Conference
European Society for Spatial Biology Annual Meeting
Spatial Biology - The Melting Pot
Book a meeting with us onsiteOctober 14 - 17
Heidelberg
Booth F06
Breaking barriers in spatial multiomics
Join us in Heidelberg for the 2nd European Society for Spatial Biology Annual Meeting!
Discover spatial multiomics on COMET™ by engaging directly with expert scientists. Experience firsthand how you can simultaneously detect RNA and protein markers within the same tissue section, all at a subcellular resolution.
Our protease-free, fully–automated workflow enables multiomics scalability for all stages of research. Discover more by browsing the posters and presentations below, scheduling a one-click meeting, or visiting the Lunaphore booth to explore real multi-omics images.
Discover COMET™ data
Poster Presentations
October 15
17:00 - 18:30
Poster #131
Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the UK, with rectal cancer accounting for over a quarter of CRC cases. Although radiotherapy (RT) is a cornerstone of treatment, response variability remains a significant clinical challenge.
In this study, we identified significant activation of JAK/STAT3 signalling following RT in a rectal cancer cell line using Phospho-Kinase Proteome Profiling and bulk RNA sequencing. This was validated in a cohort of rectal cancer biopsies sequentially collected pre- and post-RT (n=29). Bulk RNASeq analysis revealed consistent upregulation of the IL6/JAK/STAT3 pathway and STAT3 gene expression (p<0.001) across all time points. In a retrospective rectal cancer cohort (n=173), elevated pSTAT3 expression correlated with reduced cancer-specific survival (p=0.046), highlighting the potential of targeting this pathway to improve RT responses.
However, recent studies have highlighted the cell type-specific roles of inflammatory signalling within the tumour microenvironment (TME) may present a major barrier to clinical translation. Using a mini-multiplex immunofluorescence on a prospective rectal cancer biopsy cohort, we observed that RT-induced JAK/STAT signalling was initially activated in the immune compartment, particularly in macrophages, before transducing into the tumour epithelial compartment. GeoMxTM Spatial Profiling further revealed that expression of IL6 and LIF, two key JAK ligands, was highly enriched in the TME of pSTAT3-high versus pSTAT3-low patients. These transcriptomic findings were validated by sequential immunofluorescence (seqIF™) with the SPYRE™ IO panel and pSTAT3 staining on the COMET™ platform, which enabled detailed spatial analysis of tumour–immune interactions underlying RT response.
Collectively, this multi-omics approach maps the RT-induced dynamics of JAK/STAT3 signalling within the TME, suggesting that selectively targeting STAT3 in tumour-associated macrophages may offer a promising radiosensitising strategy in rectal cancer.
Speaker
Guang-Yu Lian, Ph.D.
Wolfson Wohl Cancer Research Centre, School of Cancer Sciences, College of Medical, Veterinary and Life Sciences
17:00 - 18:30
Poster #145
Background
Systemic inflammation has a long-established link with colorectal cancer (CRC). The central regulator of inflammation, NFkB, is governed by two kinases: IKKa and IKKb. Efforts to target IKKb for inhibition have been unsuccessful in clinical trial due to its vital role in maintaining normal cellular function. We hypothesize IKKa is an attractive target in CRC because of its central role in regulating inflammation and reduced toxicity. This study investigates the role of IKKa in CRC patient outcome and if the kinase can be targeted for therapeutic intervention.
Methods
A cohort of 787 stage I-III CRC patients were stained for IKKa and IKKb using immunohistochemistry (IHC), and weighted histoscores were assessed. Spatial transcriptomics, GeoMXTM Nanostring, was utilised in the same cohort to investigate transcriptomic differences between IKKa and IKKb high/low expressing protein groups. Transcriptomic results were validated using sequential immunofluorescence (seqIF™, 20-plex) staining by COMETTM Lunaphore platform, together with the SPYRE IO core panel. Patient derived explants (PDEs) were established and treated with 1mM fluorouracil (5FU) or 1mM SU1644 (novel 1st-in class IKKa inhibitor), and tissue sections were stained using bespoke NFkB focused seqIF™ panels.
