Nanotechnology

In vivo biodistribution and highly efficient tumour targeting of carbon nanotubes in mice. Liu, Z. et al. Nature Nanotech. 2, 47–52 (2007)

Determining the fate and biological effects of carbon nanotubes in vivo are crucial to their potential therapeutic applications, such as targeted drug delivery. Liu and colleagues have demonstrated efficient targeting of single-walled carbon nanotubes functionalized with phospholipids bearing polyethylene glycol to an integrin-positive tumour in mice. A high tumour accumulation was achieved, and the nanotubes exhibited relatively long circulation times and low uptake by the reticuloendothelial system.

Analgesia

An SNC9A channelopathy causes congenital inability to experience pain. Cox, J. J. et al. Nature 444, 894–498 (2006)

Cox and colleagues show that a rare autosomal recessive condition in which individuals have an inability to experience pain is caused by loss of function of the SCN9A gene, which encodes the α-subunit of the voltage-gated sodium channel Nav1.7. The finding that disruption of this single gene leads to a complete loss of nociceptive function could stimulate research for analgesics that target this ion-channel subunit.

Anticancer Drugs

Identification of NVP-TAE684, a potent, selective and efficacious inhibitor of NMP–ALK. Galkin, A. V. et al. Proc. Natl Acad. Sci. USA 104, 270–275 (2007)

Constitutive activation of the nucleophosmin–anaplastic lymphoma kinase (NPM–ALK) fusion protein drives anaplastic large-cell lymphoma (ALCL) proliferation. Galkin and colleagues have identified a selective ALK inhibitor — NVP-TAE684 — which induced apoptosis and cell-cycle arrest in vitro. In murine models of ALK-positive ALCL, NVP-TAE684 suppressed lymphomagenesis and induced regression of established lymphomas. The compound also downregulated CD30 expression, suggesting that CD30 could be used as a biomarker for NPM–ALK kinase inhibition.

Neurodegenerative Disease

Selective inhibitors of death in mutant huntingtin cells. Varma, H. et al. Nature Chem. Biol. 31 Dec 2006 (doi:10.1038/nchembio852)

Huntington's disease (HD) is caused by mutations in the huntingtin protein, which leads to cellular dysfunction, but how this contributes to HD is unclear. Varma and colleagues developed a high-throughput neuronal cell-culture assay to screen more than 40,000 compounds, of which 29 were selective inhibitors of cell death in mutant-huntingtin-expressing cells and 4 were active in diverse HD models. These results suggest a role for cell death in HD, and identify mechanistic probes and potential drug leads for this condition.