In solid tumours, the presence of regions with abnormally low oxygen levels (i.e., hypoxia) is recognised as a driver of tumour progression and therapeutic resistance. Experimental evidence suggests hypoxia contributes to tumorigenesis by reprogramming cancer cells into more aggressive phenotypes, that present several of the hallmarks of cancer. However, the connections between hypoxia-driven cancer cell reprogramming and the disease dynamics observed in vivo remain poorly understood. In this talk, I will discuss how we have used structured-population modelling to explore how the interplay of abnormal tumour oxygenation and cancer cell reprogramming contributes to emergent disease dynamics. Presenting both analysis and numerical simulations of the model, I will elucidate how hypoxia influences tumour composition and, consequently, its growth dynamics across temporal scales. If time permits, I will also discuss extensions of our work that account for treatment with radiotherapy.