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Introduction

Insulin-like growth factor binding protein-3 (IGFBP-3), macrophage migration inhibitory factor (MIF) and adrenomedullin (ADM) are connected with pancreatic ductal adenocarcinoma (PDAC) development.

Aims & Methods

Evaluation of serum levels of IGFBP-3, MIF and ADM in patients with chronic pancreatitis (CP), PDAC and control group and their potential role for differentiation of CP and PDAC.The study included 70 CP, 73 PDAC, and 23 healthy subjects as a control group. Serum concentrations of IGFBP-3, MIF, and ADM were measured with ELISA (Corgenix UK Ltd, R&D Systems). Diagnostic efficiency of the biomarkers was assessed by means of AUROC calculation. The Cambridge and TNM scales were used.

Results

Mean IGFBP-3 serum level was significantly higher in CP patients vs. controls (3.98 ± 2.44 ng/ml vs. 1.40 ± 1.45 ng/ml, p<0.05). Mean IGFBP-3 level was also higher in CP than in PDAC group (3.98 ± 2.44 ng/ml vs. 2.02 ± 1.69 ng/ml, p<0.05). Mean MIF serum level was also significantly higher in CP patients vs. control group (8589.50 ± 3607.78 pg/ml vs. 7365.76 ± 5009.52 pg/ml, p<0.05). Mean MIF level was also higher in CP vs. PDAC patients (8589.50 ± 3607.78 pg/ml vs. 8160.2 ± 4840.32 pg/ml, p>0.05), but the difference was not statistically significant. Mean ADM serum level was significantly lower in CP vs. controls (76.72 ± 135.02 ng/ml vs. 177.12 ± 348.99 ng/ml, p<0.05), but it did not differ between CP and PDAC patients (76.72 ± 135.02 ng/ml vs. 152.72 ± 285.43 ng/ml, p>0.05). Mean CA19-9 serum concentration was 50.98 +/- 153.44 U/ml in CP vs. 439.33 +/- 441.24 U/ml in PDAC; p<0.0000). Mean MIF and ADM levels did not show significant differences between CP and PDAC groups. AUROCs for MIF, IGFBP-3 and ADM ranged below 0.75, which is lower than the AUROC for CA19-9 (0.8703; 0.8120 within 95% CI). CA19-9 & IGFBP-3 taken together showed AUROC equal to 0.8676 (0.8094 within 95% CI). When additional variable IGFBP-2 was added AUROC raised to 0.8912 (0.8378 within 95% CI). When data on CA19-9, IGFBP-2 and IGFBP-3 were considered together with patients’ age and sex – AUROC was 0.9535 (0.9227 within 95% CI). Male sex and advanced age raised the probability of PDAC. When examining markers’ differentiation according to the degree of advancement of CP and PDAC, it was found that CA19-9 better differentiates groups at an early stage of disease development (1 & 2 Cambridge in CP vs. I & II TNM in PDAC), AUROC 0.9259 vs. 0,8755. The combination of CA 19-9, IGFBP-2, IGFBP-3, age and sex gave better results in the advanced group, AUROC 0.9591 vs. 0.9708.

Conclusion

Panel of IGFBP-3, MIF, ADM and CA19-9 may be useful in PDAC and CP differentiation. Further studies are necessary to confirm those findings.

PANCREATIC CANCER BIOMARKERS SUCH AS INSULIN-LIKE GROWTH FACTOR BINDING PROTEIN-3, MACROPHAGE MIGRATION INHIBITORY FACTOR AND ADRENOMEDULLIN IN THE DIFFERENTIATION OF CHRONIC PANCREATITIS FROM PANCREATIC DUCTAL ADENOCARCINOMA

Barbara Wlodarczyk 1, Lukasz Durko 1, Przemyslaw Wlodarczyk 2, Renata Talar-Wojnarowska 1, Ewa Malecka-Wojciesko 1

1 Medical University of Lodz, Lodz, Poland

2 University of Lodz, Lodz, Poland

Conference

UEG Week Vienna 2024

Topics

Pancreas

Submission format

Abstract

Session

PANCREAS (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

UEG Standards and Guidelines

Consensus

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Summary

These recommendations refer to the current management in pancreatic ductal adenocarcinoma (PDAC), a neoplasia characterised by an aggressive course and extremely poor prognosis. The recommendations regard diagnosis, surgical, adjuvant and palliative treatment, with consideration given to endoscopic and surgical methods. A vast majority of the statements are based on data obtained in clinical studies and experts’ recommendations on PDAC management, including the following guidelines: International Association of Pancreatology/European Pancreatic Club (IAP/EPC), American Society of Clinical Oncology (ASCO), European Society for Medical Oncology (ESMO), National Comprehensive Cancer Network (NCCN) and Polish Society of Gastroenterology (PSG) and The National Institute for Health and Care Excellence (NICE). All recommendations were voted on by members of the Working Group of the Polish Pancreatic Club. Results of the voting and brief comments are provided with each recommendation.

