Active Cancer Lungs & Breathing

Investigating the role of fibroblast-like cells in shaping the glioblastoma tumour microenvironment

In plain English

AI plain-English summary

Glioblastoma tumours actively remodel their own surroundings, creating physical and chemical niches that protect them from the immune system and resist treatment. This matters because glioblastoma is one of the deadliest brain cancers, and its ability to evade therapy stems largely from this hostile, heterogeneous microenvironment. While other solid tumours rely on fibroblast-like cells to drive such remodelling and immune suppression, the role of these cells in glioblastoma has been largely overlooked. This project will identify which cell types are responsible for reshaping the tumour’s extracellular matrix and how that process silences immune cells. If successful, the research could reveal new targets for therapy—for instance, drugs that block the matrix-remodelling machinery or re-awaken immune cells trapped in the tumour. This is fundamental science: it will not produce a treatment tomorrow. But understanding how glioblastoma builds its protective environment is a necessary first step toward dismantling it, much as mapping the immune-suppressive tactics of other cancers eventually led to checkpoint inhibitors.

View original technical description
Glioblastoma (GBM) remains one of the most aggressive and treatment-resistant cancers, with a poor prognosis. Treatment resistance is largely attributed to the tumour’s highly heterogeneous microenvironment. GBM consists of multiple neoplastic cell subtypes, each with distinct phenotypes and associations with extracellular matrix (ECM) remodelling, immune cell recruitment, and hypoxic gradients, creating specialised histomorphic niches. The mechanisms by which these niches arise, however, remain unclear. Increasing evidence from other solid tumours highlights the role of stromal fibroblast-like populations in driving ECM remodelling, tumour progression, and immune evasion, yet their contribution in GBM is poorly understood. This project aims to define the mechanisms underpinning the extensive ECM remodelling in GBM and investigate how this process shapes immune cell polarisation within the tumour microenvironment. We will employ a combination of in vivo, in vitro, and in silico approaches to characterise the cellular drivers of ECM remodelling and how this may contribute to immunosuppression within the tumour.

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Researchers

Argyro Olympitis (EPMC Awardee)

Related Research

Grants with similar aims, by meaning.

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Investigating the Multifaceted Effects of DNA Damage Response Inhibitors on the Glioblastoma Microenvironment
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Identifying the key mechanisms that govern T-cell mediated immune suppression in Glioblastoma

Original classification

PhD Studentship (Basic)

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