Results
Patients with IKKa high, IKKβ low expressing tumours had the poorest cancer specific survival (p=0.017), whereas IKKa low, IKKb high expressing tumours had the best patient outcome (p=0.001). At a transcriptomic level, a metabolic shift promoting pro-metastatic signaling, denoted by hallmark cholesterol homeostatic gene-set (p<0.05), was observed in pan-cytokeratin+ segments in the IKKa high patient group (previously determined from chromogenic IHC). This was validated at a protein level using bespoke seqIFTM NFkB panels, examining expression of key targets such as Cyclin D1. In PDE tissue treated with SU1644 and 5FU, analysis demonstrated a reduction of Ki67 upon treatment of SU1644, in a PDE case where 5FU did not impact Ki67 expression (p>0.001).
Conclusions
IKKa high, IKKb low expressing tumours are associated with poor patient outcome when compared to IKKa low, IKKb high tumours. Transcriptomic results suggest that high IKKa tumours undergo a metabolic shift that may facilitate metastasis. Inhibition of IKKa by SU1644 can reduce Ki67 expression in a recapitulative tissue model, indicating IKKa may represent a potential therapeutic target for chemoresistant CRC.
Speaker
Phimmada Hatthakarnkul, Ph.D.
Research Assistant, Edwards Lab
University of Glasgow
Lunch Symposium
October 16
October 16
12:30 - 1:30 PM
This talk features Lunaphore’s end-to-end solutions for spatial biology and highlights the application of these tools in Prof. Edwards’ research.
Abnormal Wnt signalling drives epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC)., but its spatial dynamics in premalignant polyps and CRC remain poorly defined.
We profiled EMT and immune–stromal features across two cohorts: premalignant polyps (n=1256) and CRC resections (n=787, stage I–IV). Wnt pathway proteins (E-cadherin, β-catenin, SOX9) were evaluated by IHC. GSEA was used for pathway enrichment using Temp-O-Seq® transcriptomics. High-plex sequential immunofluorescence (seqIF™) was performed on COMET™ (Lunaphore) using EMT and the SPYRE™ Immuno-Oncology panel. HORIZON™ supported unsupervised single-cell clustering and Visiopharm was applied for cell-type quantification and neighbourhood mapping.
In CRC, low membranous E-cadherin, high nuclear β-catenin, and high SOX9 were each associated with worse cancer-specific survival (p=0.04, p=0.05, and p=0.023, respectively). β -catenin-high tumours displayed transcriptomic enrichment for EMT, TGF-β, and MYC targets_V1, alongside downregulation of IFN-γ/IFN-α and inflammatory pathways. Pilot COMET™ analysis (polyps n=43; CRC n=64) distinguished stromal from epithelial compartments. Epithelial cells formed 18 clusters in polyps versus 22 in CRC, reflecting increased tumour heterogeneity. In polyps, over 70% of epithelial cells were E-cad⁺/β-cat⁺/SOX9⁺, with dominant clusters Snail⁺ (43%) and Snail⁻ (29%). In CRC, these populations formed 12% and 14%, respectively whereas an E-cad⁻/β-cat⁺/SOX9⁺/Snail⁻ cluster significantly increased (8% vs 0.4%), consistent with activated Wnt signalling. CRC tissues also showed higher CD4, CD8, CD11c, and stromal fractions (all p<0.001). Neighbourhood analysis revealed reduced ZEB1-rich stroma adjacent to Snail⁺ epithelium.
Spatial seqIF™ on COMET™ highlights early EMT-immune crosstalk and identifies epithelial-stromal features distinguishing benign polyps from CRC. Ongoing validation across the full INCISE/CRC cohorts aims to deliver spatially informed risk stratification for surveillance and nominate rational therapeutic strategies, such as EMT inhibition combined with immunotherapy, for future trials.
