title: Cell proliferative activity in intraductal papillary-mucinous neoplasms and invasive ductal adenocarcinomas of the pancreas: an immunohistochemical study.
abstract: OBJECTIVE
  To evaluate cell proliferative activity and expression of cytokeratins (CKs) and epithelial membrane antigen (EMA) in intraductal papillary-mucinous neoplasm of the pancreas (IPNP).
  
  
  METHODS
  We examined cell proliferative activity in normal pancreatic ducts, IPNP, and invasive ductal adenocarcinoma of the pancreas by immunohistochemistry for proliferating cell nuclear antigen (PCNA) and Ki67 antigen. Expression of CKs and EMA was also examined immunohistochemically.
  
  
  RESULTS
  In normal pancreas (n = 5), PCNA- or Ki67-positive ductal epithelia were not found. Cytokeratins (polyclonal, CAM5.2, CK-7, CK-8, CK-18, and CK-19) were expressed in the ducts and ductules but not in the acinus, and EMA expression was noted in the acinus but rarely in the ducts. In IPNP (n = 9) and invasive ductal adenocarcinoma (n = 6) of the pancreas, the overall PCNA-labeling index (PCNA-LI) was 3.2 +/- 4.1 and 16.0 +/- 7.2, respectively, and overall Ki67-LI was 2.2 +/- 2.6 and 14.5 +/- 6.3, respectively. In IPNP, the PCNA-LI and Ki67-LI were low in adenoma areas (PCNA-LI = 0.9 +/- 0.7), intermediate in dysplastic areas (PCNA-LI = 3.7 +/- 2.4), and rather high in carcinoma in situ areas (PCNA-LI = 11.5 +/- 8.4). Both CKs and EMA were noted in tumor cells.
  
  
  CONCLUSIONS
  The data suggest that cell proliferative activity is low in IPNP compared to invasive ductal adenocarcinoma, that cell proliferative activity increases with the grade of cell atypia in IPNP, and that CK expression is not changed during the neoplastic change, but EMA is newly expressed or overexpressed during the neoplastic change.
authors.affiliation: Second Department of Pathology, Tottori University Faculty of Medicine, Yonago, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Terada
authors.forename: T
authors.initials: T
authors.lastname: Ohta
authors.forename: Y
authors.initials: Y
authors.lastname: Kitamura
authors.forename: K
authors.initials: K
authors.lastname: Ashida
authors.forename: Y
authors.initials: Y
authors.lastname: Matsunaga
mesh_terms: D000368:Aged; D018270:Carcinoma, Ductal, Breast / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D002455:Cell Division / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000032:analysis; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018396:Mucin-1 / Q000032:analysis; D010190:Pancreatic Neoplasms / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis
chemical_list: D019394:Ki-67 Antigen; D018396:Mucin-1; D018809:Proliferating Cell Nuclear Antigen; D007633:Keratins