Characterization of CEL-DUP2: Complete duplication of the carboxyl ester lipase gene is unlikely to influence risk of chronic pancreatitis.


Journal

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
ISSN: 1424-3911
Titre abrégé: Pancreatology
Pays: Switzerland
ID NLM: 100966936

Informations de publication

Date de publication:
Apr 2020
Historique:
received: 06 01 2020
revised: 17 01 2020
accepted: 18 01 2020
pubmed: 3 2 2020
medline: 27 2 2021
entrez: 3 2 2020
Statut: ppublish

Résumé

Carboxyl ester lipase is a pancreatic enzyme encoded by CEL, an extremely polymorphic human gene. Pathogenic variants of CEL either increases the risk for chronic pancreatitis (CP) or cause MODY8, a syndrome of pancreatic exocrine and endocrine dysfunction. Here, we aimed to characterize a novel duplication allele of CEL (CEL-DUP2) and to investigate whether it associates with CP or pancreatic cancer. The structure of CEL-DUP2 was determined by a combination of Sanger sequencing, DNA fragment analysis, multiplex ligation-dependent probe amplification and whole-genome sequencing. We developed assays for screening of CEL-DUP2 and analyzed cohorts of idiopathic CP, alcoholic CP and pancreatic cancer. CEL protein expression was analyzed by immunohistochemistry. CEL-DUP2 consists of an extra copy of the complete CEL gene. The allele has probably arisen from non-allelic, homologous recombination involving the adjacent pseudogene of CEL. We found no association between CEL-DUP2 carrier frequency and CP in cohorts from France (cases/controls: 2.5%/2.4%; P = 1.0), China (10.3%/8.1%; P = 0.08) or Germany (1.6%/2.3%; P = 0.62). Similarly, no association with disease was observed in alcohol-induced pancreatitis (Germany: 3.2%/2.3%; P = 0.51) or pancreatic cancer (Norway; 2.5%/3.2%; P = 0.77). Notably, the carrier frequency of CEL-DUP2 was more than three-fold higher in Chinese compared with Europeans. CEL protein expression was similar in tissues from CEL-DUP2 carriers and controls. Our results support the contention that the number of CEL alleles does not influence the risk of pancreatic exocrine disease. Rather, the pathogenic CEL variants identified so far involve exon 11 sequence changes that substantially alter the protein's tail region.

Sections du résumé

BACKGROUND/OBJECTIVES OBJECTIVE
Carboxyl ester lipase is a pancreatic enzyme encoded by CEL, an extremely polymorphic human gene. Pathogenic variants of CEL either increases the risk for chronic pancreatitis (CP) or cause MODY8, a syndrome of pancreatic exocrine and endocrine dysfunction. Here, we aimed to characterize a novel duplication allele of CEL (CEL-DUP2) and to investigate whether it associates with CP or pancreatic cancer.
METHODS METHODS
The structure of CEL-DUP2 was determined by a combination of Sanger sequencing, DNA fragment analysis, multiplex ligation-dependent probe amplification and whole-genome sequencing. We developed assays for screening of CEL-DUP2 and analyzed cohorts of idiopathic CP, alcoholic CP and pancreatic cancer. CEL protein expression was analyzed by immunohistochemistry.
RESULTS RESULTS
CEL-DUP2 consists of an extra copy of the complete CEL gene. The allele has probably arisen from non-allelic, homologous recombination involving the adjacent pseudogene of CEL. We found no association between CEL-DUP2 carrier frequency and CP in cohorts from France (cases/controls: 2.5%/2.4%; P = 1.0), China (10.3%/8.1%; P = 0.08) or Germany (1.6%/2.3%; P = 0.62). Similarly, no association with disease was observed in alcohol-induced pancreatitis (Germany: 3.2%/2.3%; P = 0.51) or pancreatic cancer (Norway; 2.5%/3.2%; P = 0.77). Notably, the carrier frequency of CEL-DUP2 was more than three-fold higher in Chinese compared with Europeans. CEL protein expression was similar in tissues from CEL-DUP2 carriers and controls.
CONCLUSIONS CONCLUSIONS
Our results support the contention that the number of CEL alleles does not influence the risk of pancreatic exocrine disease. Rather, the pathogenic CEL variants identified so far involve exon 11 sequence changes that substantially alter the protein's tail region.

Identifiants

pubmed: 32007358
pii: S1424-3903(20)30029-6
doi: 10.1016/j.pan.2020.01.011
pii:
doi:

Substances chimiques

DNA 9007-49-2
CEL protein, human EC 3.1.1.3
Lipase EC 3.1.1.3

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

377-384

Informations de copyright

Copyright © 2020 IAP and EPC. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no competing financial interests.

Auteurs

Karianne Fjeld (K)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway; Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway. Electronic address: karianne.fjeld@uib.no.

Emmanuelle Masson (E)

Univ Brest, Inserm, EFS, UMR 1078, GGB, F-29200, Brest, France; CHRU Brest, Service de Génétique, Brest, France.

Jin-Huan Lin (JH)

Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China.

Patrick Michl (P)

Department of Internal Medicine I, Martin Luther University, Halle, Germany.

Tomasz Stokowy (T)

Genomics Core Facility, Department of Clinical Science, University of Bergen, Bergen, Norway.

Anny Gravdal (A)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway; Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway.

Khadija El Jellas (K)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway.

Solrun J Steine (SJ)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Dag Hoem (D)

Department of Gastrointestinal Surgery, Haukeland University Hospital, Bergen, Norway.

Bente B Johansson (BB)

Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway.

Monica Dalva (M)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway.

Claudia Ruffert (C)

Department of Internal Medicine I, Martin Luther University, Halle, Germany.

Wen-Bin Zou (WB)

Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China.

Zhao-Shen Li (ZS)

Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China.

Pål R Njølstad (PR)

Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway; Department of Pediatrics and Adolescent Medicine, Haukeland University Hospital, Bergen, Norway.

Jian-Min Chen (JM)

Univ Brest, Inserm, EFS, UMR 1078, GGB, F-29200, Brest, France.

Zhuan Liao (Z)

Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China.

Stefan Johansson (S)

Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway; Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway.

Jonas Rosendahl (J)

Department of Internal Medicine I, Martin Luther University, Halle, Germany.

Claude Férec (C)

Univ Brest, Inserm, EFS, UMR 1078, GGB, F-29200, Brest, France; CHRU Brest, Service de Génétique, Brest, France.

Anders Molven (A)

The Gade Laboratory for Pathology, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway; Department of Pathology, Haukeland University Hospital, Bergen, Norway.

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