The objective of this review is to examine the role that HIF-1 plays in the initiation of angiogenesis and in radiotherapy response. Although these two phenomena may at first seem unrelated, there are parallelisms to be drawn associated with the importance of reactive oxygen species in controlling the transcriptional activity of HIF-1, independently of its main driving force, hypoxia. Knowledge of the mechanisms underlying the control of HIF-1 leads to rationale for its inhibition in a range of clinical scenarios.
