Meningiomas arise from the membranes surrounding the brain and spinal cord, and most are driven by a combination of genetic changes, hormonal influences, and environmental exposures. They are the most common primary brain tumor, and while the majority are slow-growing and benign, understanding what triggers them helps explain why certain people are far more likely to develop one than others.
The Primary Genetic Driver
The single most common genetic change behind meningiomas is an alteration in the NF2 gene, located on chromosome 22. This gene normally produces a protein that helps regulate cell growth. When NF2 is inactivated through mutation or when part of chromosome 22 is lost, cells in the meninges can begin multiplying without the usual checks. NF2 alteration is the most frequent genetic driver in sporadic meningiomas (those that arise without a family history) and is also linked to the initiation of more aggressive tumor subtypes.
Not all meningiomas involve NF2. Roughly a quarter carry mutations in a gene called TRAF7, often paired with changes in other growth-related genes. Some tumors instead have a specific mutation in AKT1, which promotes cell survival, or in SMO, which activates a developmental signaling pathway called Hedgehog. These non-NF2 mutations are mutually exclusive of NF2 changes, meaning a given tumor typically follows one genetic path or the other. This molecular diversity is one reason meningiomas vary so much in location, behavior, and response to treatment.
Why Women Are More Affected
Women develop meningiomas at significantly higher rates than men, and the gap is widest during the reproductive years. In the 40 to 49 age group, women are about 3.4 times more likely than men to be diagnosed with a low-grade meningioma. That ratio narrows after menopause, dropping to roughly 1.6 in people over 80, which strongly implicates sex hormones in tumor growth.
The hormonal connection runs through progesterone receptors. About 72% of meningiomas express progesterone receptors, making them highly sensitive to this hormone. Interestingly, the presence of progesterone receptors is actually associated with less aggressive tumors: roughly 77% of grade 1 meningiomas express them, compared to only 17% of grade 3 tumors. Estrogen receptors appear in only about 11% of meningiomas, but when present, they correlate with faster cell proliferation and worse outcomes.
Progestogen Medications and Meningioma Risk
Some of the strongest evidence linking hormones to meningiomas comes from studies of progestogen medications. High-dose cyproterone acetate, a synthetic progestogen prescribed for conditions like severe acne, excessive hair growth, and as part of some transgender hormone regimens, carries a dramatically elevated risk. A large cohort study published in The BMJ found that women using this drug had a meningioma incidence of 23.8 per 100,000 person-years, compared to 4.5 in non-users. At cumulative doses above 60 grams, the risk was more than 20 times higher than in the general population.
Other progestogens show similar patterns. Treatment with nomegestrol acetate for five or more years multiplied the risk roughly 12-fold, while chlormadinone acetate carried about a 7-fold increase after 3.5 years of use. The encouraging finding is that these tumors appear to be hormone-dependent: in 79% of cases, tumor volume decreased after the patient stopped taking the medication. Cyproterone acetate now carries a formal contraindication for anyone with a current or past meningioma.
Radiation Exposure
Ionizing radiation to the head is the best-established environmental risk factor for meningiomas. This includes radiation therapy for childhood cancers, as well as lower-dose treatments like scalp irradiation, which was once commonly used for fungal infections. The relationship between dose and timing is striking: high-dose cranial radiation (from cancer treatment) tends to produce meningiomas roughly 12 to 25 years later, while low-dose exposure pushes the timeline out to 30 to 40 years.
A systematic review of over 900 radiation-induced meningiomas found that patients who received cranial radiotherapy developed tumors an average of 21.5 years afterward, while those who had scalp radiation for fungal infections waited an average of 40.5 years. This means childhood cancer survivors may enter their highest-risk period in early adulthood, while people who received low-dose scalp treatments face elevated risk much later in life. Radiation-induced meningiomas also tend to be more aggressive and more likely to recur than their spontaneous counterparts.
Age and Incidence Patterns
Meningioma risk climbs steadily with age. In children under 10, the incidence is vanishingly low, around 0.06 per 100,000 per year with no difference between boys and girls. By ages 50 to 59, the rate rises to about 6 per 100,000 in men and 18 per 100,000 in women. In people over 80, it reaches roughly 34 per 100,000 in men and 56 per 100,000 in women. Many meningiomas found in older adults are discovered incidentally on brain scans done for other reasons and never cause symptoms.
Obesity as a Risk Factor
Body weight plays a modest but consistent role. Multiple prospective studies have found that people with a BMI of 30 or higher face a 40% to 60% increased risk of meningioma compared to those at a normal weight. The most likely explanation ties back to hormones: fat tissue produces estrogen, and higher circulating hormone levels may promote growth in hormone-sensitive meningioma cells. Obesity also creates a state of chronic low-grade inflammation and elevated levels of growth-promoting signals like insulin, both of which could contribute to tumor development.
Inherited Genetic Syndromes
A small percentage of meningiomas occur in people with inherited conditions that predispose them to multiple tumor types. The most well-known is neurofibromatosis type 2 (NF2), which involves a germline mutation in the same NF2 gene that drives many sporadic tumors. People with this condition often develop meningiomas at younger ages and may have more than one.
Several rarer syndromes also carry elevated risk. Werner syndrome increases meningioma risk by roughly 36 times compared to the general population, and tumors tend to appear at younger ages. Cowden syndrome, caused by mutations in the PTEN gene, includes meningiomas in about 8% of affected individuals. Gorlin syndrome, better known for causing skin cancers, includes meningiomas in roughly 5% of patients. Other predisposing conditions include BAP1 tumor predisposition syndrome and familial meningiomatosis linked to mutations in the SMARCB1 and SMARCE1 genes. In one study, germline SMARCE1 mutations were found in 14% of patients under 25 who had a solitary meningioma.
Head Trauma: Debated but Unproven
The idea that a head injury could trigger a meningioma has circulated for decades. A systematic review examining 15 studies found that 9 suggested a possible relationship between traumatic brain injury and later brain tumor development. However, the evidence remains correlational rather than causal. Case reports exist, and some population-level data hint at a link, but no study has definitively shown that head trauma directly initiates meningioma growth. Detection bias is a significant concern: people who have had a serious head injury are more likely to undergo brain imaging, which increases the odds of finding an incidental tumor that was already there.
How Tumor Grade Reflects Biology
The World Health Organization classifies meningiomas into three grades, and the grading system reflects the underlying biology of what caused the tumor to become more or less aggressive. Grade 1 tumors are the most common, grow slowly, and are most likely to carry progesterone receptors. Grade 2 (atypical) meningiomas show faster cell division and are more likely to recur after treatment. Grade 3 (anaplastic) meningiomas are rare and aggressive, sometimes carrying specific molecular red flags like mutations in the TERT gene promoter or loss of tumor-suppressing genes called CDKN2A/B.
The 2021 WHO classification now treats meningioma as a single tumor type with 15 subtypes, and grading criteria apply regardless of the tumor’s microscopic appearance. This shift reflects growing understanding that the molecular changes inside the tumor predict its behavior more reliably than how the cells look under a microscope. Two tumors that look identical can carry very different genetic alterations, leading to very different outcomes.