Steve Pollard

Transcriptional control of cell fate in stem cells and cancer stem cells.

Steve Pollard is Professor of Stem Cell and Cancer Biology at the University of Edinburgh. He trained in developmental genetics at NIMR (now the Francis Crick Institute) and studied stem cell gene regulation as a postdoc with Prof Austin Smith at Cambridge. 

As a Wellcome Beit Fellow and Cancer Research UK Senior Fellow, he uncovered how brain cancers hijack neural stem cell programs. His group has also generated a suite of improved methods, tools and cell lines that have been widely shared with the community. His lab has used these to uncover novel biological processes driving brain tumours, identified new therapeutic targets, and development of first-in-class innovative gene therapy strategies that are moving into clinical testing.

portrait photo of Steve Pollard
Steve Pollard

Steve leads the CRUK Brain Cancer Centre of Excellence, is Associate Director of the CRUK Scotland Centre, and part of the leadership team for the Edinburgh-led UKRI Engineering Biology Mission Hub. In 2023, he founded Trogenix Ltd (www.trogenix.com), a spinout biotech spinout applying cancer models, synthetic biology, gene therapy, and immuno-oncology to develop precision genetic medicines for cancer.

Thibaud Aymoz-Bressot, Erika Dalmo, Kim Dilworth, Vivien Grant, Hei Ip Hong, Isabella Jamieson Morris, Heather MacPherson, Gillian Morrison, Shahida Sheraz, Zeyu Wang, Rachel White, Charles Williams, Rosie Willis, and Xinying Yeo


Many human cancers hijack the molecular programs normally reserved for immature stem cells, using them to maintain relentless self-renewal and evade terminal differentiation. In tumours, these pathways run unchecked — making them prime targets for new therapies. Our research focusses on the biochemical and cellular mechanisms regulated by a group of master regulatory transcription factors — the “command switches” that lock cells into an immature cancer stem cell state. By decoding how these powerful gene regulators work, we aim to expose vulnerabilities that can be exploited for transformative treatments.

We are developing innovative strategies to dismantle this cancer stem cell-like identity. Many of the pivotal regulators we and others have identified over the past decade are neurodevelopmental transcription factors — including members of the SOX, FOX, HOX, and bHLH families (Bulstrode et al., . These factors, often redundant and notoriously difficult to “drug” with standard medicinal chemistry, underpin the plasticity that defines both normal stem cells and cancer stem cells.

Our lab’s research combines patient-derived models (Pollard et al.), CRISPR genome editing (Bressan et al, and Dewari et al), synthetic biology, genomics, immunotherapy, and AAV-based gene therapy. Although our primary focus is the lethal brain cancer glioblastoma, our approaches have clear potential across multiple tumour types. Through collaborations with academic and industry partners, we are now extending our work to colorectal, lung, and liver cancers.

We are driven by three overarching research questions:

  • What are the key biological vulnerabilities of human cancer cells?
  • How can we target these vulnerabilities with precision and selectivity?
  • What strategies can best prevent relapse or regrowth?

Our ultimate goal is to deliver safer, more effective treatments for solid cancers.


Ferguson, K. M. et al. Modelling quiescence exit of neural stem cells reveals a FOXG1-FOXO6 axis. Dis. Model. Mech. 17, dmm052005 (2024).

Robertson, F. L. et al. Elevated FOXG1 in glioblastoma stem cells cooperates with Wnt/β-catenin to induce exit from quiescence. Cell Rep. 42, 112561 (2023).

Gangoso, E. et al. Glioblastomas acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion. Cell 184, 2454-2470.e26 (2021).

Marqués-Torrejón, M. Á. et al. LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells. Nat Commun 12, 2594 (2021).

Bressan, R. B. et al. Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants. Cell Stem Cell 28, 877-893.e9 (2021).


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