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Cancer of unknown primary site is both a challenging clinical problem and a disease that provides potential insight into the mechanisms that underlie early metastasis.
Three groups have sequenced samples of ER-positive and hormone therapy-resistant breast cancers and found point mutations inESR1, the gene encoding ERα.
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.
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.
p21-activated kinases (PAKs) have important roles in several oncogenic signalling pathways. How are PAKs activated in cancer, what are their key substrates, and how might small molecules against these enzymes best be developed and deployed for the treatment of cancer?
This Review discusses the elucidation of mechanisms whereby oestrogen drives both oestrogen receptor-α transactivation and receptor proteolysis, which might have important therapeutic implications not only for breast cancer but also for other hormone-regulated cancers.
Potassium channels are transmembrane proteins that selectively facilitate the flow of potassium ions down an electrochemical gradient. Their roles in cell proliferation, angiogenesis and cell migration have only recently been assessed. Thus, the potential importance of these channels for tumour biology is only now becoming evident.
This Review discusses recent evidence, particularly from mouse models, showing that some tetraspanin proteins have important roles in tumour initiation, promotion, metastasis and angiogenesis, and that they might therefore be valid therapeutic targets.
Although survival rates for most paediatric cancers have improved at a remarkable pace over the past four decades, the vast majority of these cancer survivors will have at least one chronic health condition by 40 years of age. How can we best understand and treat the long-term morbidity and mortality that is associated with currently successful treatments?
