Research Highlights

Short, accessible synopses of recent important articles concerning signalling pathways.

December 2008

• Signalling: Making more of a mark

  

  Melanomas are resistant to many standard therapies and often metastasize, prompting an intensive search for novel therapeutic targets. A recent study has highlighted a role for Notch signalling in melanoma development under hypoxic conditions.

  Original research paper Nature Reviews Cancer 8 906 - 907 doi:10.1038/nrc2551

• Stem cells: A new pathway for stem cell ageing and renewal

  

  Stem cells have the potential for self-renewal and are therefore able to persist throughout life in a diverse range of tissues. However, their self-renewing capacity declines with age. What mechanisms are responsible for the differences between young and ageing stem cells? The discovery of a novel pathway involving high-mobility group A2 (HMGA2), INK4A and ARF has recently provided exciting new insights.

  Original research paper Nature Reviews Cancer 8 908 doi:10.1038/nrc2547

• Development: It's all in the timing

  

  The signalling factor Sonic hedgehog (SHH) has been shown to specify the identity of motor and interneurons in the developing spinal cord in a concentration-dependent manner. Bai and colleagues now report that SHH does not act alone: WNT signalling lends a helping hand in a time-dependent fashion.

  Original research paper Nature Reviews Neuroscience 9 892 doi:10.1038/nrn2545

• Innate immunity: Seeing mTOR in a new light

  

  A recent study published in Immunity shows that the drug rapamycin has a surprisingly pro-inflammatory effect on phagocytic cells, increasing their capacity to produce cytokines, such as interleukin-12 (IL-12), and to prime T helper 1 (T_H1)- and T_H17-cell responses.

  Original research paper Nature Reviews Immunology 8 904 doi:10.1038/nri2457

• Glioblastoma: Stop acting so immature

  

  The p53 and PTEN pathways have established roles in gliomagenesis, which prompted Ron DePinho and colleagues to create mice with central nervous system (CNS)-specific deletion of the two genes. In humans, PTEN mutations are typically found in high-grade primary glioblastoma multiforme (GBM), whereas TP53 mutations are more common in secondary GBM, which develops following progression from low-grade disease. So, the authors were somewhat surprised to find that tumours in mice lacking both Pten and Trp53 in the CNS bore a striking resemblance to primary GBM in humans.

  Original research paper Nature Reviews Cancer 8 905 doi:10.1038/nrc2546