T-lineage acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy that
requires treatment with intensified chemotherapy. Studies of the long-term effects of
chemotherapy in patients with T-ALL showed that recent gains in leukemia-free survival have been
achieved at the cost of significant increases in the rates of life-threatening and debilitating toxicities.
Thus, further advances in the treatment of T-ALL require the development of effective and highly
specific molecularly targeted antileukemic drugs.
The identification of cMYB translocations and duplications in human T-ALL suggests an important
oncogenic role for this transcription factor during T-cell transformation. Nevertheless, the exact
molecular mechanisms by which cMYB contributes to the pathology of this disease remains unclear.
Here, we aim to identify the role of enhanced MYB activity in enhancer driven oncogenic
transcription in the context of malignant T-cell development and investigate the in vivo role of cMyb
in the initiation and maintenance of T-ALL. Importantly, these novel insights in the pathogenic role
of cMYB in T-cell leukemia will provide new avenues for therapeutic intervention in this aggressive