UCL Cancer Institute Seminar Series

An intact CEBPA pathway is required for myeloid differentiation, and this key transcription factor pathway is mutated, downregulated, or inactivated in many forms of Acute Myeloid Leukaemia (AML). A number of therapeutics utilized in AML actually serve to restore CEBPA expression and/or function, including all trans retinoic acid (ATRA) in Acute Promyelocytic Leukaemia; FLT3 tyrosine kinase inhibitors in FLT3-ITD positive AMLs; CDC2/CDK1 inhibitors; Histone Deacetylase (HDAC) inhibitors; CDDO; DOT1L inhibitors; and Imatinib in CML myeloid blast crisis. We and others have recently developed a number of novel therapeutics resulting in activation of CEBPA expression and/or function, including small molecules, long noncoding RNAs, and short activating RNAs. These result in more specific activation of CEBPA and subsequent differentiation of AML cells. In addition, similar approaches can be utilized to induce demethylation and activation of expression of other tumour suppressors, including p15 and p16, with potential applicability in both leukaemia and solid tumours, such as liver cancer.

Professor Daniel G. Tenen academic profile

Hosted by: Professor Tariq Enver

The seminar will be followed by a sandwich buffet lunch

Location

UCL Cancer Institute
Courtyard Café
72 Huntley Street
London, WC1E 6DD

Contact: Veronica Dominguez v.dominguez@ucl.ac.ukView M

This seminar has been sponsored in part by the Biomedical Research Centre and Cancer Research UK.