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Röring and colleagues investigate the involvement of the dimer interface in the ability of RAF to mediate downstream signalling, with implications for targeting BRAF.
Two papers have been published inNaturethat analyse genomic and transcriptomic changes in breast tumours to further understand the biology of breast cancer.
Specific delivery of small interfering RNAs directed against Polo-like kinase 1 to tumour cells using a single-chain fragmented antibody against ERBB2 can reduce xenograft tumour growth and experimental metastases, with minimal toxicities, in mice.
Timothy Thomson and colleagues have used prostate and bladder cancer models, derived from human cell lines, to show that epithelial-to-mesenchymal transition can suppress tumour-initiating potential and colonization of distant organs.
Cancer cells with mutant p53 and high expression levels of EZH2 and mitotic cyclins are likely to be sensitive to a combination of an inhibitor of the WEE1 kinase and chemotherapeutic agents that induce S phase arrest.
Pioneer factors are a special class of transcription factor that can associate with compacted chromatin to facilitate the binding of additional transcription factors. This Progress article discusses the importance of pioneer factors in breast cancer and prostate cancer.
This Review discusses the importance of spatial control of receptor tyrosine kinase (RTK) activity during development and tissue homeostasis, and how spatial deregulation of RTKs may contribute to tumorigenesis and affect the sensitivity and resistance of cancers to pharmacological RTK inhibitors.
Autophagy can have two functions in cancer: it can be tumour suppressive or tumour promoting. Therefore, defining the context-specific role for autophagy in cancer and the mechanisms involved is important for the use of autophagy-based therapeutics.
Research over the past decade has greatly increased our understanding of non-apoptotic programmed cell death events, such as lysosomal-mediated cell death, necroptosis and cell death with autophagy. This Review discusses converging and diverging features of these pathways with a view to developing new therapeutics for cancer.
Why are many metastases differentiated? This Opinion article proposes that this is due to phenotypic plasticity involving transient epithelial–mesenchymal transition (EMT). In undifferentiated metastasis, it might be that cells are genetically locked into an undifferentiated state. The therapeutic consequences of this hypothesis are also discussed.
Cannabinoids have well-established roles in palliating cancer-associated symptoms, but numerous recent studies also support their antitumorigenic activity. This Opinion article focuses on preclinical studies of the antitumour effects of cannabinoids, including the associated cellular signalling pathways and resistance mechanisms.
