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Introduction

Gastric cancer is a common malignancy worldwide. Gastric cardia cancer (GCC) is a type of gastric cancer. The Transgelin(TAGLN) is a protein that has been indicated to discriminate progression in some tumors. Tumor angiogenesis is a hallmark of cancer and is involved in the tumorigenesis of solid tumors. However, the role of TAGLN in Gastric cardia cancer and tumor angiogenesis remains unknown.

Aims & Methods

The gene expression profile of TAGLN and their corresponding clinical data were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The expression of TAGLN in GCC and non-cancerous tissue was detected by immunohistochemical staining. The correlation between TAGLN level and the survival rate of GCC patients was assessed. The TAGLN overexpression or knockdown model was constructed to evaluate its role in GC cell proliferation, migration, invasion, and angiogenesis. HUVECs were co-cultured with the conditioned medium of GC cells. A tubule formation experiment was done to examine the angiogenesis of endothelial cells. A series of in vivo experiments were conducted to help reveal the mechanisms of TAGLN in GCC.

Results

TAGLN was identified as a key risk gene in the TCGA dataset. TAGLN expression was higher in GCC tissues than in non-tumor tissues and was positively correlated with poor prognosis. TAGLN overexpression or knockdown could facilitate or inhibit the migration, invasion, proliferation, and angiogenesis of GC cells. Finally, depletion of TAGLN inhibited tumor growth in a xenograft mouse model.

Conclusion

The study highlights that TAGLN can accelerate Gastric cardia cancer progression and angiogenesis and may hold promise as a potential prognosis biomarker for the diagnosis of GCC, which can be a novel therapeutic strategy against GCC.

TRANSGELIN ACCELERATE GASTRIC CARDIA CANCER PROGRESSION AND ANGIOGENESISAS AND SERVE AS A POTENTIAL PROGNOSTIC BIOMARKER

qian ding 1, boli yang 2, Xiangxu Kong 1, Wenli Duan 1, Weilong Zhong 1, Wentian Liu 1

1 Tianjin Medical University General Hospital, Tianjin, China

2 Jincheng People's Hospital, jincheng, China

Conference

UEG Week Copenhagen 2023

Topics

Oesophagus

Submission format

Abstract

Session

PP 01 Oesophageal, gastric and duodenal disorders (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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THE EXTRACELLULAR MATRIX PROTEIN EMILIN-1 IMPACTS ON THE MICROENVIRONMENT BY HAMPERING THE DEVELOPMENT AND PROGRESSION OF GASTRIC CANCER

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Introduction

The contribution of the tumor microenvironment and extracellular matrix to the aggressive biology of Gastric Cancer (GC) has been recently characterized (1). During GC progression striking changes in the lymphatic vessels (LVs) occur and lymphatic metastasis is the commonest feature of GC spread, representing the most significant prognostic factor determining the clinical outcomes (2). Recent evidence supporting a functional link among EMILIN-1, an Extra Cellular Matrix component (ECM), tumour growth and lymph-angiogenesis has been provided. EMILIN-1 represents a key structural element in the maintenance and function of LVs and displays anti-proliferative effects through the interaction with α4β1 integrin, as demonstrated in skin and colon cancer (3,4,5). Interestingly, α4 integrin is transcriptionally repressed in GC, but not in the normal gastric epithelium (7), suggesting a crucial mechanism exerted by the integrin/EMILIN1 recognition also in this context.

Aims & Methods

The aim of this study is to analyze the possible role of EMILIN-1 as a molecular regulator in in the context of GC development and progression.
We performed Immunofluorescence staining of human gastric biopsy samples from normal and neoplastic tissues collected during the endoscopy procedures. Biopsies from pre-malignant lesions were also included. For in vivo experiments, we used the syngeneic YTN16 gastric cancer cell line (7) which was injected subcutaneously and intraperitoneally in genetically modified EMILIN-1 mice. In alternative, carcinogenesis was induced in mice using N-methyl-N-nitrosourea (MNU). GES-1 (normal stomach mucosa), and several GC cell lines representative of different GC stages and histotypes (i.e. AGS, Hs746.T, NCI-N87 and KATO-III) were employed for in vitro experiments.

Results

EMILIN-1 is diffusely deposited in normal gastric mucosa and is significantly decreased in malignant and pre-neoplastic samples; this finding correlates with the presence of aberrant LVs. EMILIN-1 mutant mice (knock out and E955A knock in) developed tumors earlier compared to WT animals: 20 days post-injection of YTN16 cells, tumors developed in EMILIN-1 mutant mice were larger and displayed a significant increase of lymphangiogenesis. Treatment of transgenic mice with MNU associated with an increased number of tumors, exacerbated aggressive lesions and higher levels of LV abnormalities.
To unveil the main mechanisms responsible for EMILIN-1 reduction we treated in vitro fibroblasts and LECs (the major cellular sources of EMILIN1 in the gastric microenvironment) with conditioned media derived from GC cells lines; dramatic effects on EMILIN1 expression were observed, both at the mRNA and protein levels. Small-RNAseq analysis on culture media allowed us to identify miR125a-5p as a possible molecular regulator of EMILIN-1 levels in this context.

Conclusion

This study demonstrates for the first time that loss of EMILIN-1 in GC leads to lymphatic dysfunction and proliferative advantages that sustain tumorigenesis, and assess the use of our animal model as a valuable tool to verify the fate of GC upon loss of EMILIN-1.

References

1. Rojas A, Araya P, Gonzalez I, Morales E. Gastric Tumor Microenvironment. Adv Exp Med Biol. 2020;1226:23–35.8
2. Deng J-Y, Liang H. Clinical significance of lymph node metastasis in gastric cancer. World J Gastroenterol. 2014;20:3967–75.
3. Capuano A, Pivetta E, Sartori G, Bosisio G, Favero A, Cover E, et al.Abrogation of EMILIN1-β1 integrin interaction promotes experimental colitis and colon carcinogenesis.Matrix Biol J Int Soc Matrix Biol. 2019;83:97–115.
4. Capuano A, Pivetta E, Baldissera F, Bosisio G, Wassermann B, Bucciotti F, et al.Integrin binding site within the gC1q domain orchestrates EMILIN-1-induced lymphangiogenesis. Matrix Biol J Int Soc Matrix Biol. 2019;81:34–49.
5. Danussi C, Petrucco A, Wassermann B, Pivetta E, Modica TM, Del Bel Belluz L, et al.EMILIN1-α4/α9 integrin interaction inhibits dermal fibroblast and keratinocyte proliferation. JCell Biol. 2011;195:131–45.
6. Park J, Song S-H, Kim TY, Choi M-C, Jong H-S, Kim T-Y, et al. Aberrant methylation of integrin alpha4 gene in human gastric cancer cells.Oncogene. 2004;23:3474–80.
7. Yamamoto M, Nomura S, Hosoi A, Nagaoka K, Iino T, Yasuda T et al. Established gastric cancer cell lines transplantable into C57BL/6 mice show fibroblast growth factor receptor 4 promotion of tumor growth. Cancer Sci. 2018 May;109(5):1480-1492.

THE EXTRACELLULAR MATRIX PROTEIN EMILIN-1 IMPACTS ON THE MICROENVIRONMENT BY HAMPERING THE DEVELOPMENT AND PROGRESSION OF GASTRIC CANCER

Alessandra Capuano 1, Maddalena Vescovo 1, Eugenio Scanziani 2, Samanta Muzzin 1, Sachiyo Nomura 3, Simone Canesi 2, Stefano Realdon 1, Stefania Maiero 1, Maria Grazia Nadin 1, Irma Valeria Albergati 4, Antonino Piruzza 4, Saveria, Lory croce' 4, Renato Cannizzaro 5, Paola Spessotto 1

1 Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, Aviano, Italy

2 University of Milan, Milan, Italy

3 University of Tokyo, Tokyo, Japan

4 University of Trieste, Trieste, Italy

5 University of Trieste, Trieste, Italy|||Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, Aviano, Italy

Event

UEG Week Vienna 2024

Topics

Digestive Oncology Mechanisms & Personalised Medicine Oesophagus Stomach & H. Pylori

Submission format

Abstract

Session

Upper GI basic: Reflux, gastritis and cancer

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

UEG Presentation

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MOLECULAR LANDSCAPES OF GASTRIC DYSPLASIA AND CANCER

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Introduction

Gastric dysplasia is a pre-malignant lesion that can progress to gastric cancer (GC), however the factors that influence its progression is still poorly understood. Here, we aim to identify molecular factors that promote the development of GC from gastric dysplasia.

Aims & Methods

We performed whole exome sequencing on 110 gastric dysplasia or GC samples from 82 patients, with an average exome coverage of 154X including the germline normal comparison. The samples were obtained from 2017 to 2019 and included (a) dysplastic samples from 34 patients without GC (b) GC samples from 20 patients without dysplasia (c) concurrent dysplasia and GC samples from 28 patients.

Results

Classification based on TCGA GC subtypes showed CIN (chromosomal unstable) GC to be more prevalent in GC without concurrent dysplasia (60% vs 21.4%; Fisher test p-value 0.030) whereas MSI (microsatellite unstable) GC tend to be concurrent with dysplasia (21.4% vs 5.0%; Fisher test p-value 0.21), suggesting acquisition of copy number alterations to be associated with rapid progression into GC. Consistent with this hypothesis, we also identified a significant increase in copy number alterations in GC samples compared to dysplasia (Wilcoxon test; p=5.1x10^-3), while somatic mutation rate was more modestly increased (Wilcoxon test; p=0.12). CIN samples were enriched with GC samples, TP53 mutations, 17q12 (ERBB2) amplification and 9p21 (CDKN2A) deletion whereas non-CIN samples showed high APC mutations, 5q23 (APC) deletion and is associated with gastric dysplasia.

Conclusion

The molecular data presented in this study is the most comprehensive to date for gastric dysplasia and early GC. Our results suggest copy number alterations may be the key driver of GC progression in dysplastic samples and molecular profiling may be used to identify patients at higher risk of developing GC.

MOLECULAR LANDSCAPES OF GASTRIC DYSPLASIA AND CANCER

Mi Jin Oh 1, Kie Kyon Huang 2, Roxanne Hui Heng Chong 3, Jimmy Bok Yan So 3, Feng Zhu 3, Patrick Tan 2, Khay Guan Yeoh 3, Hyunsoo Chung 4

1 Seoul National University College of Medicine, Seoul, Korea, Republic of

2 Duke‐NUS Medical School, Singapore, Singapore

3 National University of Singapore, Singapore, Singapore

4 Seoul National University College of Medicine, Seoul, Korea, Republic of|||National University of Singapore, Singapore, Singapore|||Seoul National University College of Medicine, Seoul, Korea, Republic of

Event

UEG Week Copenhagen 2023

Topics

Digestive Oncology Mechanisms & Personalised Medicine Oesophagus Stomach & H. Pylori

Submission format

Abstract

Session

Molecular roadway to upper GI cancer

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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Introduction

Gastric cancer (GC) has high morbidity and mortality, severely threatening public health. Its insidious onset and rapid progression often deny patients curative resection at diagnosis. The low response rate of current advanced-stage GC drugs demands urgent solutions. Thus, uncovering the molecular mechanisms of GC progression to find new therapeutic targets is crucial. ZEB1 promotes GC progression via tumor-cell-intrinsic functions like driving EMT and stem-cell-like properties and regulating stromal cell differentiation. Tumor-associated macrophages (TAMs) are key for tumor growth and metastasis, with their functions modulated during cell-cell interactions. However, whether ZEB1 in GC cells mediates crosstalk with TAMs and the related mechanisms are unknown. Apolipoprotein E (APOE), a lipid-transport protein, is linked to tumorigenesis. Clinical studies show APOE is highly expressed in GC, correlating with poor prognosis, but the underlying mechanisms remain unclear. This study explores how APOE mediates ZEB1-dependent macrophage polarization to promote GC progression, aiming to provide a basis for new therapies.

Aims & Methods

Correlations between TAMs infiltration or gene expression and prognosis were evaluated using databases (TIMER2, K-M plotter, GEPIA) and tissue analyses (Western blot, immunohistochemistry). RNA-seq, TAMs-infiltration correlation, and survival analyses were used to identify genes driving pro-tumorigenic TAMs polarization. GC cell lines with disrupted ZEB1 expression were created. CCK-8, colony formation, Transwell, and co-culture assays were used to study ZEB1's direct and TAMs-mediated indirect effects on GC cell malignancy. Proteomic profiling of ZEB1-knockdown GC cell media screened for intermediate proteins in ZEB1-regulated TAMs polarization, validated by survival, APOE expression, luciferase, and rescue experiments. In vivo validation used mouse tumor and metastasis models, combined with clinical specimen correlation and multicolor immunohistochemistry.

Results

TIMER2-based Cox regression showed TAMs infiltration was an independent poor-prognosis factor. K-M plotter and IHC indicated that high M2-TAMs infiltration correlated with worse survival. Integrated analyses identified ZEB1 as a key driver of M2-TAMs polarization. GEPIA data, tissue analyses, and functional experiments showed ZEB1 was highly expressed in GC, correlated with poor prognosis, and promoted GC cell proliferation, migration, and invasion. Transwell co-cultures revealed ZEB1 enhanced M2-TAMs polarization and suppressed M1-TAMs polarization in a paracrine-dependent way. Loss- or gain-of-function experiments showed ZEB1 in daughter cells augmented parental cell malignancy via TAMs polarization. Proteomic and related assays identified APOE as a secreted protein affecting prognosis. ZEB1 activated APOE expression, and APOE mediated ZEB1-regulated TAMs polarization. Rescue experiments reversed ZEB1-induced pro-tumorigenic TAMs polarization. In vivo, αAPOE treatment suppressed GC cell growth and reduced pro-tumorigenic TAMs infiltration. Lung-metastasis models showed APOE-mediated ZEB1-enhanced GC metastasis. Clinical specimens showed that APOE was highly expressed in GC, associated with poor prognosis, and correlated with ZEB1 and CD206.

Conclusion

ZEB1 in cancer cells directly promotes GC progression and drives APOE-mediated pro-tumorigenic TAMs polarization. APOE is a potential target for TAMs-directed GC treatment.

MECHANISM OF APOE-MEDIATED, ZEB1-DEPENDENT MACROPHAGE POLARIZATION IN GASTRIC CANCER PROGRESSION

HE NIE 1, Xiaoyi Zhao 1, Qinglin Zhang 1, Qiang Zhan 1

1 The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

Back to the basics of gastric cancer (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Early gastric cancer (EGC) represents a critical stage in preventing and controlling the progression from gastritis to advanced gastric cancer (AGC). Therefore, identifying the single-cell characteristics of EGC, particularly the cellular composition of the tumor microenvironment (TME), as well as identifying potential predictive markers and therapeutic targets, could significantly enhance the monitoring of gastric cancer and improve clinical cure rates.

Aims & Methods

We constructed a comprehensive single-cell RNA sequencing atlas for 184,426 high-quality gastric cancer cells from various stages, utilizing clinical biopsies and surgical samples. The cell composition, differential gene expression, lineage differentiation, intercellular communication, immune infiltration, and clinical correlations between tumor and microenvironment cells were analyzed. Furthermore, through the integration of clinical sample detection, ex vitro and in vivo cell function tests, organoid and endothelial cell co-culture, mouse tumorigenic models, ultrasonic vascular detection, and transcriptome sequencing, key target cell subsets and their molecular roles in EGC were identified.

Results

Our single-cell atlas highlights the cellular and molecular characteristics of EGC. Eight distinct cell lineage states were identified, and it was observed that the number of epithelial cell meta-clusters gradually decreased. In contrast, the number of T&NK, B, plasma, fibroblast, myeloid, and endothelial cells increased with disease progression. Certain epithelial subclusters ((metaplastic stem-like cells (MSCs), metaplastic stem-like cells (PMC-like), proliferating cells), T-cell subclusters (T_reg, CCR7⁺ naive, CH25H⁺ CD4⁺, TEM CD8⁺, and GFPT2⁺ CD8⁺ T cells), and endothelial subclusters (IL-33⁺ Venous-1 and AMAMTSL2⁺ Artery-2) were found to be increased in EGC. The Venous-1 subcluster was found to express high levels of IL-33. Mechanistically, it was revealed that IL-33 enhances the survival and angiogenesis of endothelial cells by upregulating the expression of adhesion proteins CD34 and PECAM1. Patient-derived EGC and AGC organoids were subsequently generated, and it was demonstrated that endothelial-derived IL-33 promoted the growth of both EGC and AGC organoids ex vitro and in vivo. Furthermore, IL-33 was found to increase the expression of KRT17 in EGC organoids. Notably, we also found that high expression of IL-33 was positively correlated with the depth of invasion and malignancy of EGC.

Conclusion

This study provides novel insights into the single-cell components involved in EGC and reveals the role of the IL-33⁺ endothelial subcluster in EGC progression.

SINGLE-CELL SEQUENCING REVEALED THAT THE IL-33<SUP>+</SUP> ENDOTHELIAL CELL SUBSET PROMOTES THE PROGRESSION OF EARLY GASTRIC CANCER

Li Zhou 1, Mei Yang 2, Chao Deng 1, Song He 1, Zhihang Zhou 1

1 The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China

2 The Third People's Hospital of Chengdu, Chongqing, China

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

Back to the basics of gastric cancer (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Inflammation is one of the key hallmarks of gastric cancer (GC) development, and the arachidonic acid (AA) pathway with more than 90 members has been shown to play a significant role in this process. Recent advances in omics technology have shed light on the molecular changes in cancer, providing a foundation for the identification of candidate biomarkers for use in diagnosis, prognosis, and screening. Thus, the purpose of this study was to revisit the AA pathway in GC using a transcriptomics approach, in order to identify which genes are particularly dysregulated and thus potentially representing targetable biomarkers.

Aims & Methods

RNA-Seq gene expression data (Level 3) and clinical data of the stomach adenocarcinoma TCGA cohort (STAD), containing 414 tumor samples, was obtained using cBioportal (http://cbioportal.org) and UCSC Xena (http://xena.ucsc.edu/). Shapiro–Wilk normality test was used to determine variable normality, and statistically significant differences of gene expression levels between tumor tissue and adjacent normal tissue were evaluated using the nonparametric Wilcoxon test. Hazard ratios for prognosis assessment were calculated using a univariate Cox regression model. Differential gene expression (DGE) analysis was performed using limma and edgeR R-packages. All statistical analyses were performed using R software (version 4.2.1), and p-values < 0.05 were considered statistically significant.

Results

A total of 53 genes were found to be differentially expressed in GC tumors compared with normal adjacent tissues. Overall, 29 genes were down regulated and 24 were up regulated, with the majority being involved in prostaglandin regulation and synthesis. The top down regulated genes include CYP4B1, AKR1C2, HPGD and AKR1C. Such genes encode proteins involved in AA metabolism and prostaglandin regulation and degradation, except for PTGS1, which encodes COX-1, an enzyme associated with prostaglandin synthesis. SOX9, GPX2, PON1, andFAAH2 accounted for the top up regulated genes. In the univariate analysis, four of the top DEGs correlated with worse overall survival: CYP11A1, SOX9, PON1 and FAAH2.

Conclusion

Overall, using a transcriptomic approach, the AA pathway was shown to be dysregulated in GC, with over half of the genes exhibiting altered expression, and going beyond inflammatory biomarkers, highlighting the pivotal role this pathway has in tumor development and progression and the potential for targetable actions.

REVISITING THE ARACHIDONIC ACID PATHWAY IN GASTRIC CANCER: A TRANCRIPTOMICS APPROACH TOWARDS THE DISCOVERY OF NOVEL BIOMARKERS

Tatiana Cruz Almeida 1, Catarina Lopes 2, Andreia Brandao 3, Mario Dinis-Ribeiro 4, Ana Carina Pereira 5

1 Portuguese Institute of Oncology of Porto (IPO Porto) - Research Center /Porto Comprehensive Cancer Center (Porto.CCC), Rise@CI-IPOP (Health Research Group), Porto, Portugal

2 Portuguese Institute of Oncology of Porto (IPO Porto) - Research Center /Porto Comprehensive Cancer Center (Porto.CCC), Rise@CI-IPOP (Health Research Group), Porto, Portugal|||CINTESIS – Center for Health Technology and Services Research, Porto, Portugal|

3 Portuguese Institute of Oncology of Porto (IPO Porto) - Research Center / Porto Comprehensive Cancer Center (Porto.CCC), Rise@CI-IPOP (Health Research Group), Porto, Portugal

4 Portuguese Institute of Oncology of Porto (IPO Porto) - Research Center /Porto Comprehensive Cancer Center (Porto.CCC), Rise@CI-IPOP (Health Research Group), Porto, Portugal|||Portuguese Institute of Oncology of Porto (IPO Porto), Porto, Portugal

5 Portuguese Institute of Oncology of Porto (IPO Porto) - Research Center /Porto Comprehensive Cancer Center (Porto.CCC), Rise@CI-IPOP (Health Research Group), Porto, Portugal|||CINTESIS – Center for Health Technology and Services Research, Porto, Portugal

Conference

UEG Week Copenhagen 2023

Topics

Oesophagus

Submission format

Abstract

Session

Molecular avatars in gastrointestinal carcinogenesis (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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Introduction

Emerging experimental and clinical data suggest that the gut microbiome can significantly influence the antitumor efficacy of key chemotherapy agents, including 5-fluorouracil, oxaliplatin, and docetaxel. These agents form the backbone of the neoadjuvant chemotherapy (NAC) regimen, FLOT, which is widely used for the treatment of locally advanced gastric cancer (GC). However, despite growing evidence from preclinical models, clinical studies investigating the direct association between gut microbiome composition and the response to NAC in GC patients remain scarce.

Aims & Methods

This study aims to address this gap in knowledge by exploring the relationship between the gut microbiome and therapeutic outcomes in this clinical context. In this longitudinal observational study, we explored the association between pre-treatment fecal microbiome composition analyzed via 16S rRNA gene sequencing and histological tumor regression, as assessed by the Becker score, in GC patients undergoing NAC with the FLOT regimen, followed by gastrectomy.

Results

Among the 38 enrolled patients, 19 (50%) achieved a Becker score of 1–2 and were classified as ‘Responders,’ while the other 19 (50%) were classified as ‘Non-responders’. Responders exhibited a higher abundance of Parabacteroides distasonis, Alistipes sp. AL-1, and Bacteroides plebeius. A combined biomarker of these species demonstrated robust predictive accuracy for a favorable response to NAC, with sensitivity of 89%, specificity of 63%, and an AUC of 0.8 (95% CI: 0.66–0.94). In contrast, non-responders showed a predominance of bacterial genera, including Ruminococcaceae UCG-014, Ruminococcus 1, Ruminococcaceae UCG-005, and the [Eubacterium] eligens group. The combined biomarker of these genera demonstrated excellent predictive performance for poor NAC response, with sensitivity of 89%, specificity of 95%, and an AUC of 0.93 (95% CI: 0.85–1.0).

Conclusion

The results of our study support the hypothesis that the pre-treatment gut microbiome composition can serve as a reliable biomarker for predicting both positive and negative responses to NAC in GC patients. By identifying specific microbial signatures associated with chemotherapy outcomes, this research provides critical insights into how microbiome-based strategies might enhance personalized treatment regimens for GC. Future studies are needed to validate these findings and explore potential therapeutic interventions targeting the microbiome to improve clinical outcomes in GC patients.

GUT MICROBIOME AS A BIOMARKER FOR PREDICTING NEOADJUVANT CHEMOTHERAPY RESPONSE IN GASTRIC CANCER

Kristina Žukauskaitė 1, Bernardas Baušys 2, Angela Horvath 1, Rasa Sabaliauskaitė 3, Kornelija Rauduvytė 4, Klaudija Bičkaitė 5, Rokas Stulpinas 6, Vanessa Stadlbauer-Köllner 1, Rimantas Baušys 7, Sonata Jarmalaitė 3, Augustinas Baušys 2

1 Medical University of Graz, Graz, Austria|||Center for Biomarker Research in Medicine (CBmed GmbH), Graz, Austria

2 Vilnius University, Vilnius, Lithuania|||Vilnius University, Vilnius, Lithuania

3 Vilnius University, Vilnius, Lithuania|||National Cancer Institute, Vilnius, Lithuania

4 National Cancer Institute, Vilnius, Lithuania|||Vilnius University, Vilnius, Lithuania

5 Vilnius University, Vilnius, Lithuania

6 Vilnius University, Vilnius, Lithuania|||Vilnius University Hospital Santaros Clinics, Vilnius, Lithuania

7 National Cancer Institute, Vilnius, Lithuania

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

OESOPHAGEAL, GASTRIC AND DUODENAL (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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