Volume 18 Issue 2, February 2018

The fusion gene consisting of fibroblast growth factor receptor 3 and transforming acidic coiled-coil-containing protein 3 is oncogenic and present in a small cancer subset. Frattini et al. have identified that this fusion gene drives peroxisomal and mitochondrial biogenesis.

Three recent papers have shed light on how the common oncogenic drivers MYC and RAS can induce an immunosuppressive tumour microenvironment.

Ubiquitin ligases (E3s) participate in many cellular processes, including cell cycle progression and cell death. This Review by Senftet al. discusses how deregulation of E3s can lead to tumorigenesis and highlights the opportunities for targeting E3s as an anticancer therapy.

Inactivating mutations in the tumour suppressor geneTP53are frequent in cancer. This Review provides a critical overview of reactivating p53 as a therapeutic strategy, describing preclinical and clinical compounds that re-establish the functions of wild-type p53 in tumours.

Recent studies have suggested that autoimmunity checkpoints (AICs) are fully functional in B cell leukaemias and lymphomas, despite malignant transformation. This Opinion article proposes that targeted engagement of AICs might represent a therapeutic opportunity to overcome drug resistance in B cell malignancies.

Differentiation therapy has shown great success in the treatment of acute promyelocytic leukaemia (APL). This Opinion article discusses the molecular basis for the success of APL treatment and the potential of drug-induced tumour cell differentiation in other malignancies.

In this Viewpoint article, we asked four scientists working in the field of epithelial to mesenchymal transition (EMT) to provide their opinions on the role of this complicated phenomenon in cancer biology as well as the challenges of this fast-moving field and the directions it should take in the future.