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Mutant JAK2, thrombopoietin receptor or calreticulin proteins on or near the cell surface result in constitutive activation of the JAK-STAT signalling pathway and chronic clonal myeloid proliferation. Additional loss or change of function mutations in the epigenetic regulators Tet2, Asxl1, Dnmt3 or PRC2 (Suz12, Eed, Ezh2) result in altered chromatin modifications and structure that promotes the transformation from chronic clonal myeloid proliferation to leukaemia.

Professor Stefan constantinescu

The Constantinescu group at Ludwig Oxford studies the link between signalling, epigenetic regulators, chromatin dynamics and differentiation in myeloid blood cancers. Overall, our objectives are to determine:

  1. The effects induced by drivers of myeloproliferative neoplasms (MPNs) on epigenetic regulators via post-translational modifications of effectors and transcriptional changes;
  2. The impact of mutations in epigenetic regulators on chromatin states that allow oncogenesis in the myeloid blood lineage;
  3. The molecular basis of progression of chronic myeloproliferative neoplasms and myelodysplasia into secondary acute myeloid leukaemia.


Find out more about research in the Constantinescu lab.


Our team