title: p73 Overexpression and angiogenesis in human colorectal carcinoma.
abstract: BACKGROUND
  Solid tumors requires neovascularization for growth and metastasis. Angiogenesis depends on the local balance between positive and negative effectors, the production of which can be regulated by oncogenes and tumor suppressor genes. The aim of this study was to investigate expression of p73, a gene homologous to the tumor suppressor gene p53, in colorectal cancer and its relationship to angiogenesis.
  
  
  METHODS
  p73 expression was examined by immunohistochemistry and western blot analysis on 56 primary colon carcinomas with matched normal mucosas. Vascular endothelial growth factor (VEGF) and microvessels were highlighted using a monoclonal antibody specific to VEGF and von Willebrand factor (vWF).
  
  
  RESULTS
  The immunoexpressions of p73 were significantly higher in the primary colorectal carcinomas than that in the matched normal mucosa (P < 0.001). Western blotting showed that 85% patients have a high level of p73 expression (more than double the normal level). A close association between p73 and VEGF expression level was observed (P = 0.016). Colorectal adenocarcinoma that expressed p73 showed significantly greater vascularity than p73-negative tumors (P = 0.012). However, no association between immunoexpression of p73 and tumor stage or differentiation was observed.
  
  
  CONCLUSIONS
  These findings suggest a potential role of p73 in tumor angiogenesis.
authors.affiliation: Center of Laboratory Medicine, Hua Shan Hospital, Fudan University, Shanghai, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Guan
authors.forename: Hai-Xia
authors.initials: HX
authors.lastname: Peng
authors.forename: Bo
authors.initials: B
authors.lastname: Yu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lu
mesh_terms: D000230:Adenocarcinoma / Q000098:blood supply / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015179:Colorectal Neoplasms / Q000098:blood supply* / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000096:biosynthesis*; D016228:Endothelial Growth Factors / Q000096:biosynthesis; D005260:Female; D016147:Genes, Tumor Suppressor; D016158:Genes, p53; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis; D007413:Intestinal Mucosa / Q000378:metabolism; D008222:Lymphokines / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D009687:Nuclear Proteins / Q000096:biosynthesis*; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014841:von Willebrand Factor / Q000096:biosynthesis
chemical_list: D004268:DNA-Binding Proteins; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D009687:Nuclear Proteins; C000606460:TP73 protein, human; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014841:von Willebrand Factor