The Beatson Institute Research Groups

The aim of our research is to understand the mechanisms that regulate cancer cell proliferation, survival and dissemination; to identify critical components of these pathways as targets for novel cancer therapies; and to help translate this knowledge to patient benefit. Our scientists are supported in this by having access to outstanding facilities and state-of-the-art services. In addition, the Institute has close ties to the University of Glasgow’s basic and clinical cancer research groups.

Click Research Groups in the right-hand menu to see what each group is working on.

Beatson publications are available as open access articles at Europe PubMed Central.

The aim of our research is to understand the mechanisms that regulate cancer cell proliferation, survival and dissemination; to identify critical components of these pathways as targets for novel cancer therapies; and to help translate this knowledge to patient benefit. Our scientists are supported in this by having access to outstanding facilities and state-of-the-art services. In addition, the Institute has close ties to the University of Glasgow's School of Cancer Sciences.

CRUK Scotland Institute publications are available as open access articles at Europe PubMed Central.

Research groups at the Scotland Institute are placing a particular emphasis on the following key themes:

  • Cancer vulnerabilities caused by energetic stress and aberrant metabolism;
  • Interplay between the tumour microenvironment, metastasis and recurrence; and
  • Biology of early disease, aimed at developing a 'precision prevention' approach.

Prof Vicky Cowling Profile

Cowling 2023

Prof Crispin Miller Profile

Miller 2023

Prof Kevin Ryan FRSE Profile

ryan 2023

Prof Owen Sansom FRSE, FMEDSci Profile


Dr Saverio Tardito Profile

Tardito 2023


LeQuesne John

The Le Quesne group combine classical molecular and quantitative microscopic imaging methods to ask questions about solid tumour biology. What can we directly observe in fully contextualised tumour tissue, the 'natural environment' of the malignant cell? How do malignant cells interact with the microenvironment of the tumour? What naturally selected strategies can we identify at cellular scale in human and mouse tumour tissues?

Our main interests lie in three areas:

  1. The dysregulation of mRNA translation in tumour cells and stroma, and how this reprogramming of the genome facilitates the malignant programme at the cellular level
  2. The refinement and development of highly multiplexed microscopic imaging methods to reveal additional levels of single-cellular detail in spatial context (e.g. quantity and subcellular localisation of multiple gene products at mRNA and protein levels)
  3. The improvement of biomarkers for the prediction of personalised treatment efficacy and patient prognostication.

We study common solid tumour types, but we have a particular emphasis on lung cancer and mesothelioma, and we have developed large focused collections of these tissues for study. In this area, we are engaged in study of how molecular and epigenetic events interact with tumour morphology in early stages of tumour development, and how morphology encodes specific survival strategies that drive tumour virulence and metastasis.




Cordero Julia

The adult intestine is a major barrier epithelium with vital endocrine, immune and metabolic roles, leading to the coordination of whole-body physiology. These functions are achieved by specialised cells such as absorptive enterocytes and secretory enteroendocrine cells, which are generated by intestinal stem cells (ISCs). Stem cells constantly repair the intestinal epithelium by adjusting their proliferation and differentiation to tissue intrinsic as well as micro- and macro-environmental signals. How do these signals integrate to preserve intestinal and whole-body health?

Work in our laboratory is devoted to deciphering the cellular and molecular mechanisms regulating ISC behaviour during tissue regeneration and tumourigenesis. We are also interested in understanding how the intestine interacts with other tissues and organs to maintain organismal balance and how these interactions are deregulated in intestinal diseases such as cancer or inflammation. We use the fruit fly Drosophila melanogaster as our primary in vivo research model system combined with suitable mammalian paradigms.

Our research aims to identify mechanisms that could be used in translational efforts to restore intestinal regeneration as well as to prevent malignant transformation of the intestine and alleviate the systemic consequences of intestinal malfunction.


Other funding:


Research Fellow, Senior Clinical Lecturer in Colorectal Surgery

Honorary Consultant Surgeon, Glasgow Royal Infirmary

Steele 2023

Colorectal cancer patients die as a result of metastatic progression or disease recurrence following surgery. Though surgery can cure some patients of colorectal cancer with liver limited disease, the vast majority cannot be treated effectively. Current systemic therapies offer modest survival benefits. Understanding the mechanisms of metastatic progression in the most aggressive forms of colorectal cancer will permit therapeutic targeting in the future alongside surgery to improve outcomes for my patients.

My current research interests focus on the immune microenvironment of locally advanced and metastatic colorectal cancer. We have identified the importance of common white blood cells – neutrophils – in driving metastatic progression in models of cancer. Using state-of-the-art in vivo models and human specimens, I am currently seeking to understand the interactions between neutrophil populations, other immune cells and tumour cells in driving progression of colorectal cancer. This work will help to identify vulnerabilities in the immune system that may be harnessed with immunotherapies to target more aggressive colorectal cancer. My clinical work at Glasgow Royal Infirmary operating on patients with locally advanced rectal cancer provides an opportunity to interact with this patient group, obtain relevant clinical samples and help prioritise my research.

