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Three recent studies have uncovered molecular links between various cancer signalling pathways and altered glutamine metabolism.

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).

Rizwan Haq and colleagues have linked the expression of PGC1α to that of oncogenic BRAF via MITF.

A new study characterizes connections between endocytosis and cellular senescence.

POT1, a component of the shelterin complex that caps the ends of telomeres, is mutated in a subset of patients with chronic lymphocytic leukaemia.

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.

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.

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.

Landau, Carter, Stojanov and colleagues characterize genetic clonal evolution in chronic lymphocytic leukaemia and connect the occurrence of clonal evolution to therapy and prognosis.

A recent paper published inBloodindicates that the interaction between AML1–ETO and the transcriptional co-repressor NCOR1 is partly responsible for limiting the leukaemogenic capacity of this fusion gene.

Burns, Lackey and colleagues find that the cytosine deaminase APOBEC3B seems to be important for the mutation rate in breast cancer.

Tumorigenic genetic and epigenetic changes in epithelial cells occur as a result of increased inflammation following the loss of transforming growth factor-β receptor 2 in stromal fibroblasts.

In medulloblastoma, placental growth factor (PLGF) may signal through a non-tyrosine kinase receptor, neuropilin 1 (NRP1), to promote tumour cell survival without having a substantial effect on angiogenesis, thus providing a rationale for targeting this pathway in these tumours.