title: Diagnostic significance of high mobility group I(Y) protein expression in intraductal papillary mucinous tumors of the pancreas.
abstract: BACKGROUND
  Overexpression of the high mobility group I(Y), [HMGI(Y)], gene/proteins has been demonstrated in many types of human malignancies, suggesting that HMGI(Y) may play a vital role in the oncogenic transformation of cells.
  
  
  OBJECTIVE
  To analyze HMGI(Y) expression in intraductal papillary mucinous tumor (IPMT) of the pancreas to verify whether determination of the HMGI(Y) expression level could provide any diagnostic advantages in the pathological diagnosis of IPMT.
  
  
  METHODS
  Thirty-three different lesions from 25 patients with IPMT, including 20 with mild dysplasia, 7 with moderate dysplasia, and 6 with carcinoma, were analyzed immunohistochemically with use of an HMGI(Y)-specific antibody.
  
  
  RESULTS
  Immunohistochemical analysis revealed that, although no significant immunoreactivity was found in cases of normal pancreatic duct or mild dysplasia, 28.6% (2/7) of moderate dysplasia showed multifocal immunoreactivity with moderate intensity. In contrast, in 50% (3/6) of the cases of carcinoma, intense multifocal or diffuse immunoreactivity occurred, almost equivalent to that observed in cases of duct cell carcinoma, whereas in the remaining 3 cases of carcinoma only a faint focal immunoreactivity occurred. Histologic examination revealed that these HMGI(Y)-positive carcinomas had an invasive growth pattern, whereas the HMGI(Y)-negative carcinomas were either carcinomas in situ or tumors with minimal invasion. Thus, an increased expression level of HMGI(Y) proteins was closely associated with the malignant phenotype in IPMT.
  
  
  CONCLUSIONS
  On the basis of these findings, we propose that HMGI(Y) proteins could play an important role(s) in a multistage process of carcinogenesis of IPMT and that the HMGI(Y) protein level could serve as a potential diagnostic marker, which may enable the identification of tumor cells with potential to be biologically malignant.
authors.affiliation: First Department of Surgery, Kyorin University School of Medicine, Tokyo, Japan. abenbtg@kyorin-u.ac.jp
authors.forename: Nobutsugu
authors.initials: N
authors.lastname: Abe
authors.forename: Takashi
authors.initials: T
authors.lastname: Watanabe
authors.forename: Yumi
authors.initials: Y
authors.lastname: Izumisato
authors.forename: Tadahiko
authors.initials: T
authors.lastname: Masaki
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Mori
authors.forename: Masanori
authors.initials: M
authors.lastname: Sugiyama
authors.forename: Gennaro
authors.initials: G
authors.lastname: Chiappetta
authors.forename: Alfredo
authors.initials: A
authors.lastname: Fusco
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Fujioka
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Atomi
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000175:diagnosis / Q000378:metabolism*; D021441:Carcinoma, Pancreatic Ductal / Q000175:diagnosis / Q000378:metabolism*; D002291:Carcinoma, Papillary / Q000175:diagnosis / Q000378:metabolism*; D025741:HMGA1a Protein / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D010190:Pancreatic Neoplasms / Q000175:diagnosis / Q000378:metabolism*
chemical_list: D025741:HMGA1a Protein