title: Annexin II overexpression correlates with stromal tenascin-C overexpression: a prognostic marker in colorectal carcinoma.
abstract: BACKGROUND
  Overexpression of annexin II, a calcium-dependent phospholipid-binding protein, has been reported in various carcinomas. One of its ligands is tenascin-C, an extracellular matrix glycoprotein with predominantly antiadhesive qualities that also has been reported to be a prognostic marker for several carcinomas. In the current study, the authors investigated the correlation between the overexpression of annexin II and tenascin-C in colorectal carcinoma.
  
  
  METHODS
  Western blot analysis of annexin II expression was examined in four human colorectal carcinoma cell lines. Using immunohistochemical methods, the authors also examined expression of annexin II and tenascin-C in 105 primary colorectal carcinoma cases.
  
  
  RESULTS
  Although annexin II was expressed in human colon carcinoma cell lines, there was no apparent correlation between its expression level and the metastatic potential of these cell lines. The authors observed overexpression of annexin II and tenascin-C proteins in 29.5% and 49.5%, respectively, of colorectal carcinoma cases. Overexpression of annexin II was found to be correlated significantly with histologic type, tumor size, depth of invasion, and pTNM stage, whereas tenascin-C overexpression was noted to be correlated significantly with histologic type, depth of invasion, lymphatic invasion, venous invasion, lymph node metastasis, and pTNM stage. Expression of annexin II was shown to be correlated significantly with that of tenascin-C. Multivariate analysis demonstrated that annexin II and tenascin-C cooverexpression was an independent factor of poor prognosis in patients with colorectal carcinoma.
  
  
  CONCLUSIONS
  The data from the current study suggest that both annexin II and tenascin-C are overexpressed in advanced colorectal carcinoma and that they may be related to the progression and metastatic spread of colorectal carcinoma.
authors.affiliation: First Department of Surgery, Nara Medical University, Kashihara, Nara, Japan. ekazu@nmu-gw.naramed-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Emoto
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: H
authors.initials: H
authors.lastname: Sawada
authors.forename: H
authors.initials: H
authors.lastname: Fujimoto
authors.forename: M
authors.initials: M
authors.lastname: Ueno
authors.forename: T
authors.initials: T
authors.lastname: Takayama
authors.forename: K
authors.initials: K
authors.lastname: Kamada
authors.forename: A
authors.initials: A
authors.lastname: Naito
authors.forename: S
authors.initials: S
authors.lastname: Hirao
authors.forename: Y
authors.initials: Y
authors.lastname: Nakajima
mesh_terms: D017306:Annexin A2 / Q000032:analysis*; D014408:Biomarkers, Tumor / Q000032:analysis*; D015153:Blotting, Western; D002460:Cell Line; D015179:Colorectal Neoplasms / Q000737:chemistry* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008207:Lymphatic Metastasis; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D011379:Prognosis; D019063:Tenascin / Q000032:analysis*; D014407:Tumor Cells, Cultured
chemical_list: D017306:Annexin A2; D014408:Biomarkers, Tumor; D019063:Tenascin