 Other funding:




Senior Clinical Lecturer in Pancreatic Cancer


Fieke Froeling

Pancreatic cancer continues to be almost universally lethal and is predicted to soon become the second highest cause of cancer death. To date, there has been little improvement in overall outcomes, with very few effective therapies available. We do, however, see exceptional tumour responses occasionally, where patients derive significant benefits and have better outcomes. Thus, there is an urgent need to personalise our patient care and better identify the right treatment for each patient.

Most of the observations in pancreatic cancer biology can be explained through basic evolutionary principles: it is a complex cancer that is adaptive, highly capable to thrive in a resource constrained environment and uniquely able to evade anti-cancer therapy. But how do cancer cells optimise their fitness, at the expense of the host, to progress into this deadly cancer? And, what can we learn from studying the alterations in the tumour and its microenvironment in the context of its host system? These are central questions driving my research, using well-annotated patient samples in conjunction with patient-derived preclinical model systems to identify novel therapeutic approaches and candidate biomarkers that can be tested in clinical trials.

Clinically, I am an Honorary Consultant Medical Oncologist at the Beatson West of Scotland Cancer Centre treating patients with pancreatic cancer. The overall goal is to develop personalised therapeutic strategies that emanate from discoveries in both basic science and reverse translation from clinical observation.

University of Glasgow- Colour



Cagan Ross The Cagan laboratory uses Drosophila to explore the biology of therapeutics. Data from several laboratories including our own have highlighted the role of genomic complexity in cancer drug resistance. To explore this, we have developed genomically complex fly models of cancer (colorectal, thyroid, breast, lung) and rare genetic diseases (primarily RASopathies). These act as a starting point for our work in mammalian models, both directly and with our collaborators.

Each personalised fly 'avatar' line models a different patient, each with typically 5-15 altered genes. While targeted therapies are effective in '2-hit' models, 12-hit models—even with many of the same cancer drivers—are often resistant to these same therapies.

We are leveraging our fly platform containing dozens of avatar lines to explore changes in transformation that come with genomic complexity. This has led to an ongoing 'fly-to-bedside' clinical trial in which 'personalised fly avatars' are used to identify therapeutic cocktails unique to each patient.

Further, we are working with chemists to address disease complexity through drug cocktails and through building a new generation of 'network-based' novel lead compounds that address tumour and rare disease complexity through multi-targeted 'polypharmacology'.

 Other funding:




Remarkable cancer cell metabolic flexibility and plasticity enable tumours to grow and combat chemotherapy. Mitochondria are essential organelles that support tumour adaptation to altered metabolic demands and environmental challenges. Accordingly, mitochondrial form and function are dynamically reprogrammed during tumorigenesis. For instance, the levels of key mitochondrial inner membrane proteins, including metabolite transporters, are fine tuned in response to nutrient and oxygen availability to support cancer cell proliferation and survival.

Metabolite transporter proteins are required to exchange small molecules including amino acids and nucleotides between the mitochondria and the rest of the cell. The tightly regulated coupling of cytosolic and mitochondrial metabolic reactions across the inner mitochondrial membrane represents an essential but poorly understood facet of tumour metabolism. Our goal is to identify mitochondrial metabolite transporters that control cancer progression using genetic screening approaches in 3D tumour models combined with genetically engineered mouse models. We will also investigate how regulated mitochondrial nucleotide transport and metabolism contribute to tumorigenesis and cancer cell responses to nucleotide-analogue chemotherapy. These studies will improve our basic understanding of mitochondrial reprogramming in tumours and may identify novel therapeutic targets for cancers that depend on metabolic flexibility and plasticity, including pancreatic cancer.


Cowling Vicky 2021

In every human cell, the expression of 25,000 genes is precisely regulated to generate the spectrum of cell types required through development and into the adult. We are interested in the signalling pathways that coordinate and regulate gene expression, and how dysregulation of these pathways is a cause or consequence of disease. Our aim is to understand how gene expression is regulated in health and disease, and to use this knowledge to develop and refine therapeutic approaches.

Our focus is on the RNA cap, a structure found on pre-mRNA and non-coding RNA that protects RNA and recruits factors involved in processing and translation. A series of RNA capping enzymes catalyses cap formation, predominantly as the transcript is being synthesised. We are interested in how these RNA capping enzymes are regulated during development and in the adult, and the impact that this has on gene expression. Currently, we are investigating RNA cap regulation in embryonic stem cell differentiation, during T cell activation and following oncogene dysregulation in cancer models.

