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Two new studies in mice have shown that disrupting the microbial balance in the gut through the use of antibiotics can affect the response to cancer therapy.
Five recent papers have looked more closely at mechanisms that underlie resistance to inhibitors of the ERK MAPK pathway in melanomas that have the BRAF-V600E mutation and have shown that several mechanisms probably contribute to resistance, even within the same patient.
A paper inNaturereports the design of small molecules that can irreversibly bind to and block the activity of oncogenic KRAS-G12C, but not wild-type KRAS.
A new study by Emerling and colleagues has shown that phosphatidylinositol 5-phosphate 4-kinase type-2α (PIP4K2α) and PIP4K2β are essential for the growth of p53-null cells and may represent a pharmaceutical target for cancers that have non-functional p53.
Three groups have sequenced samples of ER-positive and hormone therapy-resistant breast cancers and found point mutations inESR1, the gene encoding ERα.
A coordinately published set of papers inNature, Nature Geneticsand other journals report data from up to 5,000 individual cancers, including cancers of the breast, uterus, ovaries, lung, brain, head and neck, colon and rectum, bladder, kidney and blood.
The bone marrow microenvironment can support the growth and activity of leukaemia stem cells, and two recent papers suggest several ways in which these interactions might be targeted for therapeutic benefit.
A new study identifies the tumour suppressor folliculin as a GTPase-activating protein that regulates the nucleotide status of the RAG proteins, which are important regulators of mTOR complex 1 kinase activity.
A paper by Dmitry Bulavin and colleagues shows that WIP1 is involved in regulating DNA methylation-mediated silencing of heterochromatin and might contribute to C-to-T substitutions and mutation load in breast cancers.
Three papers report the discovery of recurring deleterious mutations in the cohesin subunitSTAG2in urothelial bladder cancers, but the evidence for the contribution of STAG2 loss to aneuploidy is conflicting.
A paper inCell Stem Cellthat uses lineage tracing in the pituitary shows that, although mutations in a subpopulation of stem cells can induce tumour formation, the tumour cells do not arise from the mutated stem cells.
Inhibition of macrophage colony-stimulating factor 1 receptor (CSF1R) can block glioblastoma growth by changing the phenotype of tumour-associated macrophages from pro-tumorigenic to antitumorigenic.
Two papers published inCancer Discoveryunveil the molecular mechanisms that underpin the improved response of patients with high-risk prostate cancer to ionizing radiation in the presence of androgen deprivation therapy.
Simon Boulton and colleagues have found that the 3′–5′ superfamily 2 helicase HELQ is important to prevent germ cell attrition and tumour development in mice.
