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Free for all myUEG account holders. Your access level is set automatically based on your occupation. Medical professionals get full access to all content. If you are a non-medical user, you can only access UEG Week content from congresses you attended.

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Introduction

Colorectal pinch biopsies may result in substantial histological artifacts in the form of tissue fragmentation, haemorrhage and large quantities of Muscularis Mucosa (MM) in the biopsy. Current digital Quality Control (QC) approaches on colorectal Whole Slide Images (WSIs) focus on laboratorial discrepancies and overlook quantifying the presence of such features that either confound or are irrelevant to routine scorings. Identifying these features can therefore aid in excluding inadequate slides or provide visual cues to guide histological assessment of inflammatory bowel disease (IBD). Accordingly, we built a deep learning system to identify muscularis mucosa (MM), blood, and tissue fragmentation in WSIs to streamline colorectal sample QC and the pathologist assessment process.

Aims & Methods

We trained Convolutional Neural Network (CNN) segmentation models for H&E images of bowel biopsies using 52 manually annotated WSIs, with 26 training WSIs (161 biopsy sections) and 26 testing WSIs (184 biopsy sections), developing clear-cut annotations for these features using a human-in-the-loop training paradigm. We exported 5,241 image-annotation training pairs (256*256 pixels) for MM and 3,743 for blood, applying augmentations before training a UNet++ CNN with an 80:20 split (training:validation). We implemented custom spatial postprocessing pipelines to harmonise predictions and improve overall accuracy.

Results

Our AI models accurately distinguished MM and blood in WSIs despite their similar appearance, and we quantified these relative to total tissue content in 129 patients with IBD. The MM model provided a useful visual reference for the identification of crypt shortfall and sample orientation, while the blood model helped identify sampling damage by flagging slides with high laminal blood content. We found MM accounted for 11.6% ± 10.9% of the biopsy section area across 594 WSIs. A significant presence of blood was also observed, primarily located in the lamina propria. We introduced a tissue fragmentation score and quantified it across 317 biopsies to determine areas of tissue which were damaged and showed its effectiveness as a metric for identifying degraded tissue sections.

Conclusion

Our tissue biopsy evaluation models accurately delineate MM and blood and quantify tissue fragmentation. By assessing key biopsy features often overlooked by other QC systems, our pipeline has the potential to offer valuable guidance, including re-cut recommendations, to enhance the evaluation of sample adequacy in IBD.

Disclosure

RL/DW/AM/PA/PW and CL are employees at Perspectum Ltd. EF and RG are consultants for Perspectum Ltd. All other co-authors have no conflicts of interest to declare relevant to this work.

AI MODELS FOR QC AND NON-MUCOSAL FEATURE DETECTION IN HISTOLOGICAL PINCH BIOPSIES OF INFLAMMATORY BOWEL DISEASE

Rongqi Li 1, Dylan Windell 1, Alastair Magness 1, Paul Aljabar 1, Eve Fryer 2, Robert D. Goldin 3, Phil Wakefield 1, Caitlin Langford 4, Jonathan Landy 5

1 Perspectum Ltd., Oxford, United Kingdom

2 John Radcliffe Hospital, Oxford, United Kingdom

3 Centre for Pathology, London, United Kingdom

4 Perspectum, Cambridge, United States

5 London North West University Healthcare NHS Trust, London, United Kingdom

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

The value of histology and ancillary tests (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Long-term outcome post-LTx in adults

Patrizia Burra 1

1 University of Padua-Multivisceral Transplant Unit- Gastroenterology, Padova, Italy

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Surgery

Session

New developments in liver transplantation

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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$Refractory ascites: Can we break a vicious cycle?$

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Refractory ascites: Can we break a vicious cycle?

Jonel Trebicka 1

1 Translational Hepatology - University Clinic Frankfurt, Frankfurt, Germany

Event

UEG Week Berlin 2025

Topics

Hepatobiliary

Session

ACLF and cirrhosis: Are we improving care?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Decompensated cirrhosis and limited care resources: Whom to transfer to ITU?

Andrea De Gottardi 1

1 Ente Ospedaliero Cantonale - Università della Svizzera Italiana, Lugano, Switzerland

Event

UEG Week Berlin 2025

Topics

Hepatobiliary

Session

ACLF and cirrhosis: Are we improving care?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

The adhesion G protein-coupled receptor F5 (ADGRF5) belongs to seven-transmembrane receptor family which action seems to be crucial for various cancers and immune response [1-3]. Nevertheless, limited efforts have been made to explore ADGRF5 significance in gastrointestinal cancers.