Regulation of the RNA cap can have potent effects on cell function and fate decisions via the regulation of specific gene families. We characterise the biochemical configuration of capping enzyme complexes in different cell types or disease states, follow how these configurations change during differentiation and disease, and determine the impact on gene expression and cell function and fate decisions.

Other funding:
LOGO ERC 2020                                Wellcome Trust logo                                      UKRI MR Council-Logo Horiz-RGB
                              ChineseScholarship logo                                    Royal Society logo    



Maslowski croppedNew therapies that target immune responses to kill tumours are an area of rapid growth and hope. While immune checkpoint blockade therapy has led to dramatic improvement for some patients, it still is not applicable for the majority of people affected by cancer. Challenges for immune therapies include poor immune infiltration of tumours, an inhibitory tumour microenvironment as well as immune-related toxicities.

The immune system protects us from infectious agents such as bacteria, viruses and fungi, as well as from malignant growth of our own tissues. Our lab is interested in the intersection between anti-bacterial and anti-tumour responses. Our bodies have both positive (commensals) and negative (pathogenic) interactions with bacteria. On the one hand, microbes that form our gut microbiota are important for instructing and regulating our immune system; While on the other, pathogenic or opportunistic microbes can deviate and manipulate our immune responses to aid their survival and spread, and even be involved in pro-tumourigenic processes.

The concept of bacterial cancer therapy dates to William Coley, who developed ‘Coley’s toxins’, a preparation of heat killed bacteria injected into tumours. Our work largely focuses on the use of live-attenuated Salmonella as a cancer therapy; we are dissecting the mechanisms by which attenuated Salmonella treatment leads to tumour regression, looking at the adaptation of the bacteria to the tumour environment, and the effects on cancer cells and on immune responses. With a detailed mechanistic understanding of bacterial therapy, we aim to achieve optimal engineering of Salmonella to advance towards clinical application.


Diamantopoulou headshot 2023 cropped

The recent development of liquid biopsies has opened up new directions for monitoring the progression of cancer and the formation of metastasis, bringing us one step closer to effective personalised therapies. Despite these remarkable breakthroughs, metastasis remains the leading cause of cancer-related deaths. Therefore, it is of great significance to investigate the biology of metastasis and identify the critical steps and factors that need to be targeted in order to successfully develop efficient anti-metastatic treatments.

Our work broadly aims to understand how metastasis is regulated by the circadian rhythm. We particularly focus on a very rare cancer cell population that escapes from the primary tumour and spreads throughout the body via the bloodstream to establish new tumours in different locations, named Circulating Tumour Cells (CTCs). We are interested in the circadian rhythm as it has an intriguing role during cancer development and progression. While several studies have shown that the disruption of the circadian rhythm and the resulting misalignment of sleep-wake cycles promote tumour growth, our recent ground-breaking discovery indicates that the metastatic spread of breast cancer occurs during sleep. To further explore how the circadian rhythm drives metastasis, we focus on in vivo mouse models and we employ cutting edge microfluidics and robotic technologies, genetic engineering, next generation sequencing and in vivo imaging systems. We also analyse blood samples from cancer patients to identify circadian rhythm-related molecular vulnerabilities that could be used for the development of novel therapies. Finally, we explore chronotherapy to develop new approaches to drug administration that could be beneficial to cancer patients.


Fu headshot 2023

Complex and dynamic interactions between cancer cells and elements of the tumour microenvironment (TME) underlie tumour development and contribute to therapy resistance. Facilitated by multiplex imaging and spatial omics data, architectural features of the TME organisation associated with clinical outcomes have been characterised in various types of solid tumours. One example is immune exclusion, where T lymphocytes are spatially excluded from tumour nests, limiting the effectiveness of immune checkpoint blockade-based immunotherapy. How clinically relevant TME architecture develops dynamically and how altering cellular properties and behaviours can re-sculpt TME organisation in favour of therapy response is less well established. We aim to gain insight into the dynamic delineation of, and the mechanistic basis for, clinically relevant TME organisation.

We focus on developing computational methods to map spatial features of the TME and deconstruct principles underlying the TME organisation. We are interested in a variety of approaches, including:

  • Mechanistic models and computer simulations to investigate dynamic delineation of the TME organisation, such as sculpting of tumour/stroma architecture and spatial distribution of immune cells
  • Quantitative analysis of molecular and spatial tumour data to characterise architectural features of the TME organisation, such as cell communities and neighbourhoods
  • Machine learning frameworks to infer cellular and molecular mechanisms underpinning characteristic TME architectures.

We collaborate closely with experimental and clinical research groups. In application of our computational methods to spatial and molecular data of various solid tumours, including colorectal and pancreatic cancers, our goals are to discover novel spatial TME features associated with clinical outcomes and to identify cellular and molecular mechanisms for re-sculpting TME organisation in favour of therapy response and tumour elimination.