Volume 10 Issue 4, April 2010

The seminal article by Douglas Hanahan and Robert Weinberg on the hallmarks of cancer is 10 years old this year and its contribution to how we see cancer has been substantial. But, in embracing this view, have we lost sight of what makes cancer cancer?

A new method allows the identification of rare mutations in mitochondrial DNA that differ between normal and cancer cells.

Another member of the hippo–salvador–warts pathway has been identified.

Fluorescent probes that specifically label tumours improve the surgical removal of tumours.

Recent results indicate that stringent profiling of tumours will be needed prior to the use of RAF inhibitors.

Long-range epigenetic silencing decreases transcriptional plasticity in prostate cancer.

DOK2 is frequently deleted in human lung cancer and suppresses lung cancer cell growth.

Glioblastoma radiotherapy might be improved by inhibitors of vasculogenesis rather than angiogenesis.

Tumour-derived cell lines are an important model for the discovery and development of new anticancer drugs. The recent development of large panels of cell lines and high-throughput technologies has revitalized this field, and this Review discusses how these tools can be used to screen anticancer agents.

Effects on both global protein synthesis and selective translation of specific mRNAs can contribute to cancer development and progression. How are components of the translation machinery altered in cancer, and can these be targeted therapeutically?

This Review discusses the progress made with developing drugs that specifically target the altered metabolic pathways of tumours and suggests additional targets that might also be beneficial.

Many proteases are regulated by phosphorylation, and many kinases are regulated by proteolytic cleavage. This Review examines kinase–protease interactions and their functional effects in cancer in depth, revealing the enormous diversity and complexity of this crosstalk.

Recent findings have thrust poly(ADP-ribose) polymerases (PARPs) into the limelight as potential chemotherapeutic targets. What is known about the structures and functions of the family of PARP enzymes and which questions do we need answered to guide the rational development of PARP inhibitors as anticancer agents?

Recently, MYC has been shown to serve as a direct regulator of ribosome biogenesis and therefore coordinates protein synthesis. Could the regulation of ribosome biogenesis by MYC be necessary for its role in tumorigenesis?