‘Precision Medicine for Cancer’ was held from 1 – 4 March 2015 at Neumünster Abbey, Luxembourg.Recent advances in technology have provided an unprecedented opportunity to develop platforms for implementing precision/personalised medicine in cancer. The conference focussed on the challenges that face us in implementing these approaches.Although our understanding of the pathogenesis of cancer has advanced enormously in recent years, we have only just begun to successfully translate this into improvements in the clinical management of patients. A significant opportunity is offered by the knowledge that cancer cells are ‘addicted’ to certain altered genes, a vulnerability that can be exploited therapeutically. A number of cancer-causing genes have been identified that are recurrently altered and stimulate tumour growth. These ‘driver genes’ correspond to oncogenes (or tumour suppressor genes) that are mutated or deregulated (e.g., amplified), causing the tumour to become dependent on the lesion(s) for survival and/or proliferation.This meeting was of interest to fundamental, translational and clinical cancer researchers alike, as it covered several aspects of precision treatment of cancer, ranging from tumour heterogeneity and novel metabolic targets to circulating tumour cells and new drug target discovery strategies.The topics covered included:oPrecision medicines in today’s and tomorrow’s cancer treatment.oTumour heterogeneity and drug response.oDrug resistance.oNovel strategies for drug target discovery.oCancer immunotherapyoHigh throughput approaches to analysis of tumour samplesoNext generation sequencing approachesoThe implementation of personalised medicineoBackground to the conference topicCancers are increasingly classified in terms of the ensemble of mutant genes they harbour, and targeting such genes with ‘precision’ inhibitors has resulted in profound clinical impact. The extent, duration and rate of responses can be unprecedented. Despite these advances, a large number of cancers treated with single agents become resistant soon after commencing treatment. This is caused by several mechanisms, including the pre-existence of genetic alterations in heterogeneous tumours. Thus, although significant progression has been made in identifying critical genetic factors serving as potential cancer liabilities, real benefits to patients have been modest.The meeting was highly inclusive, supported with participation grants, and set out to meet the needs of researchers of all levels of experience. Students and young researchers were particularly well catered for with opportunities for oral and poster presentations. As well as through poster defence, ‘Round table’ discussions provided opportunities for focused interactions related to the topics discussed earlier in the day. Opportunities for informal discussion were also encouraged through the provision of buffets and an evening dinner on-site.