Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
It was hoped that targeting protein prenylation would inhibit the oncogenic signalling of RAS family members. However, preclinical and clinical trials of prenyltransferase inhibitors have conflicting results. This Review discusses why these differences might occur and the future of targeting prenylation.
The US Food and Drug Administration (FDA) recently approved the immunotherapy agents sipuleucel-T and ipilimumab for the treatment of metastatic prostate cancer and melanoma, respectively. This Opinion article discusses how immunotherapy might be improved by understanding the mechanisms that are responsible for clinical benefit, identifying biomarkers that predict response or toxicity and developing combination therapies.
Epidemiological studies indicate that patients with Parkinson's disease seem to have a reduced risk of developing cancer (although exceptions exist). This Opinion article discusses the genes that are associated with Parkinson's disease and their possible roles in cancer biology.
The RAS oncogenes have far-reaching effects when they are oncogenically mutated. This Review discusses our current knowledge about the cell-autonomous and non-cell-autonomous effects of oncogenic RAS and how different RAS isoforms and substitutions seem to have different effects.
Several members of the tripartite motif (TRIM) proteins (one of the subfamilies of the RING type E3 ubiquitin ligases) seem to function as important regulators for carcinogenesis. This Review focuses on TRIM proteins that are involved in tumour development and progression.
Bradner, Mitsiades and colleagues show that inhibition of BET family proteins with the small-molecule inhibitor JQ1 selectively represses the expression ofMYC,and MYC and E2F1 target genes.
