Rate My Professor Nicholas La Thangue

His research centers on the molecular mechanisms driving tumour cell proliferation, with a focus on the pRb-E2F pathway regulating the G1/S transition, p53 stress responses, and post-translational modifications such as arginine methylation by PRMT5 and citrullination. These studies led to a hypothesis explaining how pRb accomplishes its tumour suppressor activity by negatively regulating E2F activity, which has been validated. In parallel, investigations into p53 have revealed novel pathways regulating the cellular stress response. The La Thangue Group investigates E2F family members' roles in cell cycle control and apoptosis, employing genome-wide loss-of-function screens to develop predictive biomarkers for cancer therapies. He has initiated a large cancer drug discovery programme, co-developing a novel histone deacetylase inhibitor advanced to clinical trials for haematological malignancies and diverse solid tumours. Key publications include “Separate transcription and splicing gene networks are linked and coordinated by the pRb-E2F pathway” (Carr et al., Nucleic Acids Research, 2026), “p300/CBP proteins: HATs for transcriptional bridges and scaffolds” (Chan and La Thangue, Journal of Cell Science, 2001), “Adenovirus E1a prevents the retinoblastoma gene product from complexing with a cellular transcription factor” (Bandara and La Thangue, Nature, 1991), and “Citrullination and the protein code: crosstalk between post-translational modifications in cancer” (Harada et al., Philosophical Transactions of the Royal Society B, 2023). His work has profoundly influenced oncology therapeutics.