Articles in 2013

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.

Two papers examine the nuclear and cytoplasmic function of PKM2.

The role of inflammation in tumorigenesis and tumour progression is increasingly coming into focus, and this Review discusses the current ideas about the mechanisms of inflammation-associated tumorigenesis and the association with the microbiota.

A recent study published in theJournal of Clinical Oncologyhas indicated that married cancer patients fare better than singletons.

Powers and colleagues characterize tumour-promoting fibroblast–basal breast cancer cell crosstalk.

Mutations in the metabolic gene isocitrate dehydrogenase 2 (IDH2) drive the development of leukaemia and sarcoma in vivo.

There is an emerging association between the microbiota and carcinogenesis. How might the microbiota modulate tumorigenesis, and what do we need to understand to more firmly conclude that the microbiome causes cancer?

In this Review, the authors examine the aetiological, pathogenic and clinical features that are associated with cancers harbouring oncogenic fusion kinases, the clinical outcomes with targeted therapies, and strategies to discover additional kinases that are activated by chromosomal rearrangements in solid tumours.

The influence of the microenvironment on tumour progression is becoming clearer. This Review addresses the role of transforming growth factor-β in the regulation of components of the tumour microenvironment.

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.

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.

This Opinion article outlines the roles of vesicle trafficking pathways in various phenotypes shown by cancer cells, especially loss of polarity and invasion, and argues that although these proteins are not drivers of transformation, they are integral to maintaining neoplastic phenotypes.

Two new studies have highlighted the lack of understanding many women have about their own breast cancer risk and treatment.

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.

Three papers assess the mutational landscapes of human tumours, and all three find evidence for a role of APOBECs.