Cancer-related inflammation is an important process contributing to malignant disease, with common and defined factors at different stages of progression. Until recently, the field has been driven by the hypothesis that extrinsic inflammatory pathways promote or, in some cases, initiate cancer i.e. that inflammation causes or promotes cancer. However, there is now evidence that there is an intrinsic inflammation pathway, activated by genetic events that cause neoplasia, i.e. cancer causes inflammation. Activation of oncogenes such as myc, ras and ret, or inactivation of tumour suppressors, such as pVHL, leads to constitutive production of inflammatory cytokines and chemokines by the initiated cell. Oncogene and tumour suppressor pathways are proven intracellular targets for therapies, but these recent data mean that inflammatory cytokines, and their receptors, are potential extracellular targets for the development of new drugs. These targets include TNF-α, IL-1β and IL-6, with different cytokines being implicated as major factors in different cancer models.