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Genetics

In the driving seat

Nature Reviews Cancer volume 8, pages 80–81 (2008)Cite this article

In this study FLT3 was sequenced in 222 patients with acute myeloid leukaemia who did not have the known FLT3-activating mutations. The authors identified nine non-synonymous, potentially leukaemogenic mutations; however, a major challenge was to establish which of these mutations were oncogenic (that is, driver mutations). Therefore, they investigated which of the variants could transform murine pro-B cells to cytokine-independent growth. Surprisingly, only four of the nine candidate mutations had transforming properties: one in the extracellular domain (S451F), two in the juxtamembrane domain (Y572C and V592G) and one in the kinase domain (R834Q).

Cells harbouring the remaining five mutations underwent apoptosis in the absence of cytokines, leading the researchers to believe that they are 'passenger' mutations that confer no growth advantage. However, although these mutations do not appear to activate FLT3, an alternative function might yet be found; “One can never say never!” Gilliland acknowledges, especially as, in theory, two of the mutated alleles (M737I and G831E) seem to be excellent candidates for activating mutations.

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ORIGINAL RESEARCH PAPER

  1. Fröhling, S. et al. Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles. Cancer Cell 12, 501–513 (2007)

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Authors
  1. Simone Alves
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Alves, S. In the driving seat. Nat Rev Cancer 8, 80–81 (2008). https://doi.org/10.1038/nrc2318

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  • DOI: https://doi.org/10.1038/nrc2318

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