The advanced course was held on behalf of ECNIS, aEuropean Network of Excellence (NoE). In ECNIS—Environmental Cancer, Nutrition and Individual Suscepti-bility—twenty-four different European partners are orga-nized in 15 work packages, thereby bringing togethermultidisciplinary expertise. The goal of ECNIS is tointegrate and stimulate cancer research by fostering inter-actions between epidemiologists, molecular genetics,biochemists and molecular toxicologists. The most importantinstruments to achieve science integration are scientificmeetings, such as workshops and advanced courses, jointtraining programmes, stimulation and support of scientificcooperations, exchange of researchers, shared laboratoryfacilities and generation of platforms and databases. Cur-rent knowledge, gaps, open questions and future challengesin cancer research are summarized, discussed and finallydisseminated in several review articles as well as meetingreports. Further information on ECNIS is available athttp://www.ecnis.org.The main focus of ECNIS is the identification anddevelopment of both, biomarkers of exposure and bioin-dicators of disease to analyze the potential protectiveeffects of nutritional components as well as impact ofindividual susceptibility factors on environmental cancerrisk. To achieve this goal, it is necessary to understand themolecular mechanisms of chemical carcinogenesis.Therefore, a task of ECNIS work package 10 ‘‘Mechanisticresearch to support cancer hazard and risk assessment’’coordinated by Franz Oesch (Mainz) is to elucidate andcommunicate molecular mechanisms of chemical carcino-gens to improve risk assessment (see also Oesch et al.2008). Although it is known that chemical carcinogenesisis a multistep process which typically involves activationof a pro-carcinogen to a genotoxic agent, induction of DNAdamage and mutations, clonal expansion of initiated cellsgiving rise to a tumour, followed by further mutations andprogression to a malignant cancer, this view is much toosimplistic and many aspects are still unclear. These includethe nature of dose–response relationships, especiallyextrapolation to low doses, effects of mixtures, gender-,species- and age-dependent determinants, individual sus-ceptibility factors, such as polymorphisms of genes andinfluence of circadian rhythms in chemical carcinogenesis.One important matter of debate is the nature of the cellstargeted by a chemical carcinogen or tumour promotor.Already in the nineteenth century, pathologists havehypothesized that tumours may originate from stem cells.