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基于生物信息学的胶质母细胞瘤中改变的关键基因(综述)

Key genes altered in glioblastoma based on bioinformatics (Review).

作者信息

Al Ghafari Marcelino, El Jaafari Nour, Mouallem Mariam, Maassarani Tala, El-Sibai Mirvat, Abi-Habib Ralph

机构信息

Department of Biological Sciences, Lebanese American University, Beirut 1102 2801, Lebanon.

出版信息

Oncol Lett. 2025 Mar 24;29(5):243. doi: 10.3892/ol.2025.14989. eCollection 2025 May.


DOI:10.3892/ol.2025.14989
PMID:40182607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11966088/
Abstract

Glioblastoma multiforme (GBM) is an aggressive brain tumor with poor prognosis. Recent advancements in bioinformatics have contributed to uncovering the genetic alterations that underlie the development and progression of GBM. Analysis of extensive genomic data led to the identification of significant pathways involved in GBM, such as the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK signaling pathways, alongside key genes such as EGFR, TP53 and TERT. These findings have enhanced our understanding of GBM biology and led to the identification of new therapeutic targets. Bioinformatics has become an indispensable tool in pinpointing the genetic modifications that drive GBM, paving the way for innovative treatment strategies. This approach not only aids in comprehending the complexities of GBM but also holds promise for improving outcomes in patients suffering from this devastating disease. The ongoing integration of bioinformatics in GBM research continues to be vital for advancing therapeutic options.

摘要

多形性胶质母细胞瘤(GBM)是一种侵袭性脑肿瘤,预后较差。生物信息学的最新进展有助于揭示GBM发生和发展的潜在基因改变。对大量基因组数据的分析导致确定了GBM中涉及的重要信号通路,如PI3K/AKT/mTOR和Ras/Raf/MEK/ERK信号通路,以及关键基因如EGFR、TP53和TERT。这些发现加深了我们对GBM生物学的理解,并导致确定了新的治疗靶点。生物信息学已成为确定驱动GBM的基因修饰的不可或缺的工具,为创新治疗策略铺平了道路。这种方法不仅有助于理解GBM的复杂性,而且有望改善患有这种毁灭性疾病的患者的治疗结果。生物信息学在GBM研究中的持续整合对于推进治疗选择仍然至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be8c/11966088/9e4f48a1bf3e/ol-29-05-14989-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be8c/11966088/0286038ccf53/ol-29-05-14989-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be8c/11966088/9e4f48a1bf3e/ol-29-05-14989-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be8c/11966088/0286038ccf53/ol-29-05-14989-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be8c/11966088/9e4f48a1bf3e/ol-29-05-14989-g01.jpg

相似文献

[1]
Key genes altered in glioblastoma based on bioinformatics (Review).

Oncol Lett. 2025-3-24

[2]
An update on the molecular biology of glioblastoma, with clinical implications and progress in its treatment.

Cancer Commun (Lond). 2022-11

[3]
Harnessing the role of aberrant cell signaling pathways in glioblastoma multiforme: a prospect towards the targeted therapy.

Mol Biol Rep. 2024-10-19

[4]
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Cell Commun Signal. 2023-12-18

[5]
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J Neurooncol. 2025-4

[6]
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[7]
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Int J Oncol. 2022-6

[8]
PD-L1 confers glioblastoma multiforme malignancy via Ras binding and Ras/Erk/EMT activation.

Biochim Biophys Acta Mol Basis Dis. 2018-3-3

[9]
mTOR-Rictor-EGFR axis in oncogenesis and diagnosis of glioblastoma multiforme.

Mol Biol Rep. 2021-5

[10]
Integrative analysis of glioblastoma multiforme: the power of non-coding RNAs and hub genes in cancer research.

Clin Exp Med. 2025-5-3

本文引用的文献

[1]
Integrating Molecular Perspectives: Strategies for Comprehensive Multi-Omics Integrative Data Analysis and Machine Learning Applications in Transcriptomics, Proteomics, and Metabolomics.

Biology (Basel). 2024-10-22

[2]
New sights on long non-coding RNAs in glioblastoma: A review of molecular mechanism.

Heliyon. 2024-10-23

[3]
Potential diagnostic and drug target markers in glioblastoma.

Sci Rep. 2024-3-27

[4]
Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.

Noncoding RNA Res. 2024-2-6

[5]
Epidermal Growth Factor Receptor Inhibitors in Glioblastoma: Current Status and Future Possibilities.

Int J Mol Sci. 2024-2-15

[6]
Targeted Glioma Therapy-Clinical Trials and Future Directions.

Pharmaceutics. 2024-1-11

[7]
Exploring the Role of microRNAs in Glioma Progression, Prognosis, and Therapeutic Strategies.

Cancers (Basel). 2023-8-22

[8]
A multicenter, phase II trial of GC1118, a novel anti-EGFR antibody, for recurrent glioblastoma patients with EGFR amplification.

Cancer Med. 2023-8

[9]
A complex of Wnt/planar cell polarity signaling components Vangl1 and Fzd7 drives glioblastoma multiforme malignant properties.

Cancer Lett. 2023-7-28

[10]
Molecular mechanisms of tumor resistance to radiotherapy.

Mol Cancer. 2023-6-15

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