Keywords: pancreatic ductal adenocarcinoma; recommendations; guidelines; treatment; diagnosis

Diagnostic and therapeutic recommendations in pancreatic ductal adenocarcinoma. Recommendations of the Working Group of the Polish Pancreatic Club

Katarzyna Winter, Renata Talar-Wojnarowska, Andrzej Dabrowski, Malgorzata Degowska, Anita Gąsiorowska, Marek Durlik, Stanislaw Gluszek, Grazyna Jurkowska, Aleksandra Kaczka, Pawel Lampe, Tomasz Marek, Ewa Nowakowska-Dulawa, Anna Nasierowska-Guttmejer, Grazyna Rydzewska-Wyszkowska, Janusz Strzelczyk, Ewa Malecka-Wojciesko, Zbigniew Sledzinski

Guideline

Consensus

Topics

Digestive Oncology Endoscopy Histopathology Pancreas Radiology & Imaging Surgery

Citation

Prz Gastroenterol. 2019; 14(1): 1–18

Published

2019

UEG Presentation

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Molecular targets in pancreatic cancer

Grainne O'Kane 1

1 Trinity St James's Cancer Institute, Dublin, Ireland

Event

UEG Postgraduate Teaching Programme Vienna 2024

Topics

Digestive Oncology Education & Training Mechanisms & Personalised Medicine Pancreas Standards & Guidelines

Session

Personalised therapy in locally advanced pancreatic cancer

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Introduction

Pancreatic ductal adenocarcinoma (PDAC) has poor prognosis. This bleak outlook is due to the lack of effective drug therapies for PDAC. Therefore, there is an urgent need to develop new and effective medications for PDAC.
Protein kinase R (PKR) is a ubiquitously expressed serine-threonine kinase encoded by EIF2AK2 in humans. Recent studies have uncovered a dual role for PKR in cancer; it can act as either a promoter or suppressor, depending on the type of cancer. This paradoxical effect is thought to be due to variations in PKR expression and their diverse effects on cellular regulation in different tumor microenvironments.
Our study also revealed that PKR promotes the growth of hepatocellular carcinoma cells infected with hepatitis C virus. However, the role of PKR in PDAC remains to be elucidated.

Aims & Methods

This study aimed to identify the roles and mechanisms of action of PKR in PDAC by analyzing clinical evidence and in vitro data obtained from PDAC cell lines.
We used the human pancreatic cancer cell lines (PANC-1 and MIA PaCa-2) and verified PKR expression in PDAC cell lines using RT-PCR and Western blotting. MTS assay was used to determine the effect of PKR on cell proliferation. To elucidate the mechanisms underlying the effect of PKR on PDAC, RNA-seq analysis was conducted. Flow cytometry was performed to investigate the effects of PKR knockdown on cell cycle progression and apoptosis in PDAC cells. Additionally, we used the GEPIA database to compare the expression levels of PKR (EIF2AK2) in pancreatic cancer and normal pancreatic tissues. The Kaplan-Meier Plotter tool was used to analyze the relationship between individual PKR mRNA expression and disease-free survival (DFS) in patients with PDAC.

Results

PDAC cell lines exhibited significantly reduced proliferation when transfected with PKR-targeting siRNAs or treated with PKR inhibitors. RNA-seq analysis revealed a substantial upregulation of GADD45A expression when PKR expression was inhibited. After PKR silencing, cell cycle analysis indicated a pronounced accumulation of cells in the G1 phase, which is consistent with the known role of GADD45A as a cell cycle regulator. Additionally, the inhibition of proliferation resulting from PKR knockdown was reversed upon downregulation of GADD45A, indicating an interactive effect between PKR and GADD45A in regulating PDAC cell growth. Furthermore, as mentioned above, PKR knockdown increased the percentage of cells in the G1 phase, and knockdown of both GADD45A and PKR returned the percentage of cells in the G1 phase to the same level as that in the control. These results indicated that the interaction between PKR and GADD45A plays a critical role in the proliferation of PDAC cells by regulating the cell cycle.
PKR mRNA expression levels in tumor and normal tissues were compared using the GEPIA database. Elevated PKR mRNA expression in tumor tissues compared with that in normal tissues was more pronounced in PDAC than in other carcinomas. We performed a prognostic analysis using the Kaplan-Meier Plotter database to explore the clinical significance of PKR in PDAC. The results showed that patients with elevated PKR mRNA expression had shorter disease-free survival (DFS; n=278; HR=1.84, 95% CI 1.36-2.5). In contrast, the group with high GADD45A expression showed a prolonged DFS. These data were consistent with our in vitro experimental results.

