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A paper inNature Medicinedescribes a novel, orally available splicing modulator that preferentially kills cancer cells with mutations in splicing factors in culture and in mouse models.
Activation of TGFβ signalling in invasive margins of metastatic tumours can contribute to T cell exclusion and reduced immune checkpoint therapy response. Inhibition of TGFβ in non-responders can potentially help to improve outcomes in these patients.
Xieet al. show that senescence-associated DNA methylation changes evolve independently of stochastic tumour-associated methylation changes and that a subset of commonly methylated genes with the highest gains are associated with early tumorigenesis and ageing.
A recent study published inNature Cell Biologyhas shown that tumour spheres that maintain an inverted epithelial architecture originate from primary colorectal cancers and can collectively invade the peritoneum, initiating metastasis.
Liet al. report the development of 'DNA nanorobots' carrying a thrombin protease payload that induce coagulation and necrosis at the tumour site, illustrating their therapeutic potential as drug delivery systems.
Data presented by Bakhoum, Ngo et al. suggest that chromosomal instability can promote metastasis through a cGAS–STING-dependent response to cytosolic DNA.
A subset of cancer-associated firboblasts, defined by the presence of the cell surface markers CD10 and GPR77, promotes tumour formation and chemoresistance by providing a niche for cancer stem cells.
Mitogen- and stress-activated kinase 1 (MSK1) has been identified as an epigenetic modulator of luminal gene expression in breast cancer, maintaining latency of bone micrometastases.
Two studies have shown that oncolytic virus treatment prior to surgery can prime the tumour immune microenvironment for subsequent immune checkpoint inhibition and lead to better outcomes in preclinical models of breast and brain cancers.
In this Comment, the authors outline the emerging rationale for the clinical use of tumour budding, a histological manifestation of tumour cell invasion, as a diagnostic tool and biomarker in colorectal cancer.
The fusion gene consisting of fibroblast growth factor receptor 3 and transforming acidic coiled-coil-containing protein 3 is oncogenic and present in a small cancer subset. Frattini et al. have identified that this fusion gene drives peroxisomal and mitochondrial biogenesis.
Reactive oxygen species derived from inflammatory myeloid cells is sufficient to induce mutagenesis in intestinal epithelial cells, independently of cytokines, to promote tumour initiation and progression.
