Proper homeostasis of stem cells and pluripotent progenitor is pivotal to the development of haematopoietic proliferative disorders such as myelodysplastic or myeloproliferative syndromes, leukaemia and lymphoma. It is well known that alterations in transcriptional programs lead to transformed phenotypes, which are at the basis of the insidious acquisition of stem-like phenotypes of immature cells. Our group is interested in the role of transcriptional regulators, global regulators such as c-myc, c-myb, E2F and epigenetic controllers such as PcG factors in limiting the self-renewal capacity of common myeloid and lymphoid progenitors.

Our group has two main activities: basic research aimed to unravel the molecular mechanisms responsible for the acquisition of malignant haematological phenotypes (mouse models as well as ex vivo cell models to approach the questions outlined above); and research aimed to document clinical parameters and molecular markers that may be of use to a better understanding of the progression and outcome of haematological diseases, mainly myelodysplasia, lymphoma and multiple myeloma.

Role of epigenetic and transcriptional regulators in myelodysplasia: cellular and animal models