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About CRUK Scotland Institute

Find out what we do, how we do it and why we do what we do.

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Life in Glasgow

Find out about living and working in Glasgow and Scotland.

Our Research

Explore the science at CRUK Scotland Institute. Our research groups, the people who lead them, and how we work.

Operations

The teams and services that keep the Institute running and support our research.

Partners

The networks and organisations we work with to accelerate cancer research.

Careers & Study

Jobs, studentships and opportunities for students at every stage at our world-renowned cancer research institute.

Studentships

PhD opportunities at the Institute

Studentship Vacancies

Open studentships to apply for

Internships

For undergraduate and masters students

The Rao Lab studies how transcription factor networks and chromatin regulation control epithelial cell identity – and how their disruption drives cancer initiation and progression. We are especially interested in the earliest molecular events of tumour development and how the breakdown of transcriptional programs fuels tumour evolution, cellular plasticity, and therapy resistance.

We take a systematic, functional approach to dissecting cancer regulatory networks, combining transcription factor-focused perturbation screens, CRISPR-based functional genomics, targeted protein degradation (degron) technologies, and integrative genomic and proteomic profiling. These tools are applied across complementary model systems cell lines, genetically engineered mouse models, and patient-derived samples to capture biology at multiple levels of complexity.

A central focus of the lab is defining transcription factor and epigenetic mechanisms in cancers of high unmet clinical need, particularly pancreatic cancer. By mapping the regulatory circuits that establish and maintain tumour cell identity, we aim to uncover the origins of early disease, identify biomarkers of progression, and reveal new therapeutic vulnerabilities for patients with limited treatment options.

RaoLab infographic on epigenetic control and cancer evolution, showing a circular process from normal epithelium and early molecular changes to altered cell identity, tumour progression, metastasis, and therapeutic vulnerabilities.
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Biography

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Recent Publications

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Biography

Education and qualifications

  • 2011–2015: PhD, NTNU Trondheim, Norway

Appointments

  • 2024–present: Assistant Research Professor, CRUK Cambridge Institute, UK
  • 2021–2024: Senior Research Associate, CRUK Cambridge Institute, UK
  • 2019–2020: Project Lead, Azeria Therapeutics
  • 2017–2019: Visiting Scientist, CRUK Cambridge Institute, UK
  • 2016–2017: Postdoctoral Fellow, NTNU, Trondheim, Norway

Recent Publications

2026

Pelicano, C., Chernukhin, I., Wölke, M., Cheng, P. S. W. P., Young, L., Edwards, A. R., Mannion, E., Cheng, Y., Crowshaw, M., Kupczak, S., Pinto Teles, S., Jihad, M., Kishore, K., Chilamakuri, C. S. R., Franklin, V. N. R., Papachristou, E. K., D’Santos, C., Grünwald, B., Russell, A., Carroll, J. S., Biffi, G., Rao, S. V. IL-1-activated cancer-associated fibroblasts promote STAT1-driven transcriptional reprogramming of pancreatic tumour cells. Biorxiv.

2025

Rao, S. V., Young, L., Cheeseman, D., Flynn, S., Krebs, N., Couturier, D.-L., Mack, S., Brias, R., Temple, J., Smith, A., Papachristou, E., Pelicano, C., Chilamakuri, C. S. R., Herka, K., Baba, H. A., Farah, L., Cheung, P. F., Siveke, J., Guerrier, S., Insolia, L., Gill, M., Archer-Goode, E., Kupczak, S., Cheng, Y., Borsari, G., Jodrell, D., D’Santos, C., Russell, A., Grünwald, B. T., Serrao, E., Chernukhin, I., & Carroll, J. S. Transcription factor switching drives subtype-specific pancreatic cancer. Nature Genetics. 2025;57:3016–3026.

2024

Martin PL, Pérez-Areoles FJ, Rao SV, Walsh SJ, Carroll JS, Spring DR. Towards the Targeted Protein Degradation of PRMT1. Chem Mechem. 2024 May 9:e202400269

2020

Nagarajan, S, Rao, S.V, Chernukhin, I, Sutton, J, Cheeseman, D, Dunn, S, Papachristou, E.K, Gonzalez Prada, J-E, Couturier, D-L, Kumar, S, Kishore, K, Chilamakuri, CSR, Glont, S-E, Goode, E.A, Brodie, C, Guppy, N, Natrajan, R, Bruna, A, Caldas, C, Russell, A.I, Siersbæk, R, Yusa, K and Carroll, J. S. ARID1A dictates HDAC1/BRD4 activity, intrinsic proliferative capacity and breast cancer treatment response. Nature Genetics. 2020;52:187-197.