticides is associated with brain neoplasms during childhood.[
Anti-inflammatory drugs and diets, such as curcumin, gamma-linolenic acid, ketogenic or low-calorie diets, and methionine restriction, can potentially be effective for prevention in predisposed individuals or treatment for gliomas in adults.[
About 5%–10% of gliomas occur in familial clusters in all age groups, with first-degree relatives of glioma patients having a 2-fold increased risk of having a brain tumour, mainly when the patient has developed the tumour at a younger age.[
Various inherited monogenic Mendelian cancer syndromes have increased incidence for specific glioma histologies, as mentioned previously. In general, patients with neurofibromatosis type 1, also known as von Recklinghausen disease, develop CNS lesions (4% to 45%), including optic nerve gliomas, astrocytomas, and ependymomas, among others. Neurofibromatosis type 2 (central neurofibromatosis) appears with astrocytomas, among other tumours.[
Studies have noted that children of fathers older than 40 years old at the child’s birth have an increased risk for developing brain tumours, particularly astrocytomas. Astrocytomas, along with ependymomas, are also associated with maternal age.[
Several studies have reported that childhood CNS cancer risk is associated with higher birth weight and increasing head circumference.[
Our narrative review was thorough, as we critically evaluated previous research on pediatric glioma risk factors. However, all narrative reviews have inherent limitations, such as subjectiveness in including, analyzing studies, and drawing conclusions. Also, most included studies were case-control and limited by their small sample sizes and selection bias, they had different periods of exposure, and exposure assessment was based mainly on interviews, resulting in recall bias. Thus, definitive answers for possible associations are difficult to be drawn.
Progress has been made in identifying and studying risk factors for pediatric gliomas (Fig.
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Funding
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Competing Interests
The authors have declared that no competing interests exist.