Evidence map›Paper›PMID 38483348›Full record

ArticleHuman molecular genetics2024

Common single-base insertions in the VNTR of the carboxyl ester lipase (CEL) gene are benign and also likely to arise somatically in the exocrine pancreas.

Ranveig S Brekke, Anny Gravdal, Khadija El Jellas, Grace E Curry, Jianguo Lin, Steven J Wilhelm, Solrun J Steine, Eric Mas, Stefan Johansson, Mark E Lowe and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Human molecular genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

Ranveig S BrekkeGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.ORCID 0000-0003-4824-9190
Anny GravdalGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.
Khadija El JellasGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.
Grace E CurryDepartment of Pediatrics, Washington University School of Medicine, Campus Box 8208, 660 South Euclid Ave, St. Louis, MO 63110, USA.
Jianguo LinDepartment of Pediatrics, Washington University School of Medicine, Campus Box 8208, 660 South Euclid Ave, St. Louis, MO 63110, USA.
Steven J WilhelmDepartment of Pediatrics, Washington University School of Medicine, Campus Box 8208, 660 South Euclid Ave, St. Louis, MO 63110, USA.
Solrun J SteineGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.
Eric MasCancer Research Center of Marseille, Aix Marseille University, CNRS, INSERM, Institut Paoli-Calmettes, CRCM, 27 Bd Leï Roure, 13273 Marseille Cedex 09, France.
Stefan JohanssonCenter for Diabetes Research, Department of Clinical Science, University of Bergen, Jonas Lies vei 87, 5021 Bergen, Norway.ORCID 0000-0002-2298-7008
Mark E LoweDepartment of Pediatrics, Washington University School of Medicine, Campus Box 8208, 660 South Euclid Ave, St. Louis, MO 63110, USA.
Bente B JohanssonCenter for Diabetes Research, Department of Clinical Science, University of Bergen, Jonas Lies vei 87, 5021 Bergen, Norway.
Xunjun XiaoDepartment of Pediatrics, Washington University School of Medicine, Campus Box 8208, 660 South Euclid Ave, St. Louis, MO 63110, USA.
Karianne FjeldGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.
Anders MolvenGade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Jonas Lies vei 91B, 5021 Bergen, Norway.ORCID 0000-0003-1847-3079
Haukeland University Hospital · NOWashington University in St. Louis · USSenter for Krisepsykologi · NOCentre National de la Recherche Scientifique · FR

Funding

Does Proteotoxicity Contribute to Chronic Pancreatitis in Murine Models of Human Carboxyl Ester Lipase (CEL) Genetic Risk Variants?R01DK124415 · NIDDK · WASHINGTON UNIVERSITY · PI LOWE, MARK E. · 2020 to 2023
$1.8M
National Pancreas FoundationNIDDK NIH HHS R01 DK124415NIH HHS R01 DK124415/NIDDKNorwegian Cancer Society 212734-2019Research Council of Norway 289534University of BergenWestern Norway Regional Health Authority 912057
6 · The paper itself

Abstract

The CEL gene encodes carboxyl ester lipase, a pancreatic digestive enzyme. CEL is extremely polymorphic due to a variable number tandem repeat (VNTR) located in the last exon. Single-base deletions within this VNTR cause the inherited disorder MODY8, whereas little is known about VNTR single-base insertions in pancreatic disease. We therefore mapped CEL insertion variants (CEL-INS) in 200 Norwegian patients with pancreatic neoplastic disorders. Twenty-eight samples (14.0%) carried CEL-INS alleles. Most common were insertions in repeat 9 (9.5%), which always associated with a VNTR length of 13 repeats. The combined INS allele frequency (0.078) was similar to that observed in a control material of 416 subjects (0.075). We performed functional testing in HEK293T cells of a set of CEL-INS variants, in which the insertion site varied from the first to the 12th VNTR repeat. Lipase activity showed little difference among the variants. However, CEL-INS variants with insertions occurring in the most proximal repeats led to protein aggregation and endoplasmic reticulum stress, which upregulated the unfolded protein response. Moreover, by using a CEL-INS-specific antibody, we observed patchy signals in pancreatic tissue from humans without any CEL-INS variant in the germline. Similar pancreatic staining was seen in knock-in mice expressing the most common human CEL VNTR with 16 repeats. CEL-INS proteins may therefore be constantly produced from somatic events in the normal pancreatic parenchyma. This observation along with the high population frequency of CEL-INS alleles strongly suggests that these variants are benign, with a possible exception for insertions in VNTR repeats 1-4.

Indexed as

Minisatellite RepeatsPancreas, ExocrineAllelesAnimalsFemaleGene FrequencyHEK293 CellsHumansLipaseMaleMiceMutagenesis, InsertionalPancreatic NeoplasmsCEL protein, humanLipasecarboxyl ester lipasepancreatic cancersingle-base insertionsvariable number tandem repeat

Identifiers

PMID38483348
PMCPMC11102595
OpenAlexW4392791262

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.