Increased cyclooxygenase-2 expression in juvenile polyposis syndrome

Clin Gastroenterol Hepatol. 2009 Jan;7(1):93-7. doi: 10.1016/j.cgh.2008.07.030. Epub 2008 Aug 5.


Background & aims: Gastrointestinal juvenile polyps may occur in juvenile polyposis syndrome (JPS) or sporadically. JPS is an autosomal-dominant condition caused by a germline defect in SMAD4 or BMPR1A in 50% to 60% of cases, and is characterized by multiple juvenile polyps, predominantly in the colorectum. JPS has an increased risk of gastrointestinal malignancy but sporadic juvenile polyps do not. Cyclooxygenase-2 (COX-2) expression is increased in gastrointestinal tumorigenesis and familial adenomatous polyposis. Inhibition of COX-2 leads to regression of colorectal adenomas in familial adenomatous polyposis patients and inhibits gastrointestinal tumorigenesis. To investigate the role of COX-2 in juvenile polyps, we compared the expression of COX-2 in juvenile polyps from a well-defined group of juvenile polyposis patients and sporadic juvenile polyps.

Methods: COX-2 expression was assessed in 24 genetically well-defined JPS patients and 26 patients with sporadic juvenile polyps using tissue microarray analysis. Two additional markers, Hu-antigen R, a stabilizer of messenger RNA, and CCAAT/enhancer-binding protein beta, a transcription factor, both associated with increased COX-2 expression, also were investigated.

Results: Increased COX-2 expression in JPS patients was noted compared with patients with sporadic juvenile polyps (P < .001). Also, JPS patients with a BMPR1A germline defect had higher COX-2 expression than did JPS patients in whom no germline mutation was detected. High COX-2 levels correlated with increased cytoplasmic Hu-antigen R expression in JPS polyps (P = .022), but not in sporadic juvenile polyps.

Conclusions: Juvenile polyposis and sporadic juvenile polyps show distinctive expression profiles of COX-2 that may have clinical implications.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyposis Coli / physiopathology*
  • Adolescent
  • Adult
  • Antigens, Surface / biosynthesis
  • Bone Morphogenetic Protein Receptors, Type I / genetics
  • CCAAT-Enhancer-Binding Protein-beta / biosynthesis
  • Child
  • Child, Preschool
  • Cyclooxygenase 2 / biosynthesis*
  • ELAV Proteins
  • ELAV-Like Protein 1
  • Gene Expression Profiling*
  • Humans
  • Infant
  • Middle Aged
  • Oligonucleotide Array Sequence Analysis
  • RNA-Binding Proteins / biosynthesis


  • Antigens, Surface
  • CCAAT-Enhancer-Binding Protein-beta
  • ELAV Proteins
  • ELAV-Like Protein 1
  • ELAVL1 protein, human
  • RNA-Binding Proteins
  • Cyclooxygenase 2
  • BMPR1A protein, human
  • Bone Morphogenetic Protein Receptors, Type I