Research Highlights in 2011

In vitroimaging reveals a possible mechanism for clearance of the mesothelial barrier by ovarian cancer cells during metastasis.

Two papers have examined how modifying nanoparticles can increase the specificity of tumour cell killingin vivo.

Cancer-associated cachexia is reduced in mice lacking enzymes that are crucial for triglyceride lipolysis, and a similar mechanism may operate in humans.

A new genomic-scale computer model of the cancer metabolome indicates synthetic lethal interactions.

Pollard and colleagues have examined the origin and function of metastasis-associated macrophages and implicated the chemokine CCL2 in their recruitment.

Tumorigenesis by the receptor tyrosine kinase MET requires not only activation but also increased localization and signalling on endosomes.

Dieter Saur and colleagues show that a cathepsin-activatable probe can be used to detect and diagnose early stages of pancreatic cancer.

The tumour suppressor WTX regulates mesenchymal progenitor cell fate and lineage specification.

Two papers identify new modulators of ERα expression, which has implications for responses of ERα⁺breast cancer to endocrine therapy.

A new study describes a novel mechanism of resistance to BCR–ABL1 inhibitors and suggests a therapeutic strategy for resensitization.

Semenza and colleagues identify a positive feedback loop between the pyruvate kinase PKM2 and HIF1 that may explain how PKM2 can promote metabolic reprogramming of cancer cells.

Two recent papers have shown that the E3 ubiquitin ligase COP1 is a tumour suppressor.

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.

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

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.

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

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.