Howard Elder Prize for GRE researchers January 19, 2022 Seraina Blumli Nicola Wiechens and Seraina Blümli, from Tom Owen-Hughes lab, were awarded the Howard Elder Prize at the School of Life Sciences Annual Prize giving at Review of the Year 2021. The Howard Elder Prize is for a postgraduate student or postdoctoral researcher deemed to have published the most significant paper in an area related to cancer research. The prize was introduced by Dr Howard Elder’s daughter who said her father always spoke very highly of his time at Dundee and the opportunities it gave him. Dr Elder studied medicine at St Andrews University which was located in Dundee as University College. He was in general practice for 43 years in London. He attended clinics at Great Ormond Street Hospital, a police surgeon for 30 years and taught medical students. Nicola Wiechens Nicola and Seraina jointly won for their paper ‘Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription’ published in Cell Reports. The judging panel comprising of Kevin Hiom, Albena Dinkova-Kostova and Adrian Saurin in the School of Medicine said, “As ever the decision was very difficult. Taking into account the excellence of the published paper, the contributions made by nominated researchers and the relevance of the work to cancer, the panel decided to make the award jointly to Nicola Wiechens and Seraina Blümli.” “The judges were impressed by way Nicola and Seraina used targeted protein degradation to identify the order in which chromatin, nucleosome positioning and transcription become altered in response to the loss of the key tumour suppressor ARID1A. In particular, their thoughtful and rigorous analysis of genome wide data to tease out the hierarchy of indirect and adaptive changes in the transcriptome of cells upon depletion of ARID1A. The judges congratulate Nicola and Seraina on their excellent study that has potentially important implications for targeted treatment of the many cancers in which ARID1A is defective.”