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Updated: Jun 4, 2026
Imaging Glioma Initiation In Vivo Through a Polished and Reinforced Thin-skull Cranial Window
Published on: November 20, 2012
Glioma-initiating cells and molecular pathology: implications for therapy
Atsushi Natsume1, Sayano Kinjo, Kanako Yuki
1Department of Neurosurgery, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Abstract:
There is now compelling evidence that gliomas harbor a small population of cells, termed glioma-initiating cells (GICs), characterized by their ability to undergo self-renewal and initiate tumorigenesis. The development of therapeutic strategies targeted toward GIC signaling may improve the treatment of malignant gliomas. The characterization of GICs provides a clue to elucidating histological heterogeneity and treatment failure. The role of the stem cell marker CD133 in the initiation and progression of brain tumors is still uncertain. Here, we review some of the signaling mechanisms involved in GIC biology, such as phosphatase and tensin homolog (PTEN), sonic hedgehog, Notch, and WNT signaling pathways, maternal embryonic leucine-zipper kinase (MELK), BMI1, and Janus kinase signal transducer and activator of transcription (JAK-STAT) signaling. In addition, we discuss the role of microRNAs in GICs by focusing on microRNA-21 regulation by type I interferon.
Insights
Glioma-initiating cells (GICs) drive brain tumor growth. Targeting GIC signaling pathways, including PTEN, Notch, and WNT, may lead to improved treatments for malignant gliomas.
Area of Science:
- Neuro-oncology
- Cancer Stem Cell Biology
Background:
- Gliomas contain glioma-initiating cells (GICs) responsible for tumor initiation and self-renewal.
- Understanding GIC biology is crucial for addressing histological heterogeneity and treatment resistance in malignant gliomas.
Purpose of the Study:
- To review key signaling mechanisms involved in glioma-initiating cell (GIC) biology.
- To discuss the potential of targeting GIC signaling for improved glioma therapeutics.
Main Methods:
- Literature review of signaling pathways implicated in GIC function.
- Focus on pathways such as PTEN, sonic hedgehog, Notch, WNT, MELK, BMI1, and JAK-STAT.
- Examination of microRNA roles, specifically microRNA-21 regulation.
Main Results:
- Several signaling pathways (PTEN, sonic hedgehog, Notch, WNT, MELK, BMI1, JAK-STAT) are critical for GIC maintenance and tumorigenesis.
- MicroRNAs, such as microRNA-21, play a role in GIC regulation.
- The precise role of CD133 in brain tumor initiation and progression remains under investigation.
Conclusions:
- Targeting GIC-specific signaling pathways offers a promising therapeutic avenue for malignant gliomas.
- Further research into GIC biology and regulatory mechanisms like microRNAs is essential for advancing brain tumor treatment.