Speakers
Prof. Joanne Edwards
Professor of Translational Cancer Pathology
School of Cancer Sciences, University of Glasgow
Joanne is an translational cancer research scientist with over 220 publications, more than 19,000 citations and an H-index of 72. Her research spans multiple solid tumour types and she has developed unique patient tissue cohorts with extensive linked clinical data. These resources have underpinned her international reputation for the discovery and validation of biomarkers that inform personalised cancer treatment. Joanne’s innovative approach combined traditional histopathology with cutting-edge technologies including AI computational pathology, genomics, transcriptomics, spatial biology and novel human model systems such as tissue explants, patient-derived organoids and co-culture models. These methodologies have enabled the development of predictive and prognostic biomarkers and have directly contributed to translational outputs that impact clinical settings. Despite being a non-clinical scientist, the impact of Joanne’s research has been recognised by election as a Fellow of the Royal College of Pathologists.
Joanne leads the Translational Cancer Pathology Group, a multidisciplinary team of 30 members including scientists, surgeons, oncologists and pathologists. Since 2007, she has supervised 28 PhD students, 9 MD students, 27 research assistant/associates and 15 technical staff. She is committed to fostering an inclusive and collaborative environment that supports the professional growth and wellbeing of all team members, with the School of Cancer Sciences recently recognised for its inclusive research culture by the award of a Gold Athena Swan Charter.
Joanne holds several key leadership roles, including CRC lead for the CRUK Scotland Centre, Board of Trustees and Treasurer for British Association of Cancer Research, Director of Education for the School of Cancer Sciences, where she chairs the Learning and Teaching Committee, contributes to the School’s Management and Research Strategy Boards and sits on the College Education Strategy Board. Her influence extends internationally through her role in establishing a joint PhD programme between the University of Glasgow and Mahidol University, Thailand, where she is an Associate Professor.
Joanne is an active and engaged member of the national and international research community. She co-chairs strategic and tissue access committees for key translational programmes such as TransSCOT and PRIME-RT. She is a member of the leadership team for the Cancer Research UK Scotland Experimental Cancer Medicine Centre and co-leads the Cancer Research UK Scotland Centre’s Colorectal Cancer Theme. She is also a member of and on the management board for the national CRUK collaborative Colorectal Cancer-Stratification of Therapies through Adaptive Responses (CRC-STARS). She also sits on the Scientific Advisory Board for the NHS Greater Glasgow and Clyde Biorepository.
Joanne has served on grant and interview panels for organisations including the French Institute of Cancer, Prostate Cancer Canada, the AICR Foundation (Italy) and the Irish Cancer Society. Joanne has also chaired the Clinical and Translational Research Panel for the Biochemical Society and served on their Board of Trustees (2018-2022).
Joanne’s editorial contributions include serving on the boards of Pathology and Clinical Research (2020-2023) and Cellular Signalling (2020-present). Joanne is a trustee and current Honorary Treasurer for the British Association of Cancer Research, having previously sat on their Executive Committee.
Joanne has been invited to provide expert commentary across media platforms including radio (e.g., BBC Radio Scotland), television (e.g., BBC Scotland) and the press (e.g., Holyrood magazine). She has also been invited to speak at Scottish Government events to share insights on cancer research and healthcare policy.
Under her leadership as Director of the Glasgow Tissue Research Facility (GTRF), the GTRF are actively working towards GCLP accreditation, anticipated by the end of the year, which will expand its capabilities to support a range of studies.
Joanne is committed to ensuring that her team’s research delivers meaningful impact for patients and the public. She was integral in establishing the Glasgow Colorectal Patient and Public Involvement and Engagement (PPIE) Group, which brings together patients, carers, clinicians and researchers to shape colorectal cancer research based on lived experience and public priorities.
