Articles 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.

The protein tyrosine phosphatase (Ptp) family dephosphorylates target proteins and counters the activities of protein tyrosine kinases. Accumulating evidence indicates that some PTPs have an important role in the inhibition or control of growth, whereas some PTPs exert oncogenic functions. This Review discusses the relevance of PTPs to cancer biology and their potential as therapeutic targets.

Inherent difficulties with blocking many desirable targets using conventional approaches have prompted many to consider using RNA interference (RNAi) as a therapeutic approach. This Review explores current challenges to the development of synthetic RNAi-based therapies and considers new approaches to circumvent biological barriers.

Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous disease that often recurs, prompting the field cancerization hypothesis. This Review discusses the molecular pathology of HNSCC and how its heterogeneity can be used to classify the disease and provide a model of HNSCC development.

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.

The Pim family of kinases actively collaborate with MYC in driving tumorigenesis. However, in several cancers the expression levels of PIMs can correlate with favourable prognostic outcome. This Review analyses the physiological and oncogenic activities of Pim kinases and their synergistic marriage with MYC, for better or for worse.

The survival of genetically abnormal carcinoma progenitor cells in ductal carcinomain situlesions could be driven by the hypoxic, nutrient-deprived microenvironment. Understanding the potential survival mechanisms, such as autophagy, could provide new strategies for arresting invasion at the pre-malignant stage.