3D Multiscale Moving Boundary Modelling for Malignant Solid Tumours with Focus on Glioblastoma Progression and Relapse (Keynote Speaker Talk)

TY - CONF

T1 - 3D Multiscale Moving Boundary Modelling for Malignant Solid Tumours with Focus on Glioblastoma Progression and Relapse (Keynote Speaker Talk)

AU - Trucu, Dumitru

PY - 2026/9/7

Y1 - 2026/9/7

N2 - The genuinely multiscale nature of malignant solid tumours dynamics and the challenges that these bring are illustrated in full flavour by the case of Glioblastoma (GBM) progression and relapse in the brain. Besides recent progress, the understanding of the key mechanisms for GBM invasion remains one of the greatest challenges. The complex dynamics found there brings together cell-scale and tissue scale processes that contribute to an entire range of key aspects in tumour development and spread, notably being not only proliferation, degradation of the surrounding brain environment (via proteolytic enzymatic activity), calcium mediated adhesive processes, interactions with fibrous extracellular matrix environment, but also metabolic plasticity and ability to generate therapy-resistant subpopulations under hypoxic and treatment-induced cellular stress. In this talk, we attempt to address these aspects by proposing appropriately tailored multiscale moving boundary modelling approaches. Moreover, aiming to address a higher level of complexity in describing the interlinked processes involved within GBM progression and relapse, we recently introduce three key extensions to the multiscale framework that was introduced and established in Trucu et al. 2013 and further developed in several scientific publications authored by the same group (notably in this and this). These extensions are structured on three avenues and include: (1) influence of the interfacial ECM fibres of tumour boundary movement; (2) non-local collective cell motility (“go-or-grow” behaviour); and (3) transitions from isotropic to anisotropic GBM invasion patterns. With this updated multiscale moving boundary modelling framework, we proceed to investigate further aspects in GBM dynamics, including the emergence of cellular stress and stress-induced resistance mechanisms driven by hypoxia and treatment, as well as the role of metabolic factors in relapse.

AB - The genuinely multiscale nature of malignant solid tumours dynamics and the challenges that these bring are illustrated in full flavour by the case of Glioblastoma (GBM) progression and relapse in the brain. Besides recent progress, the understanding of the key mechanisms for GBM invasion remains one of the greatest challenges. The complex dynamics found there brings together cell-scale and tissue scale processes that contribute to an entire range of key aspects in tumour development and spread, notably being not only proliferation, degradation of the surrounding brain environment (via proteolytic enzymatic activity), calcium mediated adhesive processes, interactions with fibrous extracellular matrix environment, but also metabolic plasticity and ability to generate therapy-resistant subpopulations under hypoxic and treatment-induced cellular stress. In this talk, we attempt to address these aspects by proposing appropriately tailored multiscale moving boundary modelling approaches. Moreover, aiming to address a higher level of complexity in describing the interlinked processes involved within GBM progression and relapse, we recently introduce three key extensions to the multiscale framework that was introduced and established in Trucu et al. 2013 and further developed in several scientific publications authored by the same group (notably in this and this). These extensions are structured on three avenues and include: (1) influence of the interfacial ECM fibres of tumour boundary movement; (2) non-local collective cell motility (“go-or-grow” behaviour); and (3) transitions from isotropic to anisotropic GBM invasion patterns. With this updated multiscale moving boundary modelling framework, we proceed to investigate further aspects in GBM dynamics, including the emergence of cellular stress and stress-induced resistance mechanisms driven by hypoxia and treatment, as well as the role of metabolic factors in relapse.

KW - Keynote Speaker

UR - https://www.esmtb.org/Events-announcements/13643275

M3 - Paper

T2 - Insights into Cell-Tissue Interactions via Mathematical Modelling

Y2 - 7 September 2026 through 8 September 2026

ER -