title: How many millimeters do atypical epithelia of the pancreas spread intraductally before beginning to infiltrate?
abstract: OBJECTIVE
  The pathogenesis of ordinary duct cell carcinoma of the pancreas is still unclear. The aim of this study was to identify which epithelial lesion was a precursor of duct cell carcinoma and to determine how many millimeters atypical epithelia spread intraductally before beginning to infiltrate.
  
  
  METHODS
  Small cystic dilated lesions were studied, using 1374 autopsied pancreata which were mainly taken from aged patients. Serial sections were taken at about 5-mm intervals. Small cystic dilated lesions were defined as restricted dilatations of the pancreatic branch duct, which were grossly recognizable and therefore larger than about 1-2 mm in diameter. The degree of epithelial atypia of the cystic dilated lesions was histologically divided into five groups (Group I to V).
  
  
  RESULTS
  Comparing PanIN to our classification, normal and squamous metaplasias were almost the same as Group 1. PanIN 1A and 1B almost the same as Group 2 (benign hyperplasia). PanIN-2 is almost the same as Group 3, and PanIN-3 is almost the same as Group 4, which is characterized by true cribriforming, and a loss of nuclear polarity. Of 1374 autopsy cases, small cystic dilated lesions were found in 378 pancreata (27.5%). Histological examination revealed that the incidence of each group was 47%, 33%, 18%, 2.4% and 0.6% of 507 cystic dilated lesions, respectively. Dilatation of the cystic lesion and surrounding dilated duct resembled a precursor of IPMT in four cases, but not in another five cases. Group IV epithelia just infiltrated in some of the latter cases. Invasion was found when Group IV epithelia spread about 5-8 mm, while it rarely infiltrated when it spread less than 4 mm.
  
  
  CONCLUSIONS
  The pathogenesis of ordinary duct cell carcinoma of the pancreas was speculated to begin with papillary growth of duct epithelia. Papillary atypical epithelia then begins to infiltrate when they spread intraductally about 5-8 mm.
authors.affiliation: Department of Organ Function and Controls, Yamagata University School of Medicine, 2-2-2 Iida-Nishi, Yamagata City, Yamagata 990-9585, Japan. wkimura@med.id.yamagata-u.ac.jp
authors.forename: Wataru
authors.initials: W
authors.lastname: Kimura
mesh_terms: D000328:Adult; D002278:Carcinoma in Situ / Q000473:pathology*; D021441:Carcinoma, Pancreatic Ductal / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D018450:Disease Progression; D004848:Epithelium / Q000473:pathology; D005260:Female; D006801:Humans; D006965:Hyperplasia / Q000473:pathology; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D009361:Neoplasm Invasiveness / Q000473:pathology; D010183:Pancreatic Ducts / Q000473:pathology; D011230:Precancerous Conditions / Q000473:pathology*