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.
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.
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.
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.
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).
The transcription factor FOS-related antigen 1 (FRA1) is a mediator of metastasis, and breast cancer cell lines that express FRA1 are more sensitive to antagonists of adenosine A receptors.
A paper inNaturehas identified and characterized stem cells in a transitional zone, known as the hilum, located amid the ovarian surface epithelium, the mesothelium and the uterine (Fallopian) tube epithelium, and has also found that these cells are susceptible to transformation.
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.
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 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.
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.
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.
Using malignant melanoma as a paradigm, these authors propose that therapy-induced injury to tumour tissue and the resultant inflammation can activate protective and regenerative responses that represent a shared resistance mechanism to different treatments.