Conclusion

PKR promotes PDAC cell proliferation by modulating cell cycle via regulation of GADD45A expression. These results suggest that PKR is a potential novel therapeutic target for PDAC.

PROTEIN KINASE R REGULATES THE GROWTH OF PANCREATIC DUCTAL ADENOCARCINOMA BY MODULATING THE CELL CYCLE VIA GADD45A

Yuki Numata 1, Mitsuhito Koizumi 1, Takao Watanabe 1, Osamu Yoshida 1, Yoshio Tokumoto 1, Kaori Marui 1, Sho Ishikawa 1, Masahito Kokubu 1, Yusuke Okujima 1, Yoshiki Imamura 1, Teru Kumagi 2, Yoichi Hiasa 1

1 Ehime University Graduate School of Medicine, Shitsukawa, Japan

2 Ehime University Hospital, To-on, Japan

Conference

UEG Week Vienna 2024

Topics

Pancreas

Submission format

Abstract

Session

Pancreatic cancer: Clinical and basic science (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Introduction

Both acute pancreatitis and diabetes mellitus (DM) are known risk factors for pancreatic cancer (PC) development. However, whether post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) is an independent risk factor for PC is under-investigated.

Aims & Methods

We aimed to investigate whether PEP was associated with a higher risk of PC after adjusting for known risk factors of PC among type 2 diabetes (T2D) patients.

All newly diagnosed T2D patients aged ≥18 years between January 1993 and December 2020 from Hong Kong's electronic healthcare database were studied. DM was identified by (i) two abnormal HbA1c ≥6.5% or fasting glucose ≥7 mmol/L test results, (ii) anti-DM medications use, or (iii) International Classification of Diseases Ninth Revision (ICD-9) code 250. Exclusion criteria included history of PC, pancreatic neuroendocrine tumor, serous cystadenoma, and chronic pancreatitis. Index date was defined as three years after T2D diagnosis in order to avoid reverse causality, as new onset diabetes (NOD) may signify underlying pre-existing PC. Primary outcome was PC development. Primary exposure of interest was PEP, which was identified by an amylase or lipase level at least three times the upper limit of normal more than 24 hours and within 7 days after ERCP. We divided the cohort into three groups: (i) those who had never underwent ERCP before index date [ERCP(-)], (ii) history of ERCP without PEP [ERCP(+)/PEP(-)], and (iii) history of PEP [ERCP(+)/PEP(+)]. The comparison of ERCP(+)/PEP(+) group with ERCP(+)/PEP(-) group serves to address indication bias (and hence higher PC risk) necessitating performance of ERCP. Covariates were age, sex, lifestyle factors, metabolic disorders, time-weighted mean HbA1c, cardiovascular diseases, other anti-DM medications, non-aspirin non-steroidal anti-inflammatory drugs, statins, and episode of history of acute pancreatitis. Multivariable Cox regression models were used to calculate adjusted hazard ratios (aHRs) of PC with exposure of interest.

Results

We identified 772,549 T2D patients (mean [SD] age:60.6 [12.4] years;50.3% male), of whom 751,184 (97.2%) was ERCP(-) group , 20,990 (2.7%) ERCP(+)/PEP(-) group, and 375 (0.05%) ERCP(+)/PEP(+) group. The mean (SD) duration of follow-up was 9.1 (+/-5.9) years, and 2,128 (0.3%) incident PC cases were recorded with an incidence rate of 3.0 per 10000 person-years. The PC crude incidence rate was 0.22, 4.47 and 4.76 per 10,000 person-years among ERCP(-), ERCP(+)/PEP(-) and ERCP(+)/PEP(+) groups, respectively. Compared with ERCP(-), ERCP(+)/PEP(-) and ERCP(+)/PEP(+) were associated with a higher risk of PC (aHR:16.8, 95%CI:15.5-18.3; aHR:28.0, 95%CI:15.7-50.2) (Table 1). Compared with ERCP(+)/PEP(-), the aHR of PC was 1.94 (95%CI:1.08-3.48) with ERCP(+)/PEP(+).
Table 1. Association between risk of pancreatic cancer and post-ERCP pancreatitis

	No. of patients	No. of events	Person-years*	Crude incidence rate	HR (95% CI)^†	p-value
Whole cohort
ERCP(-)	751,184	1,491	6,776,558	0.22	Ref	-
ERCP(+)/PEP(-)	20,990	1,024	228,958	4.47	16.8 (15.5 – 18.3)	<0.001
ERCP(+)/PEP(+)	375	12	2,521	4.76	28.0 (15.7 – 50.2)	<0.001
ERCP-cohort
ERCP(+)/PEP(-)	20,990	1,024	228,958	4.47	Ref	-
ERCP(+)/PEP(+)	375	12	2,521	4.76	1.94 (1.08 – 3.48)	0.025
* Person 1,0000 person-years † Adjusted for covariates mentioned above Abbreviations: ERCP, endoscopic retrograde cholangiopancreatography; PEP, post-ERCP pancreatitis; HR, hazard ratio; Ref, reference; 95% CI, 95% confidence interval

Conclusion

In a large population of T2D patients, PEP was an independent risk factor of PC development. Our study findings further consolidate the necessity of minimizing the occurrence of PEP to not just prevent short-term complications of acute pancreatitis but also PC development.

