T-cell acute lymphoblastic leukaemia was originally identified as a highly aggressive blood disorder associated with poor prognosis, but intensified therapy has since led to remarkable improvements in survival. Unfortunately, these treatment regimens (mainly combination chemotherapy) are associated with severe acute and long-term toxicities. Moreover, the prognosis of patients with relapsed and refractory disease remains extremely poor. To shift towards a personalised medicine approach, a profound understanding of the molecular basis of the progression of this leukaemia subtype is required. This thesis discusses an integrative genomics approach to functionally dissect the interplay between established and novel transcriptional regulators that take part in the rewired transcriptional networks that drive malignant transformation of thymocytes to T-ALL lymphoblasts.
(BELG J HEMATOL 2017;8(2):80–2)