Research Highlights in 2010

Two new studies identify novel BRAF inhibitor resistance mechanisms in BRAF-V600E melanoma.

Retinoblastoma controls androgen receptor-mediated signalling through the transcription factor E2F1 in the late stages of prostate cancer.

Suppression of translesion synthesis can sensitize tumour cells to chemotherapy and reduce chemotherapy-induced mutagenesis.

Yong Li and colleagues identify a feedforward loop in which miR-301A expression in pancreatic adenocarcinoma relieves suppression of NF-κB and is in turn transactivated by NF-κB.

Stem-like cells in glioblastomas can differentiate into endothelial cells, thereby generating tumour vasculature.

Paneth cells are essential for the survival of LGR5⁺stem cells in crypt of the small intestine.

Engineered RNAs are used to reprogramme the Wnt and nuclear factor-κB signalling pathways, which could be used therapeutically to control tumour cell signalling.

Restoring the function of p53 in lung tumours only affects aggressively proliferating tumour cells.

PARP inhibitors can selectively target hypoxic tumour cells.

ARTS, an inhibitor of XIAP, is required for apoptosis in haematopoietic stem and progenitor cells, and loss of ARTS can promote tumour development.

A complex interdependent regulatory network exists between YAP, ASPP1 and LATS in the control of apoptosis.

PDE4 inhibition drives melanogenesis in a mouse model of skin cancer probably by blocking a MITF–PDE4D3 negative feedback loop.

WT1is shown to be synthetic lethal withKRAS, and loss of WT1 in the context of oncogenic KRASleads to senescence.

Elsa Flores and colleagues find that TAp63 is a haploinsufficient tumour suppressor and a suppressor of metastasis.

A MYC-centred network is shown to be responsible for the similarities between ES and cancer cells; and, inDrosophila melanogaster, MYC and the Hippo transcriptional regulator Yorkie regulate each other's expression to control growth.

Cytohesins bind to the cytoplasmic domains of dimerized EGFRs and facilitate their activation through formation of asymmetric dimers.

Three genome-wide association studies identify several genes that might contribute to ovarian and breast cancer.

Two groups show that RANKL–RANK signalling is activated by the progestin MPA and that this is important for mammary tumorigenesis.

Gene expression profiles have been used to identify large chromosomal changes in iPS cells.

An alternative glycolytic pathway used by cancer cells uncouples ATP production from anabolic metabolism.