# Advancing the Study of Glioblastoma Through 3D Tumor Models

**Authors:** Karen Salmeron-Moreno, Josephine Buclez, Chris Donghyun Kim, Karthik Papisetty, Thomas McCaffery, Fadi Jacob, Rommi Kashlan, Hithardhi Duggireddy, Karthik Valiveti, Justin Maldonado, Gustavo Pradilla, Tomas Garzon-Muvdi

PMC · DOI: 10.3390/cancers18040668 · 2026-02-18

## TL;DR

This paper reviews recent advances in 3D tumor models for glioblastoma, aiming to better understand and treat this aggressive brain cancer.

## Contribution

The paper provides a comprehensive overview of how 3D tumor models can capture the complexity of glioblastoma for improved preclinical research.

## Key findings

- 3D tumor models replicate the structural and biochemical complexity of glioblastoma.
- These models offer potential to bridge preclinical research and patient care.
- Challenges remain in translating 3D models into clinical applications.

## Abstract

Glioblastoma is an aggressive brain tumor characterized by marked cellular plasticity and molecular heterogeneity, which drive therapeutic resistance and near-universal recurrence. To better reflect this complexity, researchers have developed three-dimensional tumor models that recreate key features, such as cell interactions and the biochemical environment. This review aims to describe recent advances in these models, discuss practical considerations, and provide insight into the potential of three-dimensional tumor models to strengthen the connection between preclinical research and patient care.

Glioblastoma (GBM), the most aggressive primary brain malignancy, remains a challenge to experimentally model. Accurately modeling the intra- and intertumoral heterogeneity of GBMs is essential for enhancing the predictive power of preclinical models and improving the effectiveness of current therapies. This review highlights recent advances in 3D tumor modeling, which accurately replicate the structural, cellular, and biochemical complexity of GBMs. We examine their translational potential and discuss current barriers to clinical translation.

## Linked entities

- **Diseases:** Glioblastoma (MONDO:0018177), GBM (MONDO:0018177)

## Full-text entities

- **Genes:** MGMT (O-6-methylguanine-DNA methyltransferase) [NCBI Gene 4255], PTEN (phosphatase and tensin homolog) [NCBI Gene 5728] {aka 10q23del, BZS, CWS1, DEC, GLM2, MHAM}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, EGF (epidermal growth factor) [NCBI Gene 1950] {aka HOMG4, URG}, EIF2AK3 (eukaryotic translation initiation factor 2 alpha kinase 3) [NCBI Gene 9451] {aka PEK, PERK, WRS}, WNT3A (Wnt family member 3A) [NCBI Gene 89780], RSPO1 (R-spondin 1) [NCBI Gene 284654] {aka CRISTIN3, RSPO}, MMRN1 (multimerin 1) [NCBI Gene 22915] {aka ECM, EMILIN4, GPIa*, MMRN}, CXCR4 (C-X-C motif chemokine receptor 4) [NCBI Gene 7852] {aka CD184, D2S201E, FB22, HM89, HSY3RR, LCR1}, NOG (noggin) [NCBI Gene 9241] {aka SYM1, SYNS1, SYNS1A}, PTK2 (protein tyrosine kinase 2) [NCBI Gene 5747] {aka FADK, FADK 1, FAK, FAK1, FRNK, PPP1R71}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}
- **Diseases:** hypoxic (MESH:D002534), hypoxia (MESH:D000860), glioma (MESH:D005910), injury to (MESH:D014947), inflammatory (MESH:D007249), Tumor (MESH:D009369), necrosis (MESH:D009336), brain malignancy (MESH:D001932), GBM (MESH:D005909), tumorigenic (MESH:D002471), OMSs (MESH:C000598645), TDTSs (MESH:C536408)
- **Chemicals:** glycidyl methacrylate (MESH:C007870), HA (MESH:D006820), alginate (MESH:D000464), oxygen (MESH:D010100), polyethylene glycol (MESH:D011092), glucose (MESH:D005947), CAR-T (-), temozolomide (MESH:D000077204)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939352/full.md

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Source: https://tomesphere.com/paper/PMC12939352