Bastian Nicolai, M.Sc.
Product Manager
Lunaphore
He is a molecular biotechnologist and holds an M.Sc. from the RWTH Aachen University. After more than seven years in the life science arena, joining companies focusing on immunology, immuno-oncology, and nucleic acid sample and assay technologies, Bastian is now the Product Manager at Lunaphore Technologies SA, concentrating on the applications portfolio for the spatial biology platforms COMET™ and LabSat®.
Poster Presentations
October 15
17:00 - 18:30
Poster #131
Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the UK, with rectal cancer accounting for over a quarter of CRC cases. Although radiotherapy (RT) is a cornerstone of treatment, response variability remains a significant clinical challenge.
In this study, we identified significant activation of JAK/STAT3 signalling following RT in a rectal cancer cell line using Phospho-Kinase Proteome Profiling and bulk RNA sequencing. This was validated in a cohort of rectal cancer biopsies sequentially collected pre- and post-RT (n=29). Bulk RNASeq analysis revealed consistent upregulation of the IL6/JAK/STAT3 pathway and STAT3 gene expression (p<0.001) across all time points. In a retrospective rectal cancer cohort (n=173), elevated pSTAT3 expression correlated with reduced cancer-specific survival (p=0.046), highlighting the potential of targeting this pathway to improve RT responses.
However, recent studies have highlighted the cell type-specific roles of inflammatory signalling within the tumour microenvironment (TME) may present a major barrier to clinical translation. Using a mini-multiplex immunofluorescence on a prospective rectal cancer biopsy cohort, we observed that RT-induced JAK/STAT signalling was initially activated in the immune compartment, particularly in macrophages, before transducing into the tumour epithelial compartment. GeoMxTM Spatial Profiling further revealed that expression of IL6 and LIF, two key JAK ligands, was highly enriched in the TME of pSTAT3-high versus pSTAT3-low patients. These transcriptomic findings were validated by sequential immunofluorescence (seqIF™) with the SPYRE™ IO panel and pSTAT3 staining on the COMET™ platform, which enabled detailed spatial analysis of tumour–immune interactions underlying RT response.
Collectively, this multi-omics approach maps the RT-induced dynamics of JAK/STAT3 signalling within the TME, suggesting that selectively targeting STAT3 in tumour-associated macrophages may offer a promising radiosensitising strategy in rectal cancer.
Speaker
Guang-Yu Lian, Ph.D.
Wolfson Wohl Cancer Research Centre, School of Cancer Sciences, College of Medical, Veterinary and Life Sciences
17:00 - 18:30
Poster #145
Background
Systemic inflammation has a long-established link with colorectal cancer (CRC). The central regulator of inflammation, NFkB, is governed by two kinases: IKKa and IKKb. Efforts to target IKKb for inhibition have been unsuccessful in clinical trial due to its vital role in maintaining normal cellular function. We hypothesize IKKa is an attractive target in CRC because of its central role in regulating inflammation and reduced toxicity. This study investigates the role of IKKa in CRC patient outcome and if the kinase can be targeted for therapeutic intervention.
Methods
A cohort of 787 stage I-III CRC patients were stained for IKKa and IKKb using immunohistochemistry (IHC), and weighted histoscores were assessed. Spatial transcriptomics, GeoMXTM Nanostring, was utilised in the same cohort to investigate transcriptomic differences between IKKa and IKKb high/low expressing protein groups. Transcriptomic results were validated using sequential immunofluorescence (seqIF™, 20-plex) staining by COMETTM Lunaphore platform, together with the SPYRE IO core panel. Patient derived explants (PDEs) were established and treated with 1mM fluorouracil (5FU) or 1mM SU1644 (novel 1st-in class IKKa inhibitor), and tissue sections were stained using bespoke NFkB focused seqIF™ panels.
