UCL Cancer Institute Seminar Series

We hypothesize that the process of oncogenic transformation is driven by aberrant activity of oncogene-associated chromatin modifying partners. These changes create a chromatin environment unique to the malignant state and, therefore, disruption of critical oncogenic chromatin signatures would not likely affect healthy tissues. We use acute lymphoblastic leukaemia (ALL), a highly aggressive blood cancer affecting children and adults, as our model. The presentation will be focused on two main trajectories:

a)       The critical role of a category of enzymes called ubiquitin specific peptidases (USPs) in sustaining oncogenic activity and transcriptional response. We further dissect the roles of those enzymes by using state of the art technologies, small molecule inhibitors and xenograft models of disease.

b)       Oncogene-driven formation of enhancer-promoter interaction in leukemia, changes in chromatin conformation over disease progression and the delineation of the disease-driving potential of those alterations.

Information gained from these studies will lend rationale towards targeted therapies exploiting cancer vulnerabilities for the treatment of aggressive and relapsed ALL

www.ntziachristoslab.com

Hosted by: Dr Marc Mansour

Location

Courtyard Café
UCL Cancer Institute
Paul O'Gorman Building
London, WC1E 6DD

Contact: Veronica Dominguez v.dominguez@ucl.ac.uk

This seminar has been part-sponsored by the NIHR UCLH Biomedical Research Centre and Cancer Research UK.