At the Cancer Therapeutic Resistance: Progress and Perspectives conference, in Barcelona, Spain, April 7-8, 2016, researchers, clinicians and students gathered to discuss our current understanding of intrinsic and acquired resistance of tumors to cancer therapies and to explore how to translate strategies to predict risk or overcome resistance to the clinic. The sessions covered a wide range of topics, including cancer omics, molecular classification, clinically relevant tumor models, biomarkers and novel therapeutic targets, and personalized medicine, with talks from many international experts in the field. This report highlights the main presentations that demonstrate the progress being made in predicting and identifying drug resistance in patients with cancer, personalized approaches to direct treatment and understanding the mechanisms involved. With better models of human cancer and powerful high-throughput screening techniques, translation to the clinic leading to tangible benefits for patients is attainable.

At the 17th International Symposium in the annual series of prestigious meetings organized by the Fritz Bender Foundation, 07-09 November 2013, researchers, clinicians and students gathered to discuss and exchange knowledge on individualized cancer therapies. Co-organized and hosted by the Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain, the sessions covered genetic profiling of patients, tumor characterization, tumor-host relationships and therapeutic targets, with talks from many international experts in the field. The presentations summarized in this report illustrate the current status of our knowledge and the future directions for cancer research in these broad topic areas.

MYD88 signalling can have pro- or anti-tumorigenic effects in distinct cancer models.

Hepatic encephalopathy is caused by the accumulation of gut-derived toxic substances, such as ammonia, in the bloodstream that are normally removed by the liver. Treatment usually consists of purgative ammonia-lowering therapy, such as the disaccharide lactulose, and/or nonabsorbable antibiotics.

Hepatocellular carcinoma (HCC) is often at an advanced stage before it is diagnosed and at this stage curative therapies are generally ineffective. Ling Xiao Liu and colleagues now report that cadherin-17 (CDH17), which encodes a cell surface adhesion molecule not found in healthy adult liver, is a novel oncogene in HCC and is an attractive target for therapy of this aggressive malignancy.

Tumour-initiating cells (TICs) share functional properties, such as clonogenicity and capability for multilineage differentiation, with normal stem cells. However, Howard Fine and colleagues hypothesized that there might be differences in their differentiation potential and found that epigenetic silencing of bone morphogenetic protein (BMP) receptor 1B (BMPR1B) blocks differentiation in a subset of glioblastoma TICs and contributes to their tumorigenicity.

Several solid tumours depend on intrinsic hedgehog (Hh) pathway activation for survival. Hh ligands are also expressed in all lymphoid organs and are necessary for survival of germinal centre B cells, from which some B-cell lymphomas arise.

This approach to inhibiting angiogenesis overcomes problems commonly seen with other angiogenesis inhibitors and immunotherapies.