Khadija El Jellas
University of Bergen
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Publication
Featured researches published by Khadija El Jellas.
Pancreatology | 2017
Bente B. Johansson; Karianne Fjeld; Khadija El Jellas; Anny Gravdal; Monica Dalva; Erling Tjora; Helge Ræder; Rohit N. Kulkarni; Stefan Johansson; Pål R. Njølstad
The enzyme carboxyl ester lipase (CEL), also known as bile salt-dependent or -stimulated lipase (BSDL, BSSL), hydrolyzes dietary fat, cholesteryl esters and fat-soluble vitamins in the duodenum. CEL is mainly expressed in pancreatic acinar cells and lactating mammary glands. The human CEL gene resides on chromosome 9q34.3 and contains a variable number of tandem repeats (VNTR) region that encodes a mucin-like protein tail. Although the number of normal repeats does not appear to significantly influence the risk for pancreatic disease, single-base pair deletions in the first VNTR repeat cause a syndrome of endocrine and exocrine dysfunction denoted MODY8. Hallmarks are low fecal elastase levels and pancreatic lipomatosis manifesting before the age of twenty, followed by development of diabetes and pancreatic cysts later in life. The mutant protein forms intracellular and extracellular aggregates, suggesting that MODY8 is a protein misfolding disease. Recently, a recombined allele between CEL and its pseudogene CELP was discovered. This allele (CEL-HYB) encodes a chimeric protein with impaired secretion increasing five-fold the risk for chronic pancreatitis. The CEL gene has proven to be exceptionally polymorphic due to copy number variants of the CEL-CELP locus and alterations involving the VNTR. Genome-wide association studies or deep sequencing cannot easily pick up this wealth of genetic variation. CEL is therefore an attractive candidate gene for further exploration of links to pancreatic disease.
Cancer Medicine | 2017
Khadija El Jellas; Dag Hoem; Kristin Gjerde Hagen; May Britt Kalvenes; Sura Aziz; Solrun J. Steine; Heike Immervoll; Stefan Johansson
Both serology‐based and genetic studies have reported an association between pancreatic cancer risk and ABO blood groups. We have investigated this relationship in a cohort of pancreatic cancer patients from Western Norway (n = 237) and two control materials (healthy blood donors, n = 379; unselected hospitalized patients, n = 6149). When comparing patient and blood donor ABO allele frequencies, we found only the A1 allele to be associated with significantly higher risk for pancreatic ductal adenocarcinoma (PDAC) (23.8% vs. 17.9%; OR = 1.43, P = 0.018). Analyzing phenotypes, blood group A was more frequent among PDAC cases than blood donors (50.8% vs. 40.6%; OR = 1.51, P = 0.021), an enrichment fully explained by the A1 subgroup. Blood group O frequency was lower in cases than in blood donors (33.8% vs. 42.7%; OR = 0.69, P = 0.039). This lower frequency was confirmed when cases were compared to hospitalized patients (33.8% vs. 42.9%; OR = 0.68, P = 0.012). Results for blood group B varied according to which control cohort was used for comparison. When patients were classified according to surgical treatment, the enrichment of blood group A was most prominent among unresected cases (54.0%), who also had the lowest prevalence of O (28.7%). There was a statistically significant better survival (P = 0.04) for blood group O cases than non‐O cases among unresected but not among resected patients. Secretor status did not show an association with PDAC or survival. Our study demonstrates that pancreatic cancer risk is influenced by ABO status, in particular blood groups O and A1, and that this association may reflect also in tumor resectability and survival.
Pancreatology | 2017
Monica Dalva; Khadija El Jellas; Solrun J. Steine; Bente B. Johansson; Monika Ringdal; Janniche Torsvik; Heike Immervoll; Dag Hoem; Felix Laemmerhirt; Peter Simon; Markus M. Lerch; Stefan Johansson; Pål R. Njølstad; Frank Ulrich Weiss; Karianne Fjeld
Pancreatology | 2016
Khadija El Jellas; Heike Immervoll; Ole Steffensen; Bente B. Johansson; Karianne Fjeld; Dominique Lombardo; Pĺl Rasmus Njřlstad; Eric Mas
Pancreatology | 2013
Monica Dalva; Khadija El Jellas; Solrun J. Steine; Bente B. Johansson; Monika Ringdal; Janniche Torsvik; Heike Immervoll; Dag Hoem; Felix Laemmerhirt; Peter Simon; Markus M. Lerch; Stefan Johansson; Pål R. Njølstad; Frank Ulrich Weiss; Karianne Fjeld
Pancreatology | 2018
Anny Gravdal; Ranveig Seim Brekke; Khadija El Jellas; Xunjun Xiao; Mark E. Lowe; Dominique Lombardo; Eric Mas; Bente B. Johansson; Karianne Fjeld
Pancreatology | 2018
Khadija El Jellas; Stuart M. Haslam; Man Hung Choi; Anne Dell; Bente B. Johansson; Karianne Fjeld
Pancreatology | 2018
Karianne Fjeld; Emmanuelle Masson; Patrick Michl; Tomasz Stokowy; He Lin; Solrun J. Steine; Bente B. Johansson; Monica Dalva; Khadija El Jellas; Claudia Ruffert; Wen-Bin Zou; Zhao-Shen Li; Pål R. Njølstad; Jian-Min Chen; Zhuan Liao; Stefan Johansson; Jonas Rosendahl; Claude Férec
Pancreatology | 2018
Man Hung Choi; Eline Mejlænder-Larsen; Sophia Manueldas; Khadija El Jellas; Solrun J. Steine; Kjersti Tjensvoll; Hege Aase Sætran; Stian Knappskog; Dag Hoem; Oddmund Nordgård; Randi Hovland
Journal of Biological Chemistry | 2018
Khadija El Jellas; Bente B. Johansson; Karianne Fjeld; Aristotelis Antonopoulos; Heike Immervoll; Man H. Choi; Dag Hoem; Mark E. Lowe; Dominique Lombardo; Pål R. Njølstad; Anne Dell; Eric Mas; Stuart M. Haslam