Cancer-related inflammation is an important process contributing to malignant disease, with common and defined factors at different stages of progression. For many years we have known that extrinsic inflammatory pathways promote or, in some cases, initiate cancer i.e. that inflammation causes or promotes cancer. It is now clear that an intrinsic inflammation pathway is 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. Inflammatory mediators in the tumour microenvironment act on inflammatory cells such as macrophages and neutrophils and in many cancers, these cells can be tumour-promoting, not only aiding growth and spread of malignant cells but also suppressing the activity of adaptive immune cells such as cytotoxic T cells that are able to destroy malignant cells. Therefore some types of inflammatory cells are also targets for cancer treatment.