Aims & Methods

The aim of the study was to assess the significance of ADGRF5 for macrophages function and its impact on gastrointestinal cancer progression. Bone marrow of wild type (WT) and ADGRF5 knockout (KO) mice was used to isolate macrophage population employing differentiation medium. M1 and M2 macrophage phenotype was obtained by polarization of naïve macrophages with a mixture of lipopolysaccharide (LPS) with interferon γ (IFN-γ) and interleukin (IL) 4, respectively. Macrophage phenotype was confirmed using real-time PCR. In vivo studies employing MC38 and PK5L1940 cell-derived allograft murine model of colon and pancreas cancers, respectively, were performed. Multiplex analysis was used to explore secretome in media obtained from tumors.

Results

In murine model of colon cancer, animals with ADGRF5 KO developed significantly smaller tumors which was accompanied by enhanced secretion of macrophage-related cytokines (such as macrophage colony-stimulating factor) in colon tumors compared to WT animals. Ex vivo analysis revealed overexpression of IL-12, nitric oxidase synthase 2 and tumor necrosis factor α in M1 macrophages with ADGRF5 KO compared with WT macrophages under LPS with IFN-γ treatment. In contrast, lower expression of arginase 1 was noted in M2 macrophages with ADGRF5 KO compared with WT macrophages treated with IL-4. In vivo studies employing allograft model of colon and pancreas cancers revealed that the administration of ADGRF5 KO macrophages led to a reduction in tumor size when compared to WT macrophages.

Conclusion

Collectively, ADGRF5 appears to be crucial regulator of gastrointestinal cancer progression through regulating macrophage function. Our study also noted that ADGRF5 depletion reprograms macrophages into M1 phenotype which is responsible for anti-tumor activity.

References

[1] Jacenik D., Hikisz P., Beswick E.J., Fichna J. The clinical relevance of the adhesion G protein-coupled receptor F5 for human diseases and cancers. Biochim Biophys Acta Mol Basis Dis. 2023; 1869: 166683. doi:10.1016/j.bbadis.2023.166683
[2] Kubo F., Ariestanti D.M., Oki S., Fukuzawa T., Demizu R., Sato T., Sabirin R. M., Hirose S., Nakamura N. Loss of the adhesion G-protein coupled receptor ADGRF5 in mice induces airway inflammation and the expression of CCL2 in lung endothelial cells. Respir Res. 2019; 20: 11. doi:10.1186/s12931-019-0973-6
[3] Tang X., Jin R., Qu G., Wang X., Li Z., Yuan Z., Zhao C., Siwko S., Shi T., Wang P., Xiao J., Liu M., Luo J. GPR116, an adhesion G-protein-coupled receptor, promotes breast cancer metastasis via the Gαq-p63RhoGEF-Rho GTPase pathway. Cancer Res, 2013; 73: 6206–6218. doi:10.1158/0008-5472.CAN-13-1049

THE ADHESION G PROTEIN-COUPLED RECEPTOR F5 ALTERS MACROPHAGE ACTION AND REGULATES GASTROINTESTINAL CANCER PROGRESSION

Damian Jacenik 1, Marta Zielinska 2, Ellen J. Beswick 3, Jakub Fichna 2

1 University of Lodz, Lodz, Poland

2 Medical University of Lodz, Lodz, Poland

3 University of Kentucky, Lexington, United States

Conference

UEG Week Berlin 2025

Topics

Colorectal

Submission format

Abstract

Session

DDM SUMMIT (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn’s disease, is characterized by chronic intestinal inflammation linked to dysbiosis and impaired bile acid (BA) metabolism. Recent studies have underscored the pivotal role of the gut microbiota–BA axis in modulating intestinal immunity [1]. Disruptions in this axis, particularly reduced microbial conversion of primary to secondary BAs, have been implicated in the pathogenesis of IBD [2–4]. Probiotic interventions have emerged as promising strategies to restore microbial balance and modulate BA profiles. Some probiotic bacteria express enzymes that can modify bile acids thereby influencing BA receptor signaling pathways such as GPBAR1, FXR and receptors that have recently been identified as BA-binding receptors, such as RORγt [4–6]. Building upon this framework, our previous research demonstrated that specific microbial-derived BAs, notably 3-oxo-DCA, act as dual agonists for GPBAR1 and inverse agonists for RORγt, leading to reduced Th17-mediated inflammation in murine models of colitis [7]. These findings suggest that targeted modulation of the gut microbiota–BA axis via probiotic formulations could offer therapeutic benefits in IBD management.

