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Inder Verma and colleagues provide evidence that, at least in mice, mature neurons and astrocytes can be transformed and can dedifferentiate to form gliomas.
A recent publication inNature Cell Biology indicates that the transcription factor ELF5 suppresses epithelial to mesenchymal transition and metastasis through repression of SNAI2.
Editing of a microRNA (miRNA) is impaired in gliomas, and the non-edited and edited miRNAs have different gene targets, which promote and suppress invasive activity, respectively.
A new study finds that metabolism might converge with epigenetic gene regulation to explain the context-dependent effects of the metabolite butyrate on colon cell proliferation.
Two groups have reported the discovery of small-molecule inhibitors of EZH2 that have the ability to selectively kill lymphoma cells with EZH2-activating mutations.
Three groups have used human trisomy 21 fetal liver cells or human trisomy 21 induced pluripotent stem cells (iPSCs) to examine the effects of trisomy 21 on the early stages of haematopoiesis.
The DNA damage response (DDR) is often altered in tumour cells and this Review discusses the many strategies to target the pathways that comprise the DDR as single agents and in combination to produce synthetic lethality specifically in tumour cells.
Medulloblastoma has been the subject of numerous genomics and transcriptomics studies that have led to this disease being subclassified into various clinically meaningful groups and to advances in understanding the biology of these subgroups, with implications for treatment.
Based on previous successes and failures, this Review discusses potential future directions for cancer prevention that include the use of genetic, proteomic and other molecular approaches to identify pathways that could be modified during cancer initiation. The use of immunotherapies for cancer prevention is also discussed.
Myelodysplastic syndromes (MDS) are malignant clonal disorders of haematopoietic stem cells and their microenvironment, affecting older individuals. Although emerging insights establish an association between molecular abnormalities (such as specific chromosomal abnormalities) and the phenotypic heterogeneity of MDS, as outlined in this Review the origin and progression of MDS remain enigmatic.
In recent years a new concept of immunogenic cell death (ICD) has emerged. In this Review, the authors discuss the role of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) in regulating the immunogenicity of dying cancer cells and how this might relate to therapeutic intervention.
Despite displaying characteristics of tumour suppressors, the core regulators of epithelial cell polarity are rarely mutated in tumours, and it is still unclear whether they directly contribute to cancer development. However, data from human tumour viruses provide compelling evidence of a central role for the perturbation of cell polarity in cancer.
