COMP is selectively up-regulated in degenerating acinar cells in chronic pancreatitis and in chronic-pancreatitis-like lesions in pancreatic cancer

Q. Liao, J. Kleeff, Y. Xiao, P. E. Di Cesare, Murray Korc, A. Zimmermann, M. W. Büchler, Helmut Friess

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Background: Chronic pancreatitis (CP) is an inflammatory disease of the pancreas characterized histomorphologically by progressive development of fibrosis and atrophy of the pancreatic parenchyma. Cartilage oligomeric matrix protein (COMP) is a member of the thrombospondin (TSP) family of extracellular glycoproteins that is expressed in CP tissues. In the present study, we characterized COMP mRNA and protein expression in the normal pancreas, chronic pancreatitis, and pancreatic cancer tissues. Methods: 15 normal pancreatic tissues, 14 CP tissues and 14 pancreatic cancer tissues were analyzed by Northern blotting, Western blotting, in situ hybridization and immunohistochemistry. Results: COMP mRNA and protein were detected at moderate to high levels in chronic pancreatitis tissues, at moderate levels in pancreatic cancer tissues, but at low levels in normal pancreatic tissues and in four pancreatic cancer cell lines. COMP mRNA signals and immunoreactivity were strongly present in the cytoplasm of degenerating acinar cells in CP tissues as well as in CP-like lesions in pancreatic cancer tissues. COMP protein was also present in the fibrotic tissue in CP. In contrast, COMP expression was weak to absent in the cytoplasm of cancer cells in pancreatic cancer tissues, and in ductal cells and islet cells in normal pancreatic tissues. Conclusion: COMP is preferentially expressed in degenerating acinar cells in CP and in CP-like areas in pancreatic cancer, suggesting a potential role of this gene in the course of acinar cell degeneration and dedifferentiation. COMP might thus serve as a marker for tissue destruction and disease activity in CP.

Original languageEnglish (US)
Pages (from-to)207-215
Number of pages9
JournalScandinavian Journal of Gastroenterology
Volume38
Issue number2
DOIs
StatePublished - Feb 1 2003
Externally publishedYes

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Cartilage Oligomeric Matrix Protein
Acinar Cells
Chronic Pancreatitis
Pancreatic Neoplasms
Messenger RNA
Pancreas
Cytoplasm
Cell Dedifferentiation
Thrombospondins
Proteins

Keywords

  • Chronic pancreatitis
  • COMP
  • Fibrosis
  • Pancreatic cancer

ASJC Scopus subject areas

  • Gastroenterology

Cite this

COMP is selectively up-regulated in degenerating acinar cells in chronic pancreatitis and in chronic-pancreatitis-like lesions in pancreatic cancer. / Liao, Q.; Kleeff, J.; Xiao, Y.; Di Cesare, P. E.; Korc, Murray; Zimmermann, A.; Büchler, M. W.; Friess, Helmut.

In: Scandinavian Journal of Gastroenterology, Vol. 38, No. 2, 01.02.2003, p. 207-215.

Research output: Contribution to journalArticle

Liao, Q. ; Kleeff, J. ; Xiao, Y. ; Di Cesare, P. E. ; Korc, Murray ; Zimmermann, A. ; Büchler, M. W. ; Friess, Helmut. / COMP is selectively up-regulated in degenerating acinar cells in chronic pancreatitis and in chronic-pancreatitis-like lesions in pancreatic cancer. In: Scandinavian Journal of Gastroenterology. 2003 ; Vol. 38, No. 2. pp. 207-215.
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AU - Di Cesare, P. E.

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AB - Background: Chronic pancreatitis (CP) is an inflammatory disease of the pancreas characterized histomorphologically by progressive development of fibrosis and atrophy of the pancreatic parenchyma. Cartilage oligomeric matrix protein (COMP) is a member of the thrombospondin (TSP) family of extracellular glycoproteins that is expressed in CP tissues. In the present study, we characterized COMP mRNA and protein expression in the normal pancreas, chronic pancreatitis, and pancreatic cancer tissues. Methods: 15 normal pancreatic tissues, 14 CP tissues and 14 pancreatic cancer tissues were analyzed by Northern blotting, Western blotting, in situ hybridization and immunohistochemistry. Results: COMP mRNA and protein were detected at moderate to high levels in chronic pancreatitis tissues, at moderate levels in pancreatic cancer tissues, but at low levels in normal pancreatic tissues and in four pancreatic cancer cell lines. COMP mRNA signals and immunoreactivity were strongly present in the cytoplasm of degenerating acinar cells in CP tissues as well as in CP-like lesions in pancreatic cancer tissues. COMP protein was also present in the fibrotic tissue in CP. In contrast, COMP expression was weak to absent in the cytoplasm of cancer cells in pancreatic cancer tissues, and in ductal cells and islet cells in normal pancreatic tissues. Conclusion: COMP is preferentially expressed in degenerating acinar cells in CP and in CP-like areas in pancreatic cancer, suggesting a potential role of this gene in the course of acinar cell degeneration and dedifferentiation. COMP might thus serve as a marker for tissue destruction and disease activity in CP.

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