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Pancreas. 2016 Apr;45(4):613-9. doi: 10.1097/MPA.0000000000000521.

Glucagon-Like Peptide-1 Receptor Expression in Normal and Neoplastic Human Pancreatic Tissues.

Author information

1
From the *Department of Pathology, the Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, MD; †Department of Pathology, Seoul National University College of Medicine, Seoul, South Korea; and the Departments of ‡Oncology and §Medicine, the Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, MD.

Abstract

OBJECTIVES:

Studies have proposed pro-oncogenic effects of glucagon-like peptide-1 receptor (GLP-1R) agonists in the pancreas by promoting GLP-1R overactivation in pancreatic cells. However, the expression of GLP-1R in normal and neoplastic pancreatic cells remains poorly defined, and reliable methods for detecting GLP-1R in tissue specimens are needed.

METHODS:

We used RNA in situ hybridization to quantify glp-1r RNA in surgically resected human pancreatic specimens, including pancreatic ductal adenocarcinoma (PDAC), preinvasive intraepithelial lesions (pancreatic intraepithelial neoplasia), and non-neoplastic ductal, acinar, and endocrine cells. A mixed-effect linear regression model was used to investigate the relationship between glp-1r signals and all cells, ordered by increasing grade of dysplasia.

RESULTS:

All cell types had evidence of glp-1r transcripts, with the highest expression in endocrine cells and lowest in ductal cells. The slope of the fitted line was not significantly different from zero (0.07; 95% confidence interval, -0.0094 to 0.244; P = 0.39), suggesting that progression from normal cells to PDAC is not associated with a parallel increase in glp-1r RNA. A series of pairwise comparisons between all cell types with respect to their glp-1r expression showed no significant difference in glp-1r in cancer, pancreatic intraepithelial neoplasia, and acinar and ductal cells.

CONCLUSIONS:

Our study supports the lack of evidence for GLP-1R overexpression in PDAC.

PMID:
26495786
PMCID:
PMC4783303
DOI:
10.1097/MPA.0000000000000521
[Indexed for MEDLINE]
Free PMC Article

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