title: Clinical impact of pentraxin family expression on prognosis of pancreatic carcinoma.
abstract: BACKGROUND
  Inflammatory mediators may have decisive roles at different stages of tumour development. Mediators within the pentraxin family may be used as strong biomarkers in prognosis of advanced pancreatic carcinoma patients.
  
  
  METHODS
  Using pancreatic carcinoma cell lines and gene transfectant, we measured long pentraxin (PTX3) level in culture solution and carried out cellular migration assay in vitro. In vivo study of the treatment-naive patients with advanced pancreatic carcinoma assigned to undergo gemcitabine therapy was prospectively conducted to measure and investigate the role of plasma PTX3, C-reactive protein (CRP), and eight inflammatory mediators by using collected clinical data.
  
  
  RESULTS
  Elevated PTX3 production was observed in several cell lines, and a direct relationship between migratory activity and PTX3 level was identified in vitro. High PTX3 level (117 days) was significantly less than that of patients with low PTX3 level (357 days, P<0.001). Multivariate analysis of the pancreatic carcinoma revealed a strong correlation between pentraxin family member expression and prognosis of pancreatic carcinoma. The relationship between PTX3 expression and the expression of other pro-inflammatory mediators indicated that PTX3 level is positively correlated with levels of CRP, interleukin-6, and macrophage-inhibitory factor.
  
  
  CONCLUSIONS
  Pentraxin family members, especially PTX3, may be used as promising biomarkers in the prognosis of pancreatic carcinoma patients.
authors.affiliation: Division of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, Tokyo, Japan. shkondo@ncc.go.jp
authors.forename: S
authors.initials: S
authors.lastname: Kondo
authors.forename: H
authors.initials: H
authors.lastname: Ueno
authors.forename: H
authors.initials: H
authors.lastname: Hosoi
authors.forename: J
authors.initials: J
authors.lastname: Hashimoto
authors.forename: C
authors.initials: C
authors.lastname: Morizane
authors.forename: F
authors.initials: F
authors.lastname: Koizumi
authors.forename: K
authors.initials: K
authors.lastname: Tamura
authors.forename: T
authors.initials: T
authors.lastname: Okusaka
mesh_terms: D000328:Adult; D000368:Aged; D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000096:biosynthesis / Q000097:blood; D002097:C-Reactive Protein / Q000096:biosynthesis*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000502:physiology; D003841:Deoxycytidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011379:Prognosis; D011446:Prospective Studies; D000683:Serum Amyloid P-Component / Q000096:biosynthesis*; D014162:Transfection; D016896:Treatment Outcome; D000093542:Gemcitabine; D000099153:Pentraxins
chemical_list: D000964:Antimetabolites, Antineoplastic; D014408:Biomarkers, Tumor; D002097:C-Reactive Protein; D003841:Deoxycytidine; D018836:Inflammation Mediators; D000683:Serum Amyloid P-Component; D000093542:Gemcitabine; D000099153:Pentraxins