Results
Patients with IKKa high, IKKβ low expressing tumours had the poorest cancer specific survival (p=0.017), whereas IKKa low, IKKb high expressing tumours had the best patient outcome (p=0.001). At a transcriptomic level, a metabolic shift promoting pro-metastatic signaling, denoted by hallmark cholesterol homeostatic gene-set (p<0.05), was observed in pan-cytokeratin+ segments in the IKKa high patient group (previously determined from chromogenic IHC). This was validated at a protein level using bespoke seqIFTM NFkB panels, examining expression of key targets such as Cyclin D1. In PDE tissue treated with SU1644 and 5FU, analysis demonstrated a reduction of Ki67 upon treatment of SU1644, in a PDE case where 5FU did not impact Ki67 expression (p>0.001).
Conclusions
IKKa high, IKKb low expressing tumours are associated with poor patient outcome when compared to IKKa low, IKKb high tumours. Transcriptomic results suggest that high IKKa tumours undergo a metabolic shift that may facilitate metastasis. Inhibition of IKKa by SU1644 can reduce Ki67 expression in a recapitulative tissue model, indicating IKKa may represent a potential therapeutic target for chemoresistant CRC.
Speaker
Phimmada Hatthakarnkul, Ph.D.
Research Assistant, Edwards Lab
University of Glasgow
Lunch Symposium
October 16
October 16
12:30 - 1:30 PM
This talk features Lunaphore’s end-to-end solutions for spatial biology and highlights the application of these tools in Prof. Edwards’ research.
Abnormal Wnt signalling drives epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC)., but its spatial dynamics in premalignant polyps and CRC remain poorly defined.
We profiled EMT and immune–stromal features across two cohorts: premalignant polyps (n=1256) and CRC resections (n=787, stage I–IV). Wnt pathway proteins (E-cadherin, β-catenin, SOX9) were evaluated by IHC. GSEA was used for pathway enrichment using Temp-O-Seq® transcriptomics. High-plex sequential immunofluorescence (seqIF™) was performed on COMET™ (Lunaphore) using EMT and the SPYRE™ Immuno-Oncology panel. HORIZON™ supported unsupervised single-cell clustering and Visiopharm was applied for cell-type quantification and neighbourhood mapping.
In CRC, low membranous E-cadherin, high nuclear β-catenin, and high SOX9 were each associated with worse cancer-specific survival (p=0.04, p=0.05, and p=0.023, respectively). β -catenin-high tumours displayed transcriptomic enrichment for EMT, TGF-β, and MYC targets_V1, alongside downregulation of IFN-γ/IFN-α and inflammatory pathways. Pilot COMET™ analysis (polyps n=43; CRC n=64) distinguished stromal from epithelial compartments. Epithelial cells formed 18 clusters in polyps versus 22 in CRC, reflecting increased tumour heterogeneity. In polyps, over 70% of epithelial cells were E-cad⁺/β-cat⁺/SOX9⁺, with dominant clusters Snail⁺ (43%) and Snail⁻ (29%). In CRC, these populations formed 12% and 14%, respectively whereas an E-cad⁻/β-cat⁺/SOX9⁺/Snail⁻ cluster significantly increased (8% vs 0.4%), consistent with activated Wnt signalling. CRC tissues also showed higher CD4, CD8, CD11c, and stromal fractions (all p<0.001). Neighbourhood analysis revealed reduced ZEB1-rich stroma adjacent to Snail⁺ epithelium.
Spatial seqIF™ on COMET™ highlights early EMT-immune crosstalk and identifies epithelial-stromal features distinguishing benign polyps from CRC. Ongoing validation across the full INCISE/CRC cohorts aims to deliver spatially informed risk stratification for surveillance and nominate rational therapeutic strategies, such as EMT inhibition combined with immunotherapy, for future trials.
Speakers
Prof. Joanne Edwards
Professor of Translational Cancer Pathology
School of Cancer Sciences, University of Glasgow
Bastian Nicolai, M.Sc.
Product Manager
Lunaphore