Aims & Methods

To investigate the therapeutic potential of a novel multi-strain probiotic formulation in reducing colitis. For this purpose, we employed murine models of colitis induced in male C57BL/6 mice. In the acute colitis model, disease was induced by administering a 2% dextran sulfate sodium (DSS) solution in drinking water for 9 days. Chronic colitis was induced using three cycles of 1.5% DSS administration (1 week) followed by 15 days of water to mimic the exacerbation-remission phases of human IBD. The new probiotic formulation, named Vivomixx neo9®, was administered daily by gavage at 50 × 10^9 CFU/kg. Vivomixx neo9® included nine bacterial strains: Bifidobacterium animalis subsp. lactis, Bifidobacterium breve, Lactobacillus acidophilus, Lactobacillus paracasei, Lactobacillus plantarum, Lactobacillus rhamnosus (two distinct bacterial strains), Lactobacillus lactis, and Streptococcus thermophilus. Vivomixx®, a commercial probiotic, served as the control.

Results

Our data demonstrated that treatment with both probiotic strains effectively mitigated disease severity in both acute and chronic murine models of colitis. Furthermore, the novel probiotic formulation notably ameliorated colonic mucosal injury at both macroscopic and microscopic levels and decreased fibrosis indices. DSS administration induced severe gut dysbiosis, reflected by substantial alterations in intestinal microbiota composition and disrupted BA profiles. Specifically, fecal BA analysis revealed a pronounced dysregulation characterized by diminished secondary BA levels and an elevated primary-to-secondary BA ratio. Probiotic treatment effectively reversed these dysbiotic changes, restoring fecal BA profiles comparable to those observed in naive mice. Of particular interest, the novel multi-strain probiotic enhanced the generation of oxo- and allo-BA derivatives, recognized as dual agonists for GPBAR1 and inverse agonists for RORγt, regulators of innate and adaptive immune responses.

Conclusion

Our findings indicate that Vivomixx neo9® significantly reduces colitis severity through modulation of intestinal microbiota composition and normalization of fecal bile acid profiles. These results underscore the therapeutic promise of targeting microbiota–bile acid interplay as a supplementary approach in the clinical management of IBD.

References

[1] Pan Y, Zhang H, Li M, He T, Guo S, Zhu L, et al. Novel approaches in IBD therapy: targeting the gut microbiota-bile acid axis. Gut Microbes 2024;16:2356284. https://doi.org/10.1080/19490976.2024.2356284.
[2] Bai SH, Chandnani A, Cao S. Bile Acids in Inflammatory Bowel Disease: From Pathophysiology to Treatment. Biomedicines 2024;12. https://doi.org/10.3390/biomedicines12122910.
[3] Lavelle A, Sokol H. Gut microbiota-derived metabolites as key actors in inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 2020;17:223–37. https://doi.org/10.1038/s41575-019-0258-z.
[4] Biagioli M, Marchianò S, Carino A, Di Giorgio C, Santucci L, Distrutti E, et al. Bile Acids Activated Receptors in Inflammatory Bowel Disease. Cells 2021;10:1281. https://doi.org/10.3390/cells10061281.
[5] Fiorucci S, Carino A, Baldoni M, Santucci L, Costanzi E, Graziosi L, et al. Bile Acid Signaling in Inflammatory Bowel Diseases. Dig Dis Sci 2021;66:674–93. https://doi.org/10.1007/s10620-020-06715-3.
[6] Paik D, Yao L, Zhang Y, Bae S, D’Agostino GD, Zhang M, et al. Human gut bacteria produce Τ(Η)17-modulating bile acid metabolites. Nature 2022;603:907–12. https://doi.org/10.1038/s41586-022-04480-z.
[7] Biagioli M, Di Giorgio C, Massa C, Marchianò S, Bellini R, Bordoni M, et al. Microbial-derived bile acid reverses inflammation in IBD via GPBAR1 agonism and RORγt inverse agonism. Biomed Pharmacother 2024;181:117731. https://doi.org/10.1016/j.biopha.2024.117731.

