Speaker
Description
In solid tumours, the presence of regions of abnormally low oxygen levels (i.e., hypoxia) is recognised as a major driver of tumour progression and therapeutic resistance. Yet, how exactly oxygen levels shape cancer cell responses and disease dynamics in vivo remains poorly understood. While in vitro models of hypoxia exist, they often fail to capture the complex oxygenation dynamics of real tumours. In this talk, I will discuss how mathematical modelling can be used to address the gap between in vitro and in vivo experimental conditions. As an example, I will present our work on cell-cycle dysregulation in cancer cells exposed to fluctuating oxygen environments – namely cyclic hypoxia. In this work, we have integrated mechanistic mathematical modelling and cell culture experiments to explore and predict cell responses to a wide range of (cyclic) hypoxia conditions. Our results uncover the possible multifaced role of hypoxia in shaping the heterogeneous composition of vascularized tumours.
