World neurosurgery · 2024
Traumatic Brain Injury Increasing Risk of Meningioma? From the Genetic Evidence.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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He Chunming, Long Tao, Zhou Huaiyu, Zeng Chuan, Xiong Peng, Qiu Xinyu, Song Haimin
Аннотация
BACKGROUND: Numerous studies have demonstrated a strong association between traumatic brain injury (TBI) and an increased risk of meningioma. However, this correlation remains controversial. This study utilized Mendelian randomization to explore this relationship from the perspective of genetic evidence.
METHODS: We employed 6 TBI genome-wide association study datasets from the integrative epidemiology unit genome-wide association study database. Summary statistics for meningioma were sourced from the FinnGen R10 database. We assessed heterogeneity and horizontal pleiotropy within the analyzed data. The primary method was inverse variance weighting (IVW) to investigate the causal relationship between TBI and meningioma, excluding cases with horizontal pleiotropy. Four supplementary analysis methods were also used, with abnormal results excluded based on leave-one-out sensitivity analysis.
RESULTS: All 6 Mendelian randomization analyses indicated no causal relationship between TBI and meningiomas (focal brain injury IVW P value = 0.98; diffuse brain injury IVW P value = 0.41; TBI without concussion IVW P value = 0.45; intracranial trauma IVW P value = 0.34; traumatic subdural hemorrhage IVW P value = 0.80; traumatic subarachnoid hemorrhage IVW P value = 0.92).
CONCLUSIONS: The Mendelian randomization study revealed that TBI does not increase the risk of meningioma based on genetic evidence.
METHODS: We employed 6 TBI genome-wide association study datasets from the integrative epidemiology unit genome-wide association study database. Summary statistics for meningioma were sourced from the FinnGen R10 database. We assessed heterogeneity and horizontal pleiotropy within the analyzed data. The primary method was inverse variance weighting (IVW) to investigate the causal relationship between TBI and meningioma, excluding cases with horizontal pleiotropy. Four supplementary analysis methods were also used, with abnormal results excluded based on leave-one-out sensitivity analysis.
RESULTS: All 6 Mendelian randomization analyses indicated no causal relationship between TBI and meningiomas (focal brain injury IVW P value = 0.98; diffuse brain injury IVW P value = 0.41; TBI without concussion IVW P value = 0.45; intracranial trauma IVW P value = 0.34; traumatic subdural hemorrhage IVW P value = 0.80; traumatic subarachnoid hemorrhage IVW P value = 0.92).
CONCLUSIONS: The Mendelian randomization study revealed that TBI does not increase the risk of meningioma based on genetic evidence.