Abstract Book UEG Week 2020 - 86
OP122
Tuesday, October 13, 2020
Monday, October 12, 2020
Sunday, October 11, 2020
MODELLING PLASTICITY AND DYSPLASIA OF PANCREATIC DUCTAL
ORGANOIDS DERIVED FROM HUMAN PLURIPOTENT STEM CELLS
Merkle J.1, Breunig M.1, Melzer M.K.1, Engleitner T.2,
Hermann P.C.1, Perkhofer L.1, Krüger J.1, Heller S.1, Müller M.1,
Seufferlein T.1, Rad R.2, Wagner M.1, Meier M.3, Hohwieler M.1,
Kleger A.1
1
University Hospital Ulm, Internal Medicine I, Ulm, Germany,
2
Technical University of Munich, Center for Translational Cancer
Research, Munich, Germany, 3Helmholtz Zentrum Munich,
Helmholtz Pioneer Campus, Munich, Germany
Contact E-Mail Address: jessica.merkle@uni-ulm.de
Introduction: Personalized in vitro models for dysplasia and carcinogenesis in the pancreas have been constrained by insufficient engineering approaches to generate human exocrine pancreatic tissue. Human pluripotent stem cells (hPSCs) may provide the appropriate platform for biomedical studies due to their capability to differentiate into every cell type in the
human body. We established a differentiation matrix to generate virtually
pure pancreatic duct-like organoids (PDLOs) from hPSCs. These PDLOs
showed morphological, transcriptional and functional characteristics of
human pancreatic ducts.
Aims & Methods: We generated an early in vitro cancer model by introduction of a Doxycycline-inducible piggyBac system in hPSCs which allows timed expression of oncogenic KRASG12D. Wildtype hPSCs as well as
a CRISPR/Cas-engineered CDKN2AKO/KO line both armed with oncogenic
KRAS were differentiated according to our protocol to the ductal lineage,
followed by oncogene activation in vitro and in vivo.
Results: These PDLOs showed a characteristic growth phenotype of lumen-filling after KRASG12D induction, which was further characterized on
the molecular level and demonstrated senescence and growth arrest accompanied with increased epithelia-to-mesenchymal transition (EMT).
These oncogene-induced responses were even more pronounced in PDLOs with mutated KRAS and genetic covariance of CDKN2AKO/KO. Orthotopic transplantation was additionally incorporated into the experimental
workflow. While transplanted PDLOs with oncogenic KRAS alone developed to well-differentiated tumours, PDLOs with KRAS and CDKN2A-loss
resulted in dedifferentiated human pancreatic ductal adenocarcinomas
(PDAC) in vivo.
Conclusion: Summarized, our novel and unique differentiation platform
generates human untransformed ducts and allows modelling of plasticity, dysplasia, and cancer formation in a human and genetically defined
background in the pancreas. Thereby, we also show that human ducts are
indeed permissive to generate PDAC. Tailored genome editing strategies
mimicking the mutational make-up of human PDAC will open novel opportunities to provide a unique and valuable human PDAC model.
Disclosure: Nothing to disclose
OP123
BARIATRIC SURGERY DECREASES PREVALENCE OF PANCREATIC
CANCER IN PATIENTS WITH PRIOR DIABETES AND OBESITY: A 20-YEAR
NATIONAL ANALYSIS
Syed A.1,2, Seoud T.1, Farah K.1, Eid G.1, Thakkar S.3
1
Allegheny Health Network, Gastroenterology, Pittsburgh,
United States, 2Case Western Reserve University, Internal
Medicine, Cleveland, United States, 3Allegheny Health Network,
Gastroenterology, Sewickley, United States
Contact E-Mail Address: aslam.syed@ahn.org
Introduction: The prevalence of pancreatic cancer (PC) is on the rise and
is predicted to be second-leading cause of cancer related deaths in the
near future. Obesity and type 2 diabetes (DM) are well known risk factors for PC via chronic inflammation, excess hormones and growth factors released by adipose tissue. Bariatric surgery (BS) has been shown to
improve hyperglycemia and even resolve it in many cases more so than
medical therapy alone.
Aims & Methods: We aim to evaluate the role of BS in the prevalence of PC
in patients with prior DM and obesity. We queried the population-based
Explorys database (IBM, New York) from 1999-2019 to collect aggregated de-identified electronic health records. Data was obtained using the
SNOMED-CT coding system to search for patients with "malignant tumor
of pancreas" and "type 2 diabetes mellitus." A temporal relationship was
established to observe patients with (1) DM and obesity (defined as BMI ≥
35) with or without subsequent (2) bariatric surgery (either Roux-en-Y gastric bypass or sleeve gastrectomy) and (3) lastly having a diagnosis of PC.
Results: We identified 1,435,350 patients with concomitant DM and obesity, of which 10,620 (0.7%) had record of BS subsequently. The majority
of patients did not undergo BS (98.9%). The prevalence of PC was significantly higher in patients with predisposing DM and obesity without record
of BS versus those who did have BS (0.32% vs. 0.19%, P = 0.0179). Patients
with DM and obesity that underwent BS had higher rates of being female,
younger (18-65 yrs. of age), and Caucasian or African-American (P < 0.05).
Conclusion: Bariatric surgery significantly decreased the prevalence of
pancreatic cancer with prior DM and obesity versus patients with no record of bariatric surgery. Clinicians should consider bariatric surgery in
eligible patients with metabolic disorders such as diabetes and obesity.
Disclosure: Nothing to disclose
DM-Obesity with BS
(N = 10,620)
DM-Obesity without BS
(N = 1,418,950)
P
Male
2,870 (27.0)
601,950 (42.4)
<0.0001
Female
7,750 (73.0)
816,810 (57.6)
<0.0001
Sex, n (%)
Age, n (%)
18-65
8,390 (79.0)
770,900 (54.3)
<0.0001
> 65
2,240 (21.1)
647,030 (45.6)
<0.0001
Race, n (%)
Caucasian
8,290 (78.1)
1,083,410 (76.4)
<0.0001
African American
1,960 (18.5)
244,750 (17.2)
0.0004
Asian
40 (0.4)
11,810 (0.8)
<0.0001
Hispanic/Latin
American
150 (1.4)
23,340 (1.6)
0.1016
[Baseline Demographic Data of Patients with Type 2 Diabetes and Obesity]
86
UEG Journal | Abstract Book
Abstract Book UEG Week 2020
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