PROBIOTIC FORMULATION MITIGATES MURINE COLITIS SEVERITY THROUGH MODULATION OF THE INTESTINAL MICROBIOTA-BILE ACID AXIS

Michele Biagioli 1, Cristina Di Giorgio 1, Silvia Marchianò 1, Carmen Massa 1, Ginevra Lachi 1, Eleonora Giannelli 1, Ginevra Urbani 1, Benedetta Sensini 1, Francesca Paniconi 1, Maria Rosaria Sette 1, Elva Morretta 2, Maria Chiara Monti 3, Angela Zampella 3, Stefano Fiorucci 1

1 University of Perugia, Perugia, Italy

2 University of Naples, Federico II, Naples, Italy|||University of Salerno, Salerno, Italy

3 University of Naples, Federico II, Naples, Italy

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

DDM SUMMIT (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome caused by mutations in the APC gene, a negative regulator of the Wnt signaling pathway. It is characterized by the development of hundreds to thousands of Wnt-driven adenomatous polyps in the colon. To prevent the inevitable progression to colorectal cancer, patients with FAP typically undergo total proctocolectomy in early adulthood. Currently, no effective medical therapy exists for FAP. Casein kinase I alpha (CKIα), another negative regulator of Wnt signaling, has emerged as a potential therapeutic target. Prior work in our lab demonstrated that, unlike APC loss, epithelial deletion of Csnk1a1 (CKIα) in the gut does not induce tumorigenesis. Instead, it activates a non-canonical DNA damage response, leading to robust p53 stabilization and suppression of tumorigenic changes. Given that TP53 mutations are typically late events in the adenoma–carcinoma sequence, early-stage lesions in FAP often retain wild-type p53. Unlike sporadic adenomas, which can be resected during colonoscopy, the high polyp burden in FAP precludes endoscopic management, underscoring the need for effective chemoprevention.

Aims & Methods

Our aim in this work was to investigated CKIα as a therapeutic target in preclinical models of FAP.
We employed Csnk1a1^fl/fl, APC^fl/fl, Villin-CreERT2, and CDX2-CreERT2 transgenic mice for in vivo studies, with tamoxifen-inducible gene ablation. Intestinal organoids derived from normal and tumor tissues were used for ex vivo experiments.

Results

In vivo, simultaneous deletion of APC and CKIα in intestinal epithelium did not further enhance Wnt target gene expression compared to APC loss alone. Instead, dual knockout (DKO) stabilized p53, promoted apoptosis, and blocked the dysplastic progression normally observed in APC-deficient gut tissue. In organoid models, treatment with the novel CKIα degrader BTX1050 selectively inhibited tumor-derived organoid proliferation, but did not fully eliminate tumor-initiating cells. We therefore tested A51, a dual CKIα and CDK7/9 inhibitor developed in our lab, which both stabilized and activated p53 and suppressed transcription of super-enhancer-driven oncogenes. A51 treatment significantly downregulated Myc and Mcl1, increased apoptosis in tumor organoids, but only partially suppressed tumor growth in vivo. Notably, A51 induced MAPK pathway activation, as indicated by increased pERK levels. This prompted combination therapy with A51 and the MEK inhibitor trametinib, which demonstrated potent synergistic anti-tumor activity in both organoid and mouse models.

Conclusion

CKIα depletion exerts anti-tumor effects in intestinal tumor models with wild-type p53. Our findings support the combination of A51 and MEK inhibition as a promising "chemical polypectomy" approach for FAP patients.

Disclosure

n/a

TARGETING CKIΑ AND MAPK PATHWAYS AS A “CHEMICAL POLYPECTOMY” IN FAMILIAL ADENOMATOUS POLYPOSIS

Adar Zinger 1, Maitraiy Humaney 2, Irit Snir-Alkalay 2, Yinon Ben-Neriah 2

1 Hadassah Medical Center, Jerusalem, Israel

2 The Hebrew University, Jerusalem, Israel

Conference

UEG Week Berlin 2025

Topics

Colorectal

Submission format

Abstract

Session

DDM SUMMIT (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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