Volume 11 Issue 6, June 2011

Aifantis and colleagues show that Notch signalling suppresses myeloid commitment and myeloproliferation.

ERβ can suppress prostate cancer growth through binding KLF5 and increasing transcription of the pro-apoptotic geneFOXO1.

The creation of a new model of high-grade serous ovarian carcinoma indicates that these tumours can indeed arise from the fallopian tube.

A drug that keeps the ABL1 kinase in its inactive conformation has efficacy against the ABL1 T315I gatekeeper mutation.

A new study reveals that activation of PI3K–AKT signalling is capable of inducing a state that is superficially similar to RAS-induced senescence. However, cooperative activation of both pathways promotes senescence bypass and tumour progression.

A set of p53-mutant proteins indicates that the transactivation of a small subset of p53 target genes is required for the tumour suppressive effect of p53 in response to oncogene activation.

The switch from HIF1α-dependent to HIF2α-dependent responses may be partly mediated through the ubiquitin ligase HAF, leading to increased tumour initiation and progression.

Reginald Bittner and colleagues show that muscular dystrophy-associated genes also seem to be suppressors of sarcomagenesis.

Two recent papers indicate that the function of the transcription factor NKX2-1 in tumorigenesis is complex and context dependent.

Hypoxia is common in developing and advanced tumours and could therefore provide a means for drug selectivity. As discussed in this Review, this can be achieved either by using prodrugs that are activated in hypoxic regions, or by directly targeting hypoxia-induced signalling pathways that confer survival to tumour cells.

When cancer metastasizes to bone, considerable pain and deregulated bone remodelling occurs, greatly diminishing the possibility of cure. Understanding how metastasizing tumour cells mobilize and sculpt the bone microenvironment to enhance tumour growth and promote bone invasion has uncovered new therapeutic opportunities.

DNA, mRNA and microRNA are released and circulate in the blood of cancer patients. This Review discusses the potential clinical utility of cell-free nucleic acids as blood biomarkers.

The long-term risks from new radiotherapy treatments, such as particle therapy, have not yet been determined and there is a need to try and develop risk assessments based on our current knowledge of radiation-induced carcinogenesis. Which information can we use to produce the best models?

The mutator phenotype describes a process by which tumour cells are proposed to evolve genetic alterations that contribute to the acquisition of the various attributes that are required for tumour progression. Here, Lawrence Loeb updates this hypothesis, focusing on how DNA sequencing has informed the current view of the mutator phenotype in cancer.