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.
D’Amico et al. show that, in the presence of oncogenic RAS mutations, STAT3 acts as a tumour modifier by regulating the epithelial differentiation of pancreatic and lung cancer cells via p63.
Lee, Singh et al. find that cancer-specific intronic polyadenylation events occur frequently in tumour suppressor genes in chronic lymphocytic leukaemia (CLL) and generate truncated proteins that could act as CLL drivers.
Lee, Adler et al. show that urea cycle dysregulation is common in cancer and leads to a purine to pyrimidine mutational bias that is associated with a better response to immune checkpoint inhibitors.
A recent study, published in Nature, identifies the methylcytosine dioxygenase 2 (TET2) as an epigenetic modifier that is regulated in response to glucose availability and mechanistically links higher cancer susceptibility in patients with diabetes to high blood glucose levels.
Yao et al. have established that acute lymphoblastic leukaemia cells bypass the need to metastasize via the circulation to the CNS and instead use a direct route migrating along the vascular channels that bridge the bone marrow to the meninges in an α6 integrin-dependent manner.
PI3K inhibition in solid cancers driven by PI3K catalytic subunit-α has shown limited clinical benefit. This might be due to activation of a glucose–insulin feedback loop, which can be interrupted by dietary or pharmaceutical approaches, thereby improving therapy outcome.
Two groups have used targeted sequencing to identify features of clonal haematopoiesis in healthy individuals including the number of somatic mutations, the presence of specific mutations and clonal size, which predict risk of developing acute myeloid leukaemia years before diagnosis.
Mutant KRAS has so far proven to be an undruggable target for lung adenocarcinoma and a widely held assumption is that KRAS mutations confer independence from upstream signalling. Two groups have now independently shown this might not be the case and suggest pan-ERBB inhibitors could be used to treat patients with KRAS-driven lung cancer
Priego et al. show that a subpopulation of reactive astrocytes expressing signal transducer and activator of transcription 3 (STAT3) is crucial for the development of brain metastases and report positive initial clinical data that inhibiting STAT3 can reduce metastasis.
Three studies published in Developmental Cell, Nature and Nature Medicine shed new light on mechanisms of cancer-associated cachexia in early and advanced disease.
Analyses of clinical trial patients with exceptional responses show that adoptive T cell therapy can be optimised to improve effectiveness in patients of chronic lymphocytic leukaemia and breast cancer.
Breast tumours in mice promote metabolic changes in the liver and sleep disruption through increasing activity of hypocretin (also known as orexin) neurons (HO neurons).
Increased shortening of RNA 3′ untranslated regions associated with tumorigenic transformation interferes with competing endogenous RNA (eRNA) networks, which results in trans-repression of tumour suppressors through microRNA-mediated silencing.
The gut microbiota can metabolize bile acids to affect immunosurveillance in the liver of mice and indirectly control the growth of primary liver tumours and liver metastases.
Tumour-associated neutrophils can inhibit the proliferation of pro-tumoural interleukin-17 (IL-17)+ γδ T cells via production of reactive oxygen species.
Wang, Leite de Oliveira et al. show that BRAFV600E-mutant melanomas that are resistant to BRAF and MEK inhibitors are vulnerable to increased levels of reactive oxygen species and that this can be exploited therapeutically using a histone deacetylase inhibitor.
Single-cell RNA sequencing analysis in paediatric diffuse midline gliomas with histone H3 lysine 27 to methionine mutations indicates that these aggressive tumours contain many stem-like cells and that lineage-based therapeutic targeting might be beneficial.
A recent study published in Science Translational Medicine generated a mouse model to study the link between surgical wounding and distant tumour growth, showing that the systemic wound healing response induced by surgery can promote tumour growth.
