Department of Pharmacology Seminar Series
Seminars will be held as usual in the Departmental Seminar Room at 13:00 on Fridays in Full Term. After the talk there will be tea and cake and a chance to talk informally with the speaker.
If anyone wishes to have some time with any speaker before the talk, please contact comms [@] phar.cam.ac.uk in advance.
Schedule for Easter 2026
Friday 8 May, 13:00 - 14:00
This comprises two 15-minute talks:
Speaker: Dr Camilla Ascanelli – Wilson lab
Title: Destroying MYC: Engineering Biological Degraders for Rapid Tumour Cell Death
Abstract: MYC transcription factors are central regulators of cell growth and proliferation and are deregulated in the majority of human cancers. However, their intrinsically disordered structure has made them resistant to conventional small-molecule targeting, earning MYC the label of “undruggable”. In collaboration with AstraZeneca, we applied targeted protein degradation (TPD) to overcome these limitations. While small-molecule PROTACs against MYC have been reported, they often lack specificity, achieve inefficient degradation, and can generate functional truncated protein products, limiting their utility for both therapeutic and mechanistic studies. To address this, we developed biologics-based PROTACs (bioPROTACs) that enable efficient and specific degradation of MYC. Using these tools, we demonstrate robust MYC depletion in vitro and in vivo, and reveal distinct cellular responses compared to MYC inhibition, providing new insights into MYC biology and its therapeutic targeting.
Bio: Cami is a postdoctoral researcher in Cathy Wilson’s lab. Her work focuses on developing RNA-delivered biologics for targeted protein degradation, with a particular interest in MYC-driven cancers. In collaboration with AstraZeneca, she has been developing bioPROTAC approaches to selectively degrade MYC, using these tools to probe the cellular consequences of acute MYC loss. Her research aims to translate biologics-based degradation strategies into clinically relevant approaches.
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Speaker: Dr Nick Schaum, Khaled Group
Title: Ageing in the Age of AI
Abstract: Ageing is by far the dominant risk factor for all of the most common diseases like cancer, heart disease, and dementia, yet the molecular landscape of ageing remains poorly mapped, preventing the development of therapeutics that could prevent or delay multiple diseases simultaneously. No single lab or institution can solve this alone — it demands coordinated global effort, and public-good infrastructure that the whole community can build on. The NMGN Ageing Cluster addresses this by generating a multiomic and phenotypic atlas across the mouse lifespan: two strains, four timepoints, longitudinal phenotyping, and spatial transcriptomics. But new data alone is insufficient — millions of relevant datasets already exist, scattered across public repositories in forms neither humans nor machines can readily use. Covalent.bio tackles this by building an AI-powered semantic layer over existing biological repositories, standardising metadata at global scale and making the existing corpus of transcriptomic data ML-ready. These represent two sides of the same strategy: producing the foundational data the field needs, while unlocking the vast wealth of data it already has.
Biography: Nick is a postdoc in the Khaled lab where he runs the National Mouse Genetics Network Ageing Cluster. Before coming to the UK, he built the first organism-wide single-cell atlas of ageing called Tabula Muris Senis at Stanford with the Chan Zuckerberg Biohub, and the nonprofit Rejuvenome Project at the Astera Institute. In his free time he works on his startup Covalent.bio.
Friday 15 May, 12:00 - 13:00
Speaker: Dr Laura Blenkarn - Itzhaki and Wilson Groups
Title: Design and Validation of bioPROTACs targeting Cyclin T1 in Cancer
Abstract: Cyclin T1 regulates catalytic CDK9, together forming positive transcription elongation factor b (pTEFb). This complex is essential for resumption of productive transcription after promotor-proximal pausing of RNA polymerase II (RNA polII). Proximal pausing provides an important layer of transcriptional control, acting as an opportunity to adjust expression rates of a gene or even to terminate transcriptional elongation to safeguard transcription integrity. Resumption of transcription after proximal pausing presents an opportunity to perturb gene expression synthetically in the treatment of cancer. We have used a targeted protein degradation (TPD) approach to degrade Cyclin T1 and therefore block pTEFb activity. We have used lung cancer cell lines to investigate phenotypic changes and shown that TPD of Cyclin T1 reduces global transcription and stalls cell cycling. These are promising signs that a Cyclin T1-targeting PROTAC could be used as part of a cancer treatment regime.
Bio: Laura completed her PhD in Pharmacology at the University of Cambridge in the lab groups of Dr Catherine Wilson and Prof. Laura Itzhaki, exploring targeted protein degradation of Cyclin T1 in cancer. She has since continued as a PDRA investigating the effects of her designed bioPROTACs on transcription. Prior to her PhD, Laura studied her undergraduate degree in Biological Sciences at the University of Oxford and spent a year as a Research Assistant for a clinical trial assessing a new treatment for spondylarthritis.
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Speaker: Dr Mateusz Jaskolowski, Miller Group
Title: Computational approaches to develop more advanced nanobody libraries
Abstract: Most nanobodies in use today come from camelid immunisation or from synthetic libraries designed before modern machine learning existed. I will describe the design of a new general-purpose synthetic nanobody library for phage display. From a database of roughly 20 million unique nanobody sequences, we selected optimal scaffolds for three library types, including a novel non-canonical disulfide bond nanobody library. Candidate sequences are filtered for developability and then biased, using statistical models of camelid repertoires and machine-learning tools, toward better predicted biophysical profiles. Rather than randomise the CDRs (the loops that mediate antigen binding), we control their composition exactly through pre-defined sequence arrays and generate diversity by CDR shuffling, which our analysis of those 20 million sequences suggests more closely reflects the native llama repertoire.
Bio: Mateusz Jaskolowski is an SNSF Postdoc Mobility Fellow at the University of Cambridge, working jointly in the Miller group (Pharmacology) and the Sormanni group (Chemistry). He studied at the University of Gdańsk, Poland, raised synthetic Fabs against Ebola in Anthony Kossiakoff's lab at the University of Chicago, and completed his PhD and a bridging postdoc with Nenad Ban at ETH Zürich, where he used cryo-EM to study ribosomes, ER targeting, and the co-translational N-terminal processing of nascent proteins. He joined Cambridge in October 2024.