Hypoxia is present in most solid cancers because of an imbalance between the limited oxygen delivery capacity of the abnormal vasculature and the high oxygen consumption rate of tumor cells. There is a complex and dynamic compensatory molecular response to hypoxia that enables continued cell survival and drives genomic changes leading to selection of hypoxia-adapted cells with a propensity to invade locally and metastasize. There is indisputable clinical evidence implicating hypoxia as an important determinant of cancer recurrence and poor patient survival following treatment with surgery, radiotherapy and/or chemotherapy. Despite this, measurement of tumor hypoxia is not part of routine clinical practice, in part, because there is no generally accepted method. Positron emission tomographic (PET) imaging of radiolabeled hypoxia tracers is among the most promising approaches. However, there are methodologic challenges that remain to be addressed, including the robust quantification of hypoxia in a manner that supports clinical integration. This paper will discuss the intratumoral and normal tissue transport dynamics of the radiolabeled hypoxia tracer FAZA using compartmental modelling linked to real clinical data derived from patients with pancreatic cancer. In particular, the paper will focus on qualifying hypoxia using static PET images and reference normal tissues in situations where large blood vessel are not present in the imaging field of view.