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Every population consists of individuals who vary in their traits, and each trait may, or may not, be associated with frailty or fitness. Variation in frailty and fitness traits makes population studies prone to selective depletion bias (SDB). The issue is widespread across scientific domains. When an ageing cohort exhibits declining mortality, is it individuals becoming healthier or selective depletion of the frail? In an epidemic, when growth in cumulative infections decelerates, is it individuals cautiously changing behaviour or selective depletion of the most susceptible? In microbial populations, when mutations increase population vulnerability to stress, it is individuals becoming more vulnerable or mutant populations having higher variance in fitness? In each case, the first explanation invokes individuals changing, while the second recognises that populations change due to selection on pre-existing variation. While the former are intuitive and widely adopted, explanations that rely on selective depletion are more neutral and less commonly considered due to cognitive biases and challenges in estimating all variation that matters. 

Remodelling selection (ReMS) is proposed as a general strategy of study design and analysis to address the SDB problem. I will show how the approach has been employed in specific case studies and how it has been formalised in general.

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The acquisition and maintenance of the correct cellular pattern and tissue architecture is essential for organ function in multicellular organisms. Beyond generating the required cellular diversity, developing tissues need to attain the appropriate morphology. Tissue architecture is built through symmetry breaking instabilities such as folding, branching, buckling or budding. Studying single-cell responses alone is not enough to reveal the mesoscale physical and biochemical processes that regulate tissue organization and morphology over time and scale. In our lab we investigate how the interaction between the extracellular matrix (ECM) and tissues regulates processes during development and cancer, with a focus on ECM mechanical properties. While most research in this domain has concentrated on the ECM's elasticity as a primary determinant of cell and tissue behaviour, it is important to note that the ECM possesses both viscous and elastic properties. I will present our findings demonstrating that the passive viscoelastic properties of the ECM regulate tissue architecture and patterning both during development and cancer. Specifically, we show that ECM viscoelasticity influences the spatial and temporal organization of multicellular tissues in breast and intestinal organoids. Overall, our work highlights the critical role of viscoelasticity in driving morphological symmetry breaking instabilities, a fundamental process in morphogenesis and oncogenesis, and suggests ways of controlling tissue through ECM mechanics.

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Evolution underlies the transformation of a normal cell to a cancer, yet learning the parameters defining this dynamic process from single-timepoint bulk samples is an open challenge. To understand how cancer cells evolve in vivo, we must rely on naturally occurring, heritable lineage tracing markers that encode the evolutionary history of a population of cells. Here, I shall introduce our work on identifying selectively neutral “epigenetic barcodes” and employing them as a molecular clock. By coupling this process with mathematical modelling and Bayesian inference, we characterised the evolutionary history of almost 2000 lymphoid cancers (Gabbutt et al., 2025). Across a broad range of cancer types, we demonstrated that tumour growth rates and malignancy ages differed by orders of magnitude. In 2 independent cohorts of patients with chronic lymphocytic leukaemia (CLL), a typically indolent and slow growing cancer, the inferred growth rates were highly prognostic. I shall further discuss recent work applying this approach to resolve the clonal relationship between acute myeloid leukaemia (AML) blasts and differentiated neutrophils in patients without bone marrow failure. 

Professor Pereyra will talk about; 'Physics-informed deep generative models: Applications to computational sensing'

This talk introduces a novel mathematical and computational framework for constructing high-dimensional Bayesian inversion methods that leverage state-of-the-art generative denoising diffusion models as highly informative priors. A central innovation is the construction of physics-informed generative models using Langevin diffusion processes and Markov chain Monte Carlo (MCMC) sampling techniques to develop stochastic neural network architectures capable of near-exact sampling. The obtained networks are modular and composed of interpretable layers that are directly related to statistical image priors and data likelihoods derived from forward observation models. The layers encoding the data likelihood function are designed for flexibility, enabling scene and instrument model parameters to be specified at inference time and seamlessly integrated with pre-trained foundational generative priors. To achieve high computational efficiency, we employ adversarial model distillation, which yields excellent sampling performance with as few as four Markov chain Monte Carlo steps, even in problems exceeding one million dimensions. Our approach is validated through non-asymptotic convergence analysis and extensive numerical experiments in computational image and video restoration. We conclude by discussing unsupervised training strategies that allow the models to be fine-tuned directly from measurement data, thereby bypassing the need for clean reference data.

The talk is based on recent work in physics-informed generative AI for Bayesian imaging: https://arxiv.org/abs/2503.12615 (ICCV 2025), which uses a distilled latent Stable Diffusion XL model trained on five billion clean images as a zero-shot prior, and  https://arxiv.org/pdf/2507.02686, which integrates pixel-based diffusion models with deep unfolding and diffusion distillation (TMLR 2025). The extension to video restoration is presented in https://arxiv.org/abs/2510.01339 (ICLR 2025). Our approach to unsupervised training of diffusion models is introduced in https://arxiv.org/abs/2510.11964.

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