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Haematological malignancies

Splicing the MDS genome

Nature Reviews Cancer volume 15, page 393 (2015)Cite this article

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Myelodysplastic syndrome (MDS) describes a range of haematological diseases that are associated with defective myeloid differentiation and dysplasia; in some cases, MDS progresses to acute myeloid leukaemia (AML). Three papers now present different aspects of a similar story: altered splicing can lead to MDS and even progression to AML.

To more clearly understand the pathogenesis of MDS in response to chronic DNA damage, Colla, Ong et al. used telomerase-deficient mice expressing inducible telomerase reverse transcriptase (TertER/ER mice). These mice were then crossed with each other for multiple generations (G) to degenerate their telomeres. G4 and G5 mice exhibited telomere dysfunction, DNA damage and tissue degeneration, and this phenotype was reversed by Tert induction. At 3 months, G4 and G5 mice exhibited refractory anaemia with excess blasts (RAEB; 80% of the cohort) or chronic myelomonocytic leukaemia (CMML; 20% of the cohort), both of which are types of MDS; 5% of these mice developed AML by 7 months.

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References

  1. Colla, S. et al. Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome. Cancer Cell 27, 644–657 (2015)

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  2. Kim, E. et al. SRSF2 mutations contribute to myelodysplasia by mutant-specific effects on exon recognition. Cancer Cell 27, 617–630 (2015)

    Article  CAS  Google Scholar 

  3. Shirai, C. et al. Mutant U2AF1 expression alters hematopoiesis and pre-mRNA splicing in vivo. Cancer Cell 27, 631–643 (2015)

    Article  CAS  Google Scholar 

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Authors
  1. Gemma K. Alderton
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Alderton, G. Splicing the MDS genome. Nat Rev Cancer 15, 393 (2015). https://doi.org/10.1038/nrc3975

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