title: COX-2 expression in DCIS: correlation with VEGF, HER-2/neu, prognostic molecular markers and clinicopathological features.
abstract: OBJECTIVE
  There is considerable evidence that links COX-2 to the development of cancer. The aim of our study was to assess, by immunohistochemistry, COX-2 expression in ductal carcinoma in situ (DCIS) and its possible correlation with HER-2/neu, vascular endothelial growth factor (VEGF) expression and other common immunohistochemical parameters (p53, ER, PGR, Ki67).
  
  
  RESULTS
  Tissue samples of 49 archival cases of DCIS without any invasive component were analysed for COX-2, HER-2/neu, VEGF, oestrogen and progesterone receptors, Ki67 and p53 by immunohistochemistry using specific antibodies. COX-2 expression was detected in 43 (87.8%) tissue samples, of which 12 (24.5%) were graded as weak, 22 (44.9%) as moderate and nine (8.4%) as high expression. Only six (12.2%) lesions were negative for COX-2 expression. VEGF expression was detected in 93.8% of samples; 66.7% of lesions were found to be positive for HER-2/neu expression. Furthermore, COX-2 expression was significantly correlated with VEGF expression (P = 0.003). A significant positive correlation was also observed between COX-2 and HER-2/neu expression (P < 0.0001).
  
  
  CONCLUSIONS
  Our results suggest that COX-2 is highly expressed in DCIS and takes part in the molecular pathway implicated in progression of breast cancer and may provide a rationale for targeting COX-2 in preinvasive breast cancer therapy.
authors.affiliation: Surgical Pathology, Campus Bio-Medico University, Rome, Italy. g.perrone@unicampus.it
authors.forename: G
authors.initials: G
authors.lastname: Perrone
authors.forename: D
authors.initials: D
authors.lastname: Santini
authors.forename: B
authors.initials: B
authors.lastname: Vincenzi
authors.forename: M
authors.initials: M
authors.lastname: Zagami
authors.forename: A
authors.initials: A
authors.lastname: La Cesa
authors.forename: A
authors.initials: A
authors.lastname: Bianchi
authors.forename: V
authors.initials: V
authors.lastname: Altomare
authors.forename: A
authors.initials: A
authors.lastname: Primavera
authors.forename: C
authors.initials: C
authors.lastname: Battista
authors.forename: A
authors.initials: A
authors.lastname: Vetrani
authors.forename: G
authors.initials: G
authors.lastname: Tonini
authors.forename: C
authors.initials: C
authors.lastname: Rabitti
mesh_terms: D000328:Adult; D000368:Aged; D014408:Biomarkers, Tumor / Q000032:analysis; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology*; D002278:Carcinoma in Situ / Q000378:metabolism / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism / Q000473:pathology*; D051546:Cyclooxygenase 2; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008565:Membrane Proteins; D008875:Middle Aged; D011379:Prognosis; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013223:Statistics as Topic; D016159:Tumor Suppressor Protein p53 / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D014408:Biomarkers, Tumor; D051546:Cyclooxygenase 2; D019394:Ki-67 Antigen; D008565:Membrane Proteins; D011451:Prostaglandin-Endoperoxide Synthases; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; D042461:Vascular Endothelial Growth Factor A; C496540:PTGS2 protein, human