POST-ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY PANCREATITIS WAS AN INDEPENDENT RISK FACTOR OF PANCREATIC CANCER DEVELOPMENT IN PATIENTS WITH TYPE 2 DIABETES

Ka Shing Cheung 1, Jing Tong Tan 2, Xianhua Mao 3, Wai-Kay Seto 3

1 The University of Hong Kong, Hong Kong, Hong Kong|||The University of Hong Kong-Shenzhen Hospital, Shenzhen, China

2 The University of Hong Kong, Hong Kong, Hong Kong

3 The University of Hong Kong-Shenzhen Hospital, Shenzhen, China|||The University of Hong Kong, Hong Kong, Hong Kong

Conference

UEG Week Vienna 2024

Topics

Pancreas

Submission format

Abstract

Session

PANCREAS (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Introduction

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer that poses significant therapeutic challenges. In this regard, the identification of prognostic biomarkers is crucial to improve the prediction of clinical outcomes and guide therapeutic decisions. Tumour-associated autoantibodies (TAAbs) have been identified as prognostic biomarkers in several types of cancer, as they can be generated before the first clinically detectable signs of disease.

Aims & Methods

The aim of this study was to identify TAAbs that can be used as prognostic biomarkers in PDAC. 80 sera from patients with PDAC, divided into four groups according to disease stage, were included in the study: patients with premalignant lesions (n = 20), patients undergoing curative resection after diagnosis (CR) (n = 20), patients with unresectable advanced locoregional disease (LA) (n = 20) and patients with metastatic disease (MT) (n = 20). Sera from each group were analysed divided into 4 pools of 5 samples each using the HuProt Human Protreome microarray v4.0 (CDI Laboratories, Baltimore, MD). Candidate TAAbs with high specific reactivity in MT and/or LA samples were selected according to the following criteria: z-score ≥ 3 in at least 2/4 pools and fold-change > 1.2. The RNAseq data collected in the Human Protein Atlas were used to determine protein expression levels and prognostic value. The GSE15471, GSE28735 and GSE16515 databases were used to compare expression levels with those of healthy subjects without the disease.

Results

43 TAAbs demonstrated high levels of specific reactivity in samples from MT and/or LA patients. Of these highly recognised proteins, 15 were selected for showing notable levels of expression in tumour tissue from PDAC patients and prognostic capacity in some types of cancer. Of these 15, 2 proteins involved in tumour development were identified. Survival analyses showed that six of the 15 selected proteins were significantly associated with a worse prognosis in PDAC patients (p < 0.05). Finally, in the comparison with control tumour tissue, 5 proteins were identified with significantly higher expression in patients diagnosed with the disease (p < 0.05 in at least 2 of the cohorts used).

Conclusion

15 TAAbs have been identified as promising candidates for prognostic biomarkers in PDAC. Further validation studies are required to confirm their prognostic value and to develop a robust biomarker signature with potential for clinical application and market translation.

TUMOUR-ASSOCIATED AUTOANTIBODIES AS PROGNOSTIC BIOMARKERS IN PANCREATIC ADENOCARCINOMA: RESULTS OF A DISCOVERY STUDY BASED ON PROTEIN MICROARRAYS

Cristina Regueiro Expósito 1, Carme García 2, Ainhoa Lapitz 3, Beatriz Coelho 4, Jesús M. Bañales 5, Luis Bujanda Fernández de Piérola 6, Joaquín Cubiella 7

1 Galician Public Foundation for Biomedical Research Galicia Sur, Ourense, Spain

2 Complexo Hospitalario Universitario de Ourense, Ourense, Spain

3 Biodonostia Health Research Institute, San Sebastian, Spain

4 Biodonostia Health Research Institute, University Hospital of Donostia, University of the Basque Country, San Sebastian, Spain

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

6 Instituto Biodonostia, San Sebastián, Spain

7 Complejo Hospitalario de Ourense, Ourense, Spain

Conference

UEG Week Berlin 2025

Topics

Pancreas

Submission format

Abstract

Session

PANCREAS (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Podcast Episode

Journal Podcast

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Are we providing the correct pancreatic enzyme treatment in chronic pancreatitis?

Iago Rodríguez-Lago 1, Friedemann Erchinger 2

1 Hospital Universitario de Galdakao, Bilbao, Spain

2 Kanalspesialistene AS, Bergen, Norway

Topics

Pancreas

Published

2023

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