The development of a complex functional multicellular organism from a single cell involves tightly regulated and coordinated cell behaviours coupled through short- and long-range biochemical and mechanical signals. To truly comprehend this complexity, alongside experimental approaches we need mathematical and computational models, which can link observations to mechanisms in a quantitative, predictive, and experimentally verifiable way. In this talk I will describe our efforts to model aspects of embryonic development, focusing in particular on the planar polarised behaviours of cells in epithelial tissues, and discuss the mathematical and computational challenges associated with this work. I will also highlight some of our work to improve the reproducibility and re-use of such models through the ongoing development of Chaste (https://github.com/chaste), an open-source C++ library for multiscale modelling of biological tissues and cell populations.

Cell and tissue movement during development, immune response, and cancer invasion depends on chemical or mechanical guidance cues. In many systems, this guidance arises not from long-range, pre-patterned cues but from self-generated gradients locally shaped by cells. However, how heterogeneous cell mixtures coordinate their migration by self-generated gradients remains largely unexplored. In this talk, I will first summarize our recent discovery that immune cells steer their long-range migration using self-generated chemotactic cues (Alanko et al., 2023). I will then introduce a multi-component Keller-Segel model that describes migration and patterning strategies of heterogeneous cell populations (Ucar et al., 2025). Our model predicts that the relative chemotactic sensitivities of different cell populations determine the shape and speed of traveling density waves, while boundary conditions such as external cell and attractant reservoirs substantially influence the migration dynamics. We quantitatively corroborate these predictions with in vitro experiments on co-migrating immune cell mixtures. Interestingly, immune cell co-migration occurs near the optimal parameter regime predicted by theory for coupled and colocalized migration. Finally, I will discuss the role of mechanical interactions, revealing a non-trivial interplay between chemotactic and mechanical non-reciprocity in driving collective migration.
 

Motivated by pattern formations and cell movements, many evolution equations incorporating spatial convolution with suitable integral kernel have been proposed. Numerical simulations of these nonlocal evolution equations can reproduce various patterns depending on the shape and form of integral kernel.The solutions to nonlocal evolution equations are similar to the patterns obtained by reaction-diffusion system and Keller-Segel system models. In this talk, we classify nonlocal interactions into two types, and investigate their relationship with reaction-diffusion systems and Keller-Segel systems, respectively. In these partial differential equation systems, we introduce multiple auxiliary diffusive substances and consider the singular limit of the quasi-steady state to approximate nonlocal interactions. In particular, we introduce how the parameters of the partial differential equation system are determined by the given integral kernel. These analyses demonstrate that, under certain conditions, nonlocal interactions and partial differential equation systems can be treated within a unified framework.  
This talk is based on collaborations with Hiroshi Ishii of Hokkaido University and Hideki Murakawa of Ryukoku University. 

Extra-chromosomal DNA (ecDNA) is a genetic error found in more than 30% of tumour samples across various cancer types. It is a key driver of oncogene amplification promoting tumour progression and therapeutic resistance, and is correlated to the worse clinical outcomes. Different from chromosomal DNA where genetic materials are on average equally divided to daughter cells controlled by centromeres during mitosis, the segregation of ecDNA copies is random partition and leads to a fast accumulation of cell-to-cell heterogeneity in copy numbers.  I will present our analytical and computational modeling of ecDNA dynamics under random segregation, examining the impact of copy-number-dependent versus -independent fitness, as well as the maintenance and de-mixing of multiple ecDNA species or variants within single cells. By integrating experimental and clinical data, our results demonstrate that ecDNA is not merely a by-product but a driving force in tumor progression. Intra-tumor heterogeneity exists not only in copy number but also in genetic and phenotypic diversity. Furthermore, ecDNA fitness can be copy-number dependent, which has significant implications for treatment.

Please register for the event via https://sites.google.com/view/oxwmathbio2025

We will discuss local regularity properties for solutions to non-local equations naturally arising in kinetic theory. We will focus on the Strong Harnack inequality for global solutions to a non-local kinetic equation in divergence form. We will explain the connection to the Boltzmann equation and we will mention a few consequences on the asymptotic behaviour of the solutions.