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Introduction

Pancreatic cancer is estimated to be the second leading cause of cancer-related deaths in Europe by 2030 and remains a significant challenge with limited risk factors. Pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasms (IPMN), and mucinous cystic neoplasia (MCN) are three common precursor lesions for this disease. The risk of pancreatic cancer in first-degree relatives (FDRs) of individuals with precursors however remains unknown.

Aims & Methods

This study aims to analyze the absolute incidence and relative risk of pancreatic cancer by family history of precursors using a population-based cohort study in Sweden. We included all patients who had been pathologically diagnosed with precursor lesions of pancreatic cancer between 1965 and 2016 in Sweden and up to 5 matched reference individuals from the general population based on birth year, sex, calendar year, and residency. We identified all their FDRs (parents, full siblings, and offspring) using the Swedish multigeneration registry. All FDRs were followed up through national registries from birth or year 1959 when cancer registry was launched, until the date of pancreatic cancer diagnosis, death, migration, or end of follow-up (January 1^st, 2020). The absolute cancer incidence rate was computed as the number of observed cases divided by person-years and relative risk was calculated as multivariable-adjusted hazard ratio (HR) using Cox proportional hazards regression.

Results

A total of 27,862 FDRs were included in the analyses, among which 4647 were FDRs of 1036 precursor patients and 23,157 were FDRs of 5067 matched reference individuals. During the follow-up, 149 FDRs developed pancreatic cancer, with an incidence rate of 10 (95% CI 8-12) per 100,000 person-years for FDRs of reference individuals, and 21 (16-28) for FDRs of precursor individuals. Compared to FDRs of reference individuals, FDRs of precursor had a 2.24 (1.58-3.18) times higher risk of developing pancreatic cancer during their lifetime. When stratified by subtype of precursors, similar HRs were found for PanIN (2.37 [1.52-3.70]) and IPMN (2.31 [1.29-4.11]), but not for MCN (1.84 [0.89-3.78]). Individuals whose parents had been diagnosed with precursors had 4.94 (2.10-11.62) times higher risk for pancreatic cancer than those without. To facilitate clinical application, we also assessed the association of pancreatic cancer risk after known diagnosis of precursors in FDRs. Compared to reference counterparts, an HR of 4.46 (2.37-8.38) was found for those with known precursors in FDRs.

Conclusion

A family history of precursor lesions of pancreatic cancer can be an indicative risk factor for pancreatic cancer and risk estimates varies by precursor subtypes and type of FDRs with precursors. Precursor lesions in FDR should be considered as a positive phenotype in individuals at risk.

Disclosure

Dr. Wolpin reported receiving grants from AstraZeneca, Celgene, Bristol Myers Squibb, Eli Lilly, Novartis, and Revolution Medicines and receiving personal fees from BioLineRx, Mirati, Ipsen, GRAIL, Celgene, Bristol Myers Squibb, and Third Rock Ventures. Dr. Ludvigsson has coordinated an unrelated study on behalf of the Swedish IBD quality register (SWIBREG). This study has received funding from the Janssen corporation. Dr Ludvigsson has also received financial support from MSD to develop a paper reviewing national healthcare registers in China. Dr Vujasinovic and Dr Löhr have received lecture fees from Abbott and Viatris. Dr Vujasinovic and Dr Löhr have also received financial support for writing a scientific book from Viatris. All other authors declare that they have no conflicts of interest and nothing to declare.

RISK OF PANCREATIC CANCER IN FIRST-DEGREE RELATIVES OF INDIVIDUALS WITH PRECURSORS: A SWEDISH NATIONWIDE COHORT STUDY

Qiao-Li Wang 1, Jiangwei Sun 2, Chen Yuan 3, Miroslav Vujasinovic 4, Matthias Löhr 4, Brian Wolpin 3, Jonas F Ludvigsson 5

1 Karolinska Institutet, Stockholm, Sweden|||Dana-Farber Cancer Institute, Boston, United States|||Karolinska Institutet, Stockholm, Sweden

2 Karolinska Institutet, Stockholm, Sweden

3 Dana-Farber Cancer Institute, Boston, United States

4 Karolinska Institutet, Stockholm, Sweden|||Karolinska University Hospital, Stockholm, Sweden

5 Karolinska Institutet, Stockholm, Sweden|||Örebro University Hospital, Örebro, Sweden|||Columbia University Medical Center, New York, United States|||University of Nottingham, Nottingham, United Kingdom

Conference

UEG Week Vienna 2024

Topics

Pancreas

Submission format

Abstract

Session

Pancreatic cancer: Cinical (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Diagnosis and management of pancreatic insufficiency

Juan Enrique Dominguez-Munoz 1

1 University Hospital of Santiago de Compostela - Gastroenterology and Hepatology, University Hospital, Santiago de Compostela, Spain

Event

UEG Week Berlin 2025

Topics

Immunology Pancreas

Session

Chronic pancreatitis and rare etiologies

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Chronic pancreatitis aetiology: Where does it come from?

Lucía Guilabert 1

1 Dr. Balmis General University Hospital from Alicante, Alicante, Spain

Event

UEG Postgraduate Teaching Programme Vienna 2024

Topics

Education & Training Mechanisms & Personalised Medicine Pancreas Primary Care

Session

A personalised approach to chronic pancreatitis

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Case report of "unusual" foreign bodies in the oesophagus

Katarina Karlovic 1

1 KBC Rijeka, Rijeka, Croatia

Event

UEG Week Vienna 2024

Topics

Nurses

Session

Abstracts II: Patient care and endoscopic techniques

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Introduction

One possible treatment option for Eosinophilic Esophagitis (EoE) is Protone Pump Inhibitor (PPI) therapy. The possible mechanisms of action discussed include acid suppression and a direct anti-inflammatory effect. However, only up to 50% of EoE patients respond to PPI therapy. Predicting the therapeutic response is challenging, so the aim of this study was to identify potential predictors for a response to such therapy.

Aims & Methods

Patients with active EoE (defined as the presence of esophageal symptoms and simultaneous detection of >15 eosinophilic granulocytes per high-power field [HPF] in at least one biopsy from the esophagus) were retrospectively identified from the hospital database of a tertiary university referral center over 5 years. These patients had received sufficient PPI therapy (defined as double standard dose for at least four weeks). The analysis focused on their therapeutic response and potential predictors including clinical, histological and functional parameters of treatment success.

Results

151 EoE patients were screened and of them 57 patients (mean age: 41 years; 81% male; mean maximum eosinophil count: 55/HPF) who had received PPI therapy at double standard dose for at least 4 weeks (mean duration: 62 days) were finally included. Histopathological complete remission (defined as <5 eosinophils/HPF) was achieved in 18 of 57 patients (31.6%) following PPI treatment, while partial remission (defined as <15 eosinophils/HPF) was observed in 25 of 57 patients (43.9%). No response to PPI therapy was noted in 14 of 57 patients (24.6%). There were no significant differences of the assessed predictors in EoE patients with and without PPI response, although patients with PPI response showed a distally emphasized esophageal eosinophilia and a higher acid exposure time in pH-metry (both non-significant).

Conclusion

No definitive predictors for the response to PPI therapy in EoE patients could be identified. However, a distally predominant esophageal eosinophilia and higher acid exposure time in patients responding to PPI therapy may suggest a contributory role of gastroesophageal reflux in this cohort.

References

PREDICTORS OF TREATMENT RESPONSE OF PPI THERAPY IN PATIENTS WITH EOSINOPHILIC ESOPHAGITIS

Helena Antwerpen 1, Simon Nennstiel 2, Simon Weidlich 3, Christoph Schlag 2

1 Klinikum rechts der Isar TU München, München, Germany

2 Klinikum rechts der Isar TU München, München, Germany|||University Hospital Zurich, Zürich, Switzerland

3 Klinikum rechts der Isar TU München, München, Germany

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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Summary: Liver and pregnancy - Beware of dangerous liaisons

Christophe Moreno 1

1 Hôpital Erasme (gastro) - Hôpital Erasme (gastro); Maransart/BE, Brussels, Belgium

Event

UEG Postgraduate Teaching Programme Berlin 2025

Topics

Hepatobiliary Paediatrics

Session

Liver and pregnancy: Beware of dangerous liaisons

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Pancreatic cancer, known for its poor prognosis, can potentially be cured if diagnosed early, specifically when the tumor is 10 mm or less in diameter, referred to as Small Pancreatic Cancer (SPC).¹ Despite recent advancements of AI diagnostic models for various diseases, detecting SPC remains a significant challenge.^2,3,4 This difficulty arises because the detection rate decreases as SPC tumors diminish in size, necessitating an imaging interpretation approach different from that used for general pancreatic cancer. SPC complicates direct identification through imaging, necessitating reliance on indirect image findings such as partial pancreatic parenchymal atrophy and abnormalities in the main pancreatic duct.^5,6,7 These subtle findings demand advanced interpretive skills. Furthermore, the rarity of SPC complicates the collection of a sufficient dataset for research and diagnosis.

Aims & Methods

This study aims to construct an SPC-specific AI-based diagnostic model by incorporating indirect image findings, achieved through collaboration with multiple institutions that specialize in SPC diagnosis to ensure a sufficient number of cases. We first analyzed portal phase CT scans of 30 SPC cases and 30 normal pancreas (NP) cases from our institution. Two specialists annotated the abnormal areas, including indirect image findings of SPC, and the entire pancreas for NP, from which small region images, each measuring 28×28 pixels, were randomly extracted. These images were converted into feature vectors using a pretrained deep learning model (ResNet-50), and the feature distribution of each small region was compared and classified using a machine learning model. Following this initial experiment, we conducted external validation using SPC cases collected from three other institutions.

Results

In our institution's SPC cases, abnormalities in the main pancreatic duct were seen in 77%, partial pancreatic parenchymal atrophy in 40%, and upstream pancreatic parenchymal atrophy in 16%. In cases from the other institutions, these figures were 71%, 46%, and 13%, respectively. t-SNE plotting of feature vectors indicated a trend of separation between small regions of SPC and NP, with SPC displaying varied features among cases, while NP exhibited similar features. Classification using the LightGBM model, a type of decision tree-based learning algorithm, achieved an average accuracy of 0.944 through 5-fold cross-validation, and an accuracy of 0.919 for cases from other institutions.

Conclusion

Using the indirect image findings of SPC enabled good classification performance for small regions of NP. A slight decrease in accuracy was observed in cases from the other institutions, suggesting the influence of imaging conditions and equipment. Through multi-institutional collaboration, we have amassed a dataset of over 100 SPC cases, which we will utilize to further refine and enhance our model. Our future work will focus on improving preprocessing methods and expanding the dataset with additional multi-institutional data. Achieving these goals will enable AI to support clinicians in the reliable diagnosis of SPC, potentially leading to an increase in the number of pancreatic cancer patients who can undergo curative surgical treatments.

References

1. Kanno A, et al. Pancreatology 2018; 18(1): 61-7.
2. Chu LC, et al. AJR Am J Roentgenol 2019; 213(2): 349-57.
3. Kenner BJ, et al. Pancreas 2021; 50(7): 916-22.
4. Chen PT, et al. Radiology 2023; 306(1): 172-82.
5. Yamao K, et al. Diagnostics 2020; 10(7): 445.
6. Sagami R, et al. Cancers 2021; 13(5): 945.
7. Nakahodo J, et al. Pancreatology 2022; 22(8): 1148-58.

DEVELOPMENT OF AN AI MODEL FOR EARLY DETECTION OF SMALL PANCREATIC CANCER USING INDIRECT IMAGE FINDINGS

Hidekazu Takahashi 1, Kentaro Yamao 2, Hideo Yokota 3, Satoko Takemoto 3, Jun Nakahodo 4, Ryuki Minami 5, Ryota Sagami 6, Takuya Ishikawa 2, Yasuyuki Mizutani 7, Tadashi Iida 7, Kota Uetsuki 7, Unknown Unknown 7

1 Nagoya University Graduate School of Medicine, Nagoya, Japan|||RIKEN, Center for Advanced Photonics, Wako, Japan|||Pancreatic Cancer Research for Secure Salvage Young Investigators (PASSYON), Osaka-Sayama, Japan

2 Nagoya University Graduate School of Medicine, Nagoya, Japan|||Pancreatic Cancer Research for Secure Salvage Young Investigators (PASSYON), Osaka-Sayama, Japan

3 RIKEN, Center for Advanced Photonics, Wako, Japan

4 Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital, Tokyo, Japan|||Pancreatic Cancer Research for Secure Salvage Young Investigators (PASSYON), Osaka-Sayama, Japan

5 Tenri Hospital, Tenri, Japan|||Pancreatic Cancer Research for Secure Salvage Young Investigators (PASSYON), Osaka-Sayama, Japan

6 Oita University, Faculty of Medicine, Oita, Japan|||Pancreatic Cancer Research for Secure Salvage Young Investigators (PASSYON), Osaka-Sayama, Japan

7 Nagoya University Graduate School of Medicine, Nagoya, Japan

Conference

UEG Week Vienna 2024

Topics

Pancreas

Submission format

Abstract

Session

Molecular and clinical therapies in HPB (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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