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Updated: Jan 20, 2026

Live-Cell Imaging Assays to Study Glioblastoma Brain Tumor Stem Cell Migration and Invasion
Published on: August 29, 2018
Molecular and Clinical Insights into the Invasive Capacity of Glioblastoma Cells
Carlos Velásquez1,2, Sheila Mansouri3, Carla Mora1
1Department of Neurological Surgery and Spine Unit, Hospital Universitario Marqués de Valdecilla and Instituto de Investigación Marqués de Valdecilla (IDIVAL), Santander, Spain.
Abstract:
The invasive capacity of GBM is one of the key tumoral features associated with treatment resistance, recurrence, and poor overall survival. The molecular machinery underlying GBM invasiveness comprises an intricate network of signaling pathways and interactions with the extracellular matrix and host cells. Among them, PI3k/Akt, Wnt, Hedgehog, and NFkB play a crucial role in the cellular processes related to invasion. A better understanding of these pathways could potentially help in developing new therapeutic approaches with better outcomes. Nevertheless, despite significant advances made over the last decade on these molecular and cellular mechanisms, they have not been translated into the clinical practice. Moreover, targeting the infiltrative tumor and its significance regarding outcome is still a major clinical challenge. For instance, the pre- and intraoperative methods used to identify the infiltrative tumor are limited when trying to accurately define the tumor boundaries and the burden of tumor cells in the infiltrated parenchyma. Besides, the impact of treating the infiltrative tumor remains unclear. Here we aim to highlight the molecular and clinical hallmarks of invasion in GBM.
Insights
Glioblastoma (GBM) invasion drives treatment resistance and poor survival. Understanding its molecular pathways and clinical challenges is crucial for developing new therapies targeting invasive tumor cells.
Area of Science:
- Neuro-oncology
- Cancer Biology
- Molecular Medicine
Background:
- Glioblastoma (GBM) exhibits invasive properties, correlating with treatment resistance, recurrence, and reduced patient survival.
- GBM invasiveness is governed by complex molecular pathways, including PI3K/Akt, Wnt, Hedgehog, and NFkB, interacting with the tumor microenvironment.
- Despite advances in understanding GBM invasion mechanisms, clinical translation remains limited, posing significant challenges in treatment and outcome prediction.
Purpose of the Study:
- To elucidate the molecular and cellular hallmarks of glioblastoma invasion.
- To highlight the clinical challenges associated with identifying and treating invasive GBM components.
- To bridge the gap between molecular understanding and clinical application for GBM invasion.
Main Methods:
- Review of molecular signaling pathways implicated in GBM invasion (PI3K/Akt, Wnt, Hedgehog, NFkB).
- Analysis of extracellular matrix and host cell interactions in GBM.
- Evaluation of current pre- and intraoperative methods for defining GBM tumor boundaries.
- Discussion of the clinical significance and impact of treating infiltrative GBM.
Main Results:
- Key signaling pathways (PI3K/Akt, Wnt, Hedgehog, NFkB) are central to GBM cellular invasion.
- Current methods for delineating invasive GBM are insufficient, complicating treatment strategies.
- The clinical impact of targeting infiltrative GBM remains poorly understood.
Conclusions:
- Targeting GBM invasion requires a deeper understanding of its molecular underpinnings.
- Improved diagnostic and therapeutic strategies are needed to address the clinical challenge of infiltrative GBM.
- Further research is essential to translate molecular insights into effective clinical interventions for GBM patients.
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