News Feature |
Featured
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Letter |
Stage-specific sensitivity to p53 restoration during lung cancer progression
p53 is an important tumour suppressor gene. Two papers now show in a Kras-driven lung cancer model that p53-mediated tumour suppression is only engaged late during tumour progression, when the Kras oncogenic signal reaches a threshold sufficient to activate the ARF–p53 pathway. Therefore, p53 re-expression in p53-deficient lung tumours does not restrict early stages of tumorigenesis, but induces tumour regression of more aggressive tumours.
- David M. Feldser
- , Kamena K. Kostova
- & Tyler Jacks
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Letter |
Selective activation of p53-mediated tumour suppression in high-grade tumours
p53 is an important tumour suppressor gene. Two papers now show in a Kras-driven lung cancer model that p53-mediated tumour suppression is only engaged late during tumour progression, when the Kras oncogenic signal reaches a threshold sufficient to activate the ARF–p53 pathway. Therefore, p53 re-expression in p53-deficient lung tumours does not restrict early stages of tumorigenesis, but induces tumour regression of more aggressive tumours.
- Melissa R. Junttila
- , Anthony N. Karnezis
- & Carla P. Martins
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Letter |
Tumour angiogenesis is reduced in the Tc1 mouse model of Down’s syndrome
Down's syndrome is caused by trisomy of chromosome 21, and it is known that the growth of certain tumours is reduced in this genetic disorder. Using a mouse model of Down's syndrome, several individual genes on chromosome 21 are now being proposed to mediate the effect on tumour growth and angiogenesis.
- Louise E. Reynolds
- , Alan R. Watson
- & Kairbaan M. Hodivala-Dilke
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Letter |
The mutation spectrum revealed by paired genome sequences from a lung cancer patient
Complete genome sequencing has already provided insights into the mutation spectra of several cancer types. Here, the first complete sequences are provided of a primary lung tumour and adjacent normal tissue. Comparison of the two reveals a variety of somatic mutations in the cancer genome, including changes in the KRAS proto-oncogene. The results reveal a distinct pattern of selection against mutations within expressed genes compared to non-expressed genes, and selection against mutations in promoter regions.
- William Lee
- , Zhaoshi Jiang
- & Zemin Zhang
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Research Highlights |
Cancer biology: Cells combat chemo
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Letter |
Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal
Genomic instability has been implicated in tumour development. Here, a new mouse model of Kras-driven lung tumours has been developed, in which genomic instability is caused by overexpression of the mitotic checkpoint protein Mad2. In this model, inhibiting Kras leads to tumour regression, as shown previously. But tumours recur at a much higher rate.
- Rocio Sotillo
- , Juan-Manuel Schvartzman
- & Robert Benezra
Epidemiology: Fear in the dust