title: Tumoral Versus Flat Intraepithelial Neoplasia of Pancreatobiliary Tract, Gallbladder, and Ampulla of Vater.
abstract: BACKGROUND
  -The identification of a precursor lesion is important to understanding the histopathologic and genetic alterations in carcinogenesis. There are a plethora of terminologies that describe precursor lesions of the pancreatobiliary tract, ampulla of Vater, and gallbladder. The current terminologies for precursor lesions may make it difficult to understand the tumor biology. Here, we propose the concept of tumoral and flat intraepithelial neoplasia to improve our understanding of precursor lesions of many epithelial organs, including the pancreatobiliary tract, ampulla of Vater, and gallbladder.
  
  
  OBJECTIVE
  -To understand the dichotomous pattern of tumoral and flat intraepithelial neoplasia in carcinogenesis of pancreatobiliary tract, ampulla of Vater, and gallbladder.
  
  
  METHODS
  -Review of relevant literatures indexed in PubMed.
  
  
  CONCLUSIONS
  -Tumoral intraepithelial neoplasia presents as an intraluminal or intraductal, mass-forming, polypoid lesion or a macroscopic, visible, cystic lesion without intracystic papillae. Microscopically, tumoral intraepithelial neoplasia shows various proportions of papillary and tubular architecture, often with a mixed pattern, such as papillary, tubular, and papillary-tubular. The malignant potential depends on the degree of dysplasia and the cell phenotype of the epithelium. Flat intraepithelial neoplasia presents as a flat or superficial, spreading, mucosal lesion that is frequently accompanied by an invasive carcinoma. Tumoral and flat intraepithelial neoplasias are not homogeneous entities and may exhibit histopathologic spectrum changes and different genetic profiles. Although intraepithelial neoplasia showed a dichotomous pattern in the tumoral versus flat types, they can coexist. Tumoral and flat intraepithelial neoplasia can be interpreted as part of a spectrum of changes in the carcinogenesis pathway of each organ.
authors.forename: Kee-Taek
authors.initials: KT
authors.lastname: Jang
authors.affiliation: From the Department of Pathology and Translational Genomics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea (Dr Jang); and the Department of Pathology, Pusan National University Hospital and the Pusan National University School of Medicine, and the Biomedical Research Institute, Pusan National University Hospital, Pusan, Korea (Dr Ahn).
authors.forename: Sangjeong
authors.initials: S
authors.lastname: Ahn
mesh_terms: D065311:Adenocarcinoma in Situ / Q000175:diagnosis* / Q000473:pathology; D002288:Adenocarcinoma, Mucinous / Q000175:diagnosis / Q000473:pathology; D014670:Ampulla of Vater / Q000000981:diagnostic imaging / Q000473:pathology; D001661:Biliary Tract Neoplasms / Q000175:diagnosis* / Q000473:pathology; D063646:Carcinