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Introduction

Cholangiocarcinoma (CCA) comprises a heterogeneous group of malignant tumours with dismal prognosis. During the last years, different studies have highlighted the key role of the immune system in the development of intrahepatic CCA (iCCA) and several combinational therapies targeting the tumour microenvironment (TME) have shown promising results for anti-cancer therapy. In this regard, the macrophage receptor with collagenous structure (MARCO) is a class A scavenger receptor found on particular subsets of macrophages that has been described to play a determining role in macrophage polarization and consequently in adaptive immune responses in many solid tumours. However, its role in iCCA is still unknown. This study aims to unravel the role of MARCO in iCCA development and progression.

Aims & Methods

The cell-type specific MARCO expression was examined in iCCA human tumors by using publicly available single-cell RNA sequencing data from different studies and MARCO-expressing tumor-associated macrophages (TAMs) were phenotypically characterized. MARCO mRNA expression was analyzed in human control and iCCA liver tissue samples and associated to different immune cell types and immune-functionality scores employing state-of-the-art technologies as ConsensusTME, Tumour Immune Dysfunction and Exclusion (TIDE) tool and Tumour Immunophenotype Profiling (TIP). To study the role of MARCO in murine cholangiocarcinogenesis, wild type (WT) and Marco^-/- mice were subjected to 3 different iCCA murine models and flow cytometry analysis of the TME was carried out to characterize different lymphocytic and myeloid populations.

Results

Single-cell RNA sequencing data indicate that MARCO is expressed in a specific subtype of TAMs in patients with iCCA. Besides, high MARCO expression levels in the liver samples of patients with iCCA are linked with worse clinical outcome. In line with this, MARCO expression in human iCCA tumours is associated to cell types involved in tumour progression such as M2 macrophages, and related with T cell dysfunction. Regarding the potential role of MARCO in murine models of iCCA, Marco^-/- mice show a trend to be protected from iCCA development, the mechanisms behind this effect being likely associated to a reduction of the innate immune cells such as CD9⁺Ly6C^-F4/80⁺ resident macrophages and type-2 innate lymphoid cells (ILC2). Noteworthy, in a context of a syngeneic orthotopic experimental model, Marco^-/- mice exhibit a reduced presence of immune checkpoint molecules in innate and adaptive immune cells, including a lower percentage of PD-L1⁺Ly6C^-F4/80⁺ resident macrophages and, PD-1⁺ and CTLA-4⁺ cytotoxic CD8⁺ T cells in comparison to WT mice. In addition, MARCO deficiency significantly improves the overall survival of mice subjected to the orthotopic injection of syngeneic CCA cells into the liver, due to a reduction of the tumour metastasis in the lungs.

Conclusion

High MARCO expression is associated to a worse outcome in patients with iCCA and is associated to an immunosuppressive TME. Importantly, Marco^-/- mice display a reduced presence of immunosuppressive cell populations and present an increased overall survival. Therefore, MARCO arises as a novel therapeutic target for iCCA.

SCAVENGER RECEPTOR MARCO IS ASSOCIATED WITH AN IMMUNOSUPPRESSIVE MICROENVIRONMENT AND TUMOR PROGRESSION IN INTRAHEPATIC CHOLANGIOCARCINOMA

Aloña Agirre Lizaso 1, Maider Huici-Izagirre 1, Colm J. O'Rourke 2, Ekaterina Zhuravleva 2, Ana Korosec 3, Mikel Azkargorta 4, Felix Elortza 4, Sumera I. Ilyas 5, Gregory J. Gores 5, Jesper B. Andersen 2, Gernot Schabbauer 3, Luis Bujanda Fernández de Piérola 6, Pedro M. Rodrigues 7, Omar Sharif 3, Jesús M. Bañales 8, María Jesús Perugorria 9

1 Donostia University Hospital, University of the Basque Country (UPV/EHU), San Sebastian, Spain

2 Biotech Research and Innovation Centre (BRIC), Department of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

3 Institute for Vascular Biology, Centre for Physiology and Pharmacology, Medical University Vienna, Christian Doppler Laboratory for Arginine Metabolism in Rheumatoid Arthritis and Multiple Sclerosis, Vienna, Austria

4 CIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain|||Proteomics Platform, CIC bioGUNE, ProteoRed-ISCIII, Bizkaia Science and Technology Park, Derio, Spain

5 Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, United States

6 Donostia University Hospital, University of the Basque Country (UPV/EHU), San Sebastian, Spain|||CIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain

7 CIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain|||Donostia University Hospital, University of the Basque Country (UPV/EHU), San Sebastian, Spain|||IKERBASQUE, Basque Foundation for Science, Bilbao, Spain

8 Donostia University Hospital, University of the Basque Country (UPV/EHU), San Sebastian, Spain|||CIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain|||IKERBASQUE, Basque Foundation for Science, Bilbao, Spain|||University of Navarra, Pamplona,

9 Donostia University Hospital, University of the Basque Country (UPV/EHU), San Sebastian, Spain|||CIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain|||Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain

Conference

UEG Week Copenhagen 2023

Topics

Hepatobiliary

Submission format

Abstract

Session

Oncology, transplantation and encephalopathy (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

UEG Standards and Guidelines

Clinical Practice Guideline

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Summary

Intrahepatic cholangiocarcinoma (iCCA) develops inside the liver, between bile ductules and the second-order bile ducts. It is the second most frequent primary liver cancer after hepatocellular carcinoma, and its global incidence is increasing. It is associated with an alarming mortality rate owing to its silent presentation (often leading to late diagnosis), highly aggressive nature and resistance to treatment. Early diagnosis, molecular characterisation, accurate staging and personalised multidisciplinary treatments represent current challenges for researchers and physicians. Unfortunately, these challenges are beset by the high heterogeneity of iCCA at the clinical, genomic, epigenetic and molecular levels, very often precluding successful management. Nonetheless, in the last few years, progress has been made in molecular characterisation, surgical management, and targeted therapy. Recent advances together with the awareness that iCCA represents a distinct entity amongst the CCA family, led the ILCA and EASL governing boards to commission international experts to draft dedicated evidence-based guidelines for physicians involved in the diagnostic, prognostic, and therapeutic management of iCCA.

Keywords

Diagnosis, intrahepatic cholangiocarcinoma, management, risk factors, staging, targeted therapy

EASL-ILCA Clinical Practice Guidelines on the management of intrahepatic cholangiocarcinoma

Publisher

European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Digestive Oncology Hepatobiliary

Citation

Journal of Hepatology, July 2023. vol. 79, 181–208

Published

2023

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Risk factors, epidemiology and prognosis of cholangiocarcinoma

Iago Rodríguez-Lago 1, Nina Barner-Rasmussen 2

1 Hospital Universitario de Galdakao, Bilbao, Spain

2 Helsinki University Hospital, Finland

Topics

Hepatobiliary

Published

2022

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Introduction

Cholangiocarcinoma (CCA) comprises a heterogeneous group of malignant tumors with poor prognosis. Etiopathogenesis remains obscure and it is urgent to find novel therapeutic targets in order to develop effective therapies. Krüppel-like factors (KLF) are a family of transcription factors involved in large variety of biological processes, including organogenesis, differentiation and cellular homeostasis. However, the role of KLFs during cholangiocarcinogenesis is yet to be unveiled.

Aims & Methods

Here, we investigated the role of KLF5 in cholangiocarcinogenesis and evaluated the therapeutic potential of its inhibition during CCA tumorigenesis. KLF5 expression was determined in human CCA tissues [Copenhagen (n=210), TCGA (n=36), Job (n=78), TIGER-LC (n=90) and San Sebastian cohorts (n=12)] and cell lines. KLF5^-/- CCA cells were generated by CRISPR/Cas9. Proteomic analyses were carried out by mass spectrometry and the functional effects of KLF5 genetic ablation or chemical inhibition with ML264 were evaluated in vitro and in vivo.

Results

KLF5 expression was upregulated in human CCA tissues from 5 different patient cohorts compared to surrounding normal liver tissue and/or normal bile ducts. Importantly, KLF5 upregulation was observed independently on tumor mutational background. High KLF5 levels correlated with lymph node invasion and worse overall survival, being an important prognostic factor. In vitro, KLF5 protein and mRNA levels were found upregulated in human CCA cells compared to normal human cholangiocytes. Proteomic analysis of KLF5^-/- CCA cells revealed that most of the altered pathways are related with the modulation of cell cycle, proliferation, survival and migration. In agreement, KLF5^-/- CCAcells displayed decreased cell proliferation, colony formation and migration while promoting cell cycle arrest at G1/S and apoptosis in vitro, when compared with CCA control cells. Instead, no signs of tumor development were evident after subcutaneous or orthotopic injection in a xenograft animal model of CCA. Likewise, pharmacological inhibition of KLF5 with ML264 hampered CCA cells proliferation and migration in vitro, halting the progression of cell cycle and blocking tumor growth in vivo in distinct animal models. Lastly, both genetic and pharmacological inhibition of KLF5 sensitized CCA cells to chemotherapy-induced apoptosis in vitro, and the combination of the standard of care chemotherapy (gemcitabine + cisplatin) and ML264 completely halted CCA tumor growth in mice. Accordingly, KLF5^-/-CCA cells displayed altered levels of several proteins related to chemoresistance when compared to control cells, that were shown to significantly correlate with KLF5 expression in human CCA tissues

Conclusion

Increased KLF5 is a general event in CCA, contributing to cancer progression by promoting cell survival and proliferation, as well as, chemoresistance. KLF5 inhibition with ML264 may represent a potential therapeutic strategy for CCA.

KLF5 UPREGULATION IS A COMMON EVENT IN CHOLANGIOCARCINOMA, ACTING AS AN ONCOGENE AND CONSTITUTING A BAD PROGNOSTIC FACTOR

Pedro M. Rodrigues 1, Oihane Erice 2, Ana Landa-Magdalena 2, Nuno André Paiva 2, Maite García Fernandez-Barrena 3, Paula Olaizola 4, Ainhoa Lapitz 4, Irene Olaizola 2, Colm J. O'Rourke 5, Santiago Iturbe-Rey 2, Jesper B. Andersen 5, Diego F. Calvisi 6, Mikel Azkargorta 7, Felix Elortza 7, Ibai Goicoechea 8, Charles H. Lawrie 9, Luis Bujanda Fernández de Piérola 4, María Jesús Perugorria 10, Jesús M. Bañales 11

1 Biodonostia Health Research Institute, San Sebastian, Spain|||National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||IKERBASQUE, Basque Foundation for Science, Bilbao, Spain

2 Biodonostia Health Research Institute, San Sebastian, Spain

3 Division of Hepatology, CIMA-University of Navarra, Pamplona, Spain

4 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Biodonostia Health Research Institute, San Sebastian, Spain

5 Biotech Research and Innovation Centre (BRIC), Department of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

6 Institute of Pathology, University of Regensburg, Regensburg, Germany

7 Proteomics Platform, CIC bioGUNE, CIBERehd, ProteoRed-ISCIII, Bizkaia Science and Technology Park, Derio, Spain

8 Molecular Oncology group, Biodonostia Research Institute, San Sebastian,, San Sebastian, Spain

9 Molecular Oncology group, Biodonostia Research Institute, San Sebastian,, San Sebastian, Spain|||Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom

10 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Department of Medicine, Faculty of Medicine and Nursing, University of the Basque Country UPV/EHU, Leioa, Spain|||Biodonos

11 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||IKERBASQUE, Basque Foundation for Science, Bilbao, Spain|||Department of Biochemistry and Genetics, School of Sciences, Un

Conference

UEG Week Copenhagen 2023

Topics

Hepatobiliary

Submission format

Abstract

Session

Oncology, transplantation and encephalopathy (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

UEG Standards and Guidelines

Clinical Practice Guideline

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Summary

Recent years have witnessed significant advances in the imaging, molecular profiling, and systemic treatment of cholangiocarcinoma (CCA). Despite this progress, the early detection, precise classification, and effective management of CCA remain challenging. Owing to recent developments and the significant differences in CCA subtypes, EASL commissioned a panel of experts to draft evidence-based recommendations on the management of extrahepatic CCA, comprising distal and perihilar CCA. Particular attention is given to the need for accurate classification systems, the integration of emerging molecular insights, and practical strategies for diagnosis and treatment that reflect real-world clinical scenarios.

EASL Clinical Practice Guidelines on the management of extrahepatic cholangiocarcinoma

Publisher

European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Digestive Oncology Hepatobiliary

Citation

Journal of Hepatology, Volume 83, Issue 1, 211 - 238

Published

2025

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Introduction

Cholangiocarcinoma (CCA) comprises a heterogeneous group of malignant tumors with dismal prognosis. Alterations in post-translational modifications (PTMs), including SUMOylation, result in abnormal protein dynamics, cell disturbances and disease. Here, we investigate the role of SUMOylation in CCA development and progression.

Aims & Methods

Levels and function of SUMOylation, together with response to S-adenosylmethionine (SAMe) and ML792 (SUMOylation inhibitors) or CRISPR/Cas9 against UBE2I were evaluated in vitro, in vivo and/or in patients with CCA. The impact of SUMOylation in CCA cells on tumor-stroma crosstalk was assessed performing co-culture experiments with CCA-derived cancer-associated fibroblasts (CAFs), human endothelial cells and monocytes. Proteomic analyses were carried out by mass spectrometry.

Results

The SUMOylation machinery was found overexpressed and overactivated in human CCA cells and tumors, correlating with poor prognosis. Most SUMOylated proteins found upregulated in CCA cells, after SUMO1-immunoprecipitation and further proteomics, participate in cell proliferation, survival or cell homeostasis. Genetic (CRISPR/Cas9-UBE2I) and pharmacological (SAMe and ML792) inhibition of SUMOylation reduced CCA cell proliferation and impeded colony formation in vitro. Moreover, both SAMe and ML792 induced apoptotic cell death in CCA cells in vitro. SUMOylation depletion (SAMe, ML792 or CRISPR/Cas9-UBE2I) halted tumorigenesis in subcutaneous models of CCA in vivo. Furthermore, SUMOylation deficiency in CCA cells reduced cancer-associated fibroblast and endothelial cell proliferation and impaired macrophage polarization towards an anti-inflammatory M2-like phenotype.

Conclusion

Aberrant protein SUMOylation contributes to cholangiocarcinogenesis by promoting cell survival and proliferation. Moreover, SUMOylation impacts the CCA-stroma crosstalk. Impaired SUMOylation halts CCA growth and, thus, may represent a potential new therapeutic strategy for patients with CCA.

THERAPEUTIC POTENTIAL OF TARGETING PROTEIN HYPER-SUMOYLATION IN CHOLANGIOCARCINOMA

Paula Olaizola 1, Irene Olaizola 2, Marta Fernandez de Ara 2, Maite G. Fernandez-Barrena 3, Laura Alvarez 4, Mikel Azkargorta 5, Colm J. O'Rourke 6, Pui-Yuen Lee-Law 7, Luiz M. Nova-Camacho 8, Jose Juan Marin 9, Maria L. Martinez-Chantar 10, Matias A. Avila 3, Patricia Aspichueta 11, Felix Elortza 5, Jesper B. Andersen 6, Luis Bujanda Fernández de Piérola 1, Pedro M. Rodrigues 12, María Jesús Perugorria 13, Jesús M. Bañales 12

1 Biodonostia Health Research Institute - Donostia University Hospital, San Sebastian, Spain|||National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain

2 Biodonostia Health Research Institute - Donostia University Hospital, San Sebastian, Spain

3 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Hepatology Program, CIMA, University of Navarra, Pamplona, Spain|||Instituto de Investigaciones Sanitarias de Navarra (Idi

4 Hepatology Program, CIMA, University of Navarra, Pamplona, Spain

5 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Proteomics Platform, CIC bioGUNE, CIBERehd, ProteoRed-ISCIII, Bizkaia Science and Technology Park, Derio, Spain

6 Biotech Research and Innovation Centre (BRIC), Department of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

7 Biodonostia Health Research Institute - Donostia University Hospital, San Sebastian, Spain|||Radboud University Nijmegen Medical Center, Nijmegen, Netherlands

8 Osakidetza Basque Health Service, Donostialdea IHO, Donostia University Hospital, Department of Pathology, San Sebastian, Spain

9 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Experimental Hepatology and Drug Targeting (HEVEPHARM) Group, Institute of Biomedical Research of Salamanca (IBSAL), Unive

10 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Liver Disease Laboratory, CIC bioGUNE, Basque Research and Technology Alliance (BRTA), Bilbao, Spain

11 National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain|||Biocruces Bizkaia Health Resea

12 Biodonostia Health Research Institute - Donostia University Hospital, San Sebastian, Spain|||National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||IKERBASQUE, Basque Foundation

13 Biodonostia Health Research Institute - Donostia University Hospital, San Sebastian, Spain|||National Institute for the Study of Liver and Gastrointestinal Diseases (CIBERehd, “Instituto de Salud Carlos III”), Madrid, Spain|||Faculty of Medicine and Nursi

Conference

UEG Week Copenhagen 2023

Topics

Hepatobiliary

Submission format

Abstract

Session

PP 07 Liver & biliary (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

UEG Presentation

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IMMUNO-ONCOLOGY BIOMARKERS FOR IMPROVED DIAGNOSIS OF CHOLANGIOCARCINOMA IN PRIMARY SCLEROSING CHOLANGITIS: INSIGHTS FROM THE INFLAMMATORY AND FIBROTIC TUMOUR MICROENVIRONMENT

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Introduction

Cholangiocarcinoma (CCA) is a rare but highly aggressive malignancy that arises from the epithelial cells of the biliary tree. Unfortunately, CCA is often asymptomatic in its early stages, making it difficult to diagnose and treat effectively. As a result, CCA patients have a poor prognosis (5-year survival <10%). Patients with underlying primary sclerosing cholangitis (PSC), a chronic autoimmune disease that causes inflammation and fibrosis of the bile ducts, are at increased risk of developing CCA, making them candidates for monitoring. However, there are no reliable markers to predict progression from PSC to CCA.

Aims & Methods

We aimed to identify potential immuno-oncology biomarkers that could improve the early diagnosis of CCA in patients with PSC and determine whether some biomarkers could also be useful for the diagnosis of patients with CCA of other aetiologies. A proteomic analysis was performed on serum samples from 35 PSC, 35 sporadic CCA, 12 CCA patients with a background of PSC, and 20 healthy controls using the Olink® Explore 384-plex inflammation and oncology panels and Luminex ProcartaPlex immune-monitoring assays. The resulting serum protein signatures were analysed to discriminate PSC from CCA, as well as PSC-CCA from PSC and PSC-CCA from CCA. The biological relevance of these markers was further explored using spatial proteomics (Nanostring GeoMx platform) on representative tissue sections from each group of comparison.

Results

Several serum protein signatures were identified that could distinguish PSC from CCA as well as PSC-CCA from PSC and from sporadic CCA. The identified immuno-oncology biomarkers included proteins involved in immune system regulation, extracellular matrix remodelling, and cell growth and differentiation. Spatially-resolved proteomic analysis confirmed a dysregulation of the inflammatory and fibrotic tumour microenvironment in CCA developing on a background of PSC.

Conclusion

The identification of immuno-oncology biomarkers that can differentiate PSC from CCA and PSC-CCA from PSC or CCA is an important step towards improving the early diagnosis of CCA in PSC. These biomarkers provide insights into the complex interplay between inflammation and fibrosis in the tumour microenvironment and have the potential to be used as early diagnostic and prognostic markers for CCA in PSC. Early detection of CCA is critical for increasing the chances of successful treatment and improving patient outcomes.

IMMUNO-ONCOLOGY BIOMARKERS FOR IMPROVED DIAGNOSIS OF CHOLANGIOCARCINOMA IN PRIMARY SCLEROSING CHOLANGITIS: INSIGHTS FROM THE INFLAMMATORY AND FIBROTIC TUMOUR MICROENVIRONMENT

Andres Garcia Sampedro 1, Rocio Macias 2, Kevin Litchfield 3, Alberto Quaglia 4, Douglas Thorburn 5, Massimo Pinzani 1, Stephen P Pereira 1, Pilar Acedo 1

1 University College London, London, United Kingdom

2 Carlos III Health Institute, Madrid, Spain|||Institute for Biomedical Research of Salamanca (IBSAL), Salamanca, Spain

3 University College London Cancer Institute, London, United Kingdom

4 King's College Hospital NHS Foundation Trust, London, United Kingdom|||Royal Free London NHS Foundation Trust, London, United Kingdom

5 University College London, London, United Kingdom|||University College London, London, United Kingdom

Event

UEG Week Copenhagen 2023

Topics

Digestive Oncology Hepatobiliary Pancreas

Submission format

Abstract

Session

Hepatobiliary and pancreatic cancer: Basic meets clinical practice

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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