生物钟（CC）对神经胶质瘤具有生物学和临床意义。大多数研究集中在CC对肿瘤微环境的影响和时间疗法的应用。本研究重点关注 CC 基因表达模式和细胞内致癌活性。神经胶质瘤基因表达数据来自人类癌症基因组图谱 (TCGA) 项目。应用纳入和排除标准后，我们​​从 TCGA-GBM 和 TCGA-LGG 项目中选择了 666 名患者，并纳入了重要的临床病理变量。对整个队列进行聚类分析，并根据统计、生物学和临床标准分为 CC1 和 CC2 亚型。 CC2 胶质瘤表现出较高的 BMAL1 和 CRY1 表达以及较低的 CRY2 和 PER2 表达（调整后的 P < .001）。 CC2 神经胶质瘤具有更高的细胞增殖、代谢重编程、血管生成、缺氧和许多致癌信号活性 (P < .001)。 CC2 亚型胶质母细胞瘤比例较高 (P < .001)，且预后较差 (P < .001)。分层 Kaplan-Meier 和多变量 Cox 分析表明，CC 亚型是临床病理特征 (P < .001)、遗传畸变 (P = .006) 和生物过程 (P < .001) 的独立预后因素。因此，这项研究显示了成人神经胶质瘤中 CC 亚型及其生物学和临床病理学意义的统计证据。© 作者 2024。由牛津大学出版社代表美国神经病理学家协会出版。保留所有权利。如需权限，请发送电子邮件至：journals.permissions@oup.com。

The circadian clock (CC) has biological and clinical implications in gliomas. Most studies focused on CC effects on the tumor microenvironment and the application of chronotherapy. The present study focused on CC gene expression patterns and intracellular oncogenic activities. Glioma gene expression data were collected from The Human Cancer Genome Atlas (TCGA) project. After applying inclusion and exclusion criteria, we selected 666 patients from TCGA-GBM and TCGA-LGG projects and included important clinicopathological variables. The entire cohort was subjected to clustering analysis and divided into CC1 and CC2 subtypes based on statistical, biological, and clinical criteria. CC2 gliomas showed higher expression of BMAL1 and CRY1 and lower expression of CRY2 and PER2 (adjusted P < .001). CC2 gliomas had q higher activity of cell proliferation, metabolic reprogramming, angiogenesis, hypoxia, and many oncogenic signals (P < .001). The CC2 subtype contained a higher proportion of glioblastomas (P < .001) and had a worse prognosis (P < .001). Stratified Kaplan-Meier and multivariable Cox analyses illustrated that the CC subtype is an independent prognostic factor to clinicopathological characteristics (P < .001), genetic aberrations (P = .006), and biological processes (P < .001). Thus, this study shows statistical evidence of CC subtypes and their biological, and clinicopathological significance in adult gliomas.© The Author(s) 2024. Published by Oxford University Press on behalf of American Association of Neuropathologists, Inc. All rights reserved. For permissions, please email: journals.permissions@oup.com.