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This study aims to establish and evaluate an in vivo mouse model of glioblastoma using high-resolution imaging techniques.

February 16, 2026Open Access

Tumor visualization and evaluation of glioblastoma in mice using small animal 9.4T MRI and PET‑CT with high resolution

Key Points

This study aims to establish and evaluate an in vivo mouse model of glioblastoma using high-resolution imaging techniques.
Developed a mouse model for glioblastoma using GL261 cell injection.
Utilized MRI and PET-CT for non-invasive tumor imaging.
Compared metabolites in tumor and normal brain tissue using 1H-MRS.
Performed pharmacokinetic analysis of FDG distribution in brain and tumor tissue.
MRI detected tumors 7 days post-cell injection, with sizes increasing over time (1.263 to 13.85 mm3).
1H-MRS analysis revealed elevated lactate and choline levels in tumor tissue compared to normal brain.
PET-CT confirmed MRI tumor detections, showing increased SUV in tumor tissue post-FDG administration.
Pharmacokinetic analysis indicated specific model parameters for brain and tumor tissue.

Abstract

Glioblastoma (GBM) is the most prevalent type of malignant primary brain tumor. Preclinical research serves a key role in investigating the development and mechanism of GBM tumor. However, the dynamic and non‑invasive evaluation of tumors in animals faces challenges, such as the limited sensitivity of clinical instruments and insufficient spatial resolution for mouse brain tumors. The present study aimed to establish an in vivo mouse GBM model and evaluate the model using high resolution small animal positron emission tomography‑computed tomography (PET‑CT) and magnetic resonance imaging (MRI). Metabolism was compared between the normal brain and tumor tissue by using 1H‑magnetic resonance spectroscopy (1H‑MRS). T2‑weighted imaging (T2WI) MRI detected the tumor in the brain 7 days after injection of GL261 cells, with tumor sizes of 1.263, 4.917 and 13.85 mm3 on days 7, 14 and 21, respectively. 1H‑MRS demonstrated that the levels of tissue metabolites such as lactate and total choline increased, while those representing neurological function of the brain such as total N‑acetylaspartate decreased in tumor compared with the normal brain tissues. PET‑CT imaging confirmed the tumor detected by MRI. At 6‑120 min post 18F‑fluorodeoxyglucose (FDG) administration, the standard uptake value (SUV) in tumor tissue gradually increased, while the SUV value in normal brain tissue gradually decreased. SUV in the liver and kidneys decreased, while SUV in the bladder increased in a time‑dependent manner. Pharmacokinetic analysis showed that the distribution of FDG in brain and tumor tissue conformed to a two‑tissue compartment model. This model consists of a plasma compartment and two tissue compartments representing free FDG and phosphorylated FDG within brain or tumor tissue. The model parameters are defined as follows: Fractional blood volume (vB)=3.6%, k1 (forward transport rate)=1.844, k2 (reverse transport rate)=3.844 and k3 (phosphorylation rate)=0.280 in brain and vB=2.3%, k1=0.797, k2=2.722 and k3=0.319 in tumor tissue, respectively. The tumors observed by MRI and PET‑CT imaging were ultimately confirmed through morphological and pathological analysis. Compared with normal brain tissue, glioma tissue exhibited significantly elevated glucose transporter type 1 protein levels. In conclusion, the model was confirmed by high‑resolution small animal PET‑CT and MRI, as well as morphological and pathological approaches.

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