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Abstract:

Cancer cells survive by navigating a fundamental trade-off between proliferation and arrest. During tumour development and in response to therapy, they dynamically switch between cell division and G0 arrest to withstand intrinsic stress and environmental pressure. Yet how these transitions are constrained by tumour evolution and organised within the tumour microenvironment remains unclear. In this talk, I will show how integrating single-cell and spatial transcriptomics with AI- and ecology-inspired analytical frameworks reveals the genomic and regulatory architecture underlying proliferation–G0 decisions in cancer. We demonstrate that patterns of genomic instability and stress-responsive transcriptional programmes systematically bias tumour cells toward distinct adaptive trajectories. These analyses uncover a long-lived, G0-arrested, immune-evasive cancer niche marked by proteostasis dysregulation, with potential implications for therapeutic resistance. In parallel, I will present complementary work dissecting spatial heterogeneity in DNA damage and repair pathway activity. By quantifying how homologous recombination and related repair programmes vary across tumour tissues, we link mutational processes to local microenvironmental adaptation. Together, our work provides a framework for understanding how genome instability and spatial context jointly shape cancer survival strategies under selective pressure.

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By: Paula Amiet-West
Last updated: Tuesday, 17 February 2026