<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.12720</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>脑膜瘤预后相关生物标记物研究进展</title><url>https://artdesignp.com/journal/MRP/3/2/10.61369/MRP.12720</url><author>陆立权,柳夫义</author><pub-date pub-type="publication-year"><year>2025</year></pub-date><volume>3</volume><issue>2</issue><history><date date-type="pub"><published-time>2025-02-20</published-time></date></history><abstract>脑膜瘤是常见的原发性颅内肿瘤，发病率约占成人颅内肿瘤中的 30%~40%， 多数良性脑膜瘤手术切除后预后良好，但部分恶性脑膜瘤侵袭性强、易复发，治疗难度较大。[1] 目前临床对脑膜瘤预后评估主要依赖于组织学分级、手术切除程度、肿瘤生长部位及大小等传统指标，难以全面反映患者个体差异和肿瘤生物学特性，因此寻找更为精准可靠的预后生物标记物成为脑膜瘤研究重点。近年来，分子生物学技术发展推动了脑膜瘤分子分型与预后生物标记物研究的突破。本文系统综述脑膜瘤预后相关生物标记物的研究进展，探讨其在预后评估、个体化治疗及临床决策中的应用价值，以期为脑膜瘤的临床诊疗提供新的思路。</abstract><keywords>脑膜瘤,生物标记物,预后</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]曾 明 慧, 王飞. 小型脑膜瘤的治疗现状及其研究进展[J]. 中 华神经外科杂志, 2023,39(3):306-311.[2]Ostrom Q T, Price M, Neff C, et al. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2015-2019.[J]. Neuro-oncology, 2022,24(5):1-95.[3]郑莉梅, 张声, 王行富. 第 5 版 WHO 中枢神经系统肿瘤分类脑膜瘤分类解读[J]. 中 华病理学杂志, 2023,52(2):107-111.[4]Louis D N, Perry A, Wesseling P, et al. The 2021 WHO classification of tumors of the central nervous system: a summary[J]. Neuro-oncology, 2021, 23(8): 1231-1251.[5]Wang J Z, Landry A P, Raleigh D R, et al. Meningioma: International Consortium on Meningiomas consensus review on scientific advances and treatment paradigms for clinicians, researchers, and patients[J]. Neuro-oncology, 2024, 26(10): 1742-1780.[6]Nigim F, Esaki S, Hood M, et al. A new patient-derived orthotopic malignant meningioma model treated with oncolytic herpes simplex virus[J]. Neuro-oncology, 2016, 18(9): 1278-1287.[7]Berghoff A S, Hielscher T, Ricken G, et al. Prognostic impact of genetic alterations and methylation classes in meningioma[J]. Brain Pathology, 2022, 32(2): e12970.[8]Xu D, Yin S, Shu Y. NF2: An underestimated player in cancer metabolic reprogramming and tumor immunity[J]. NPJ Precision Oncology, 2024, 8(1): 133.[9]Roehrkasse A M, Peterson J E G, Fung K M, et al. The discrepancy between standard histologic WHO grading of meningioma and molecular profile: a single institution series[J]. Frontiers in Oncology, 2022, 12: 846232.[10]Ren L, Xie Q, Deng J, et al. Association of frequent NF2 mutations with spinal location predominance and worse outcomes in psammomatous meningiomas[J]. Journal of Neurosurgery, 2024, 141(3): 593-601.[11]Leao R, Apolonio J D, Lee D, et al. Mechanisms of human telomerase reverse transcriptase (hTERT) regulation: clinical impacts in cancer[J]. Journal of biomedical science, 2018,25(1):22.[12]Mirian C, Duun-Henriksen A K, Juratli T, et al. Poor prognosis associated with TERT gene alterations in meningioma is independent of the WHO classification: an individual patient data meta-analysis[J]. Journal of Neurology, Neurosurgery &amp;amp; Psychiatry, 2020, 91(4): 378-387.[13]Zhang J, Liu Z, Jia J. Mechanisms of Smoothened Regulation in Hedgehog Signaling[J]. Cells, 2021, 10(8).[14]Clark V E, Harmancı A S, Bai H, et al. Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas[J]. Nature genetics, 2016, 48(10): 1253-1259.[15]Strickland M R, Gill C M, Nayyar N, et al. Targeted sequencing of SMO and AKT1 in anterior skull base meningiomas[J]. Journal of neurosurgery, 2017, 127(2): 438-444.[16]Boetto J, Bielle F, Sanson M, et al. SMO mutation status defines a distinct and frequent molecular subgroup in olfactory groove meningiomas[J]. Neuro-oncology, 2017, 19(3): 345-351.[17]Kumar B H, Kabekkodu S P, Pai K S R. Structural insights of AKT and its activation mechanism for drug development[J]. Molecular Diversity, 2025: 1-21.[18]John P, Waldt N, Liebich J, et al. AKT1E17K‐mutated meningioma cell lines respond to treatment with the AKT inhibitor AZD5363[J]. Neuropathology and Applied Neurobiology, 2022, 48(2): e12780.[19]Clark V E, Erson-Omay E Z, Serin A, et al. Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO[J]. Science, 2013, 339(6123): 1077-1080.[20]牛蕴泽, 郭太, 刘彦伟. 细胞周期依赖激酶抑制基因 2A/B 纯合缺失在组织病理 2 或 3级脑胶质瘤中的临床意义[J]. 国际神经病学神经外科学杂志, 2023,50(5):1-7.[21]杨益言, 王卫东. p53 动力学：从细胞命运到炎症免疫[J]. 中华放射医学与防护杂志, 2024,44(12):1090-1094.[22]王琳玲, 徐欣怡, 潘红宇,等影像组学列线图预测 IDH 突变型星形细胞瘤 CDKN 2A/B 纯合缺失状态[J]. 实用放射学杂志, 2024,40(11):1770-1774.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
