Meningioma risk factor
Intrinsic Risk Factors
Several Familial Tumor Syndromes of the Central Nervous systems are characterized by increased meningioma risk, and the genetics of these syndromes provides mechanistic insight into sporadic disease. The best defined of these syndromes is neurofibromatosis type 2, which is caused by a mutation in the NF2 gene and has a meningioma incidence of approximately 50%. This finding led to the subsequent discovery that NF2 loss-of-function occurs in up to 60% of sporadic tumors. Other important familial diseases with increased meningioma risk include nevoid basal cell carcinoma syndrome, multiple endocrine neoplasia 1 (MEN1), Cowden syndrome, Werner syndrome, BAP1 tumor predisposition syndrome, Rubinstein Taybi syndrome, and familial meningiomatosis caused by germline mutations in the SMARCB1 and SMARCE1 genes.
Other intrinsic risk factors (gender, ethnic groups, allergic conditions, familial and personal history, genetic polymorphisms)
Exogenous risk factors
They have been suspected to play a role in the etiology of meningiomas and their changes with time is likely to impact incidence trends. A causal link has been established only for ionising radiation but the role of many other factors have been hypothesised: electromagnetic fields, nutrition, pesticides, hormonal as well as reproductive factors. Considering the serious or even lethal potentiality of some meningiomas and the apparent rise in their incidence, all practitioners involved in neuro-oncology should feel concerned today of the necessity to better assess their public health burden and to study their epidemiological features 1).
Obesity but not overweight is associated with an increased risk of meningioma. Due to the limited number of studies, further research is needed to confirm the association 2).
Pregnancy has been associated with diagnosis or growth of meningiomas in several case reports, which has led to the hypothesis that pregnancy may be a meningioma risk factors. The aim of a study of Pettersson-Segerlind et al. was to test this hypothesis in a large population-based cohort study. Women born in Sweden 1958-2000 (N = 2,204,126) were identified and matched with the Medical Birth Register and the Cancer Register. The expected number of meningioma cases and risk ratios were calculated for parous and nulliparous women and compared to the observed number of cases. Compared to parous women, meningiomas were more common among nulliparous (SIR = 1.73; 95% CI 1.52-1.95). The number of meningioma cases detected during pregnancy was lower than the expected (SIR = 0.40; 95% CI 0.20-0.72). Moreover, no increased risk was found in the first-year post-partum (SIR = 1.04; 95% CI 0.74-1.41). Contrary to this hypothesis, there was no increased risk for diagnosing a meningioma during pregnancy or 1-year post-partum. A lower detection rate during pregnancy, may reflect under-utilization of diagnostic procedures, but the actual number of meningiomas was homogenously lower among parous than nulliparous women throughout the study period, indicating that pregnancy is not a risk factor for meningioma 3).