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A paper published inCancer Discovery shows that H3 G34R or G34V mutations result in the altered binding of proteins that recognize trimethylated H3K36. This results in a gene expression signature that is more commonly seen in the developing forebrain and that is associated with increased MYCNtranscription.
Phase I clinical trial data presented at the 2013 American Association for Cancer Research (AACR) meeting support the use of combination immunotherapy involving a personalized dendritic cell vaccine and adoptive T cell transfer in patients with advanced ovarian cancer.
The incidence of most cancers increases with age, and there are various ageing-associated changes that might contribute to increased tumorigenesis, and paradoxically, to decreased tumorigenesis. Lessons may be learned from diseases conferring premature ageing or longevity, and this Opinion article discusses our current understanding of the connections between ageing and cancer.
The transforming growth factor-β (TGFβ) ligands have important functions in cancer. However, it is now becoming apparent that many of the other TGFβ superfamily members (bone morphogenetic proteins (BMPs), activins, NODAL, and growth and differentiation factors (GDFs)) have crucial roles in tumorigenesis and metastasis; these are the focus of this Review.
Increasing evidence indicates that components of the RNA polymerase complexes are altered in cancer. This Review discusses how all three classes of human RNA polymerase activity are dysregulated in cancer and the opportunities to therapeutically target RNA polymerase activity.
The regulation of iron metabolism is altered in tumour cells. Changes in iron regulation enhance iron influx and retention. This leads to altered cellular processes that foster cancer growth and metastasis, and provides an opportunity for the development of therapeutics that target iron availability.
Eric Snyder, Tyler Jacks and colleagues have shown the transcription factor NKX2-1 promotes a pulmonary cell fate and that this suppresses a latent gastrointestinal differentiation programme, which might explain why lung adenocarcinomas lacking NKX2-1 can adopt a glandular and mucinous phenotype.
For more than four decades, cells have been studied in space. This work has provided insight into how normal cells and cancer cells grow and aggregate into complex architectures and respond to extrinsic forces. This Review discusses what we have learned about cell biology from space-based research and how this might be applied to cancer research on Earth.
The contribution of epigenetic changes to malignant behaviour has been investigated using induced pluripotent stem cell (iPSC) reprogramming techniques to reset the epigenome of glioblastoma stem cells, and the results suggest that the resetting of cancer-specific methylation abnormalities is not sufficient to suppress tumorigenesis.
A paper published inScienceindicates that one of two common histone mutations found in paediatric glioblastoma is a gain-of-function mutation that inhibits histone trimethylation that is mediated by the Polycomb repressive complex 2 (PRC2).
