Phenotypic variation modulates the growth dynamics and response to radiotherapy of solid tumours under normoxia and hypoxia

In cancer, treatment failure and disease recurrence have been associated with small subpopulations of cancer cells a stem-like phenotype. this paper, we develop investigate phenotype-structured model solid tumour growth in which are structured by stemness level, varies continuously between terminally differentiated behaviours. Cell evolution is driven proliferation death, as well advection diffusion respect to the structure variable. Here, magnitude sign advective flux allowed vary oxygen level. We use how environment, particular levels, affects tumour’s population dynamics composition, its response radiotherapy. combination numerical analytical techniques quantify under physiological levels evolve phenotype low level (i.e., hypoxia) they de-differentiate. Under normoxia, proportion stem typically negligible may ultimately become extinct whereas hypoxia comprise dominant volume, enhancing radio-resistance favouring long-term survival. then such phenotypic heterogeneity impacts radiotherapy normoxia hypoxia. Of interest establishing presence radio-resistant can facilitate regrowth following also show radiation-induced changes give rise complex re-growth dynamics. For example, transient periods induced damage blood vessels rescue cell from extinction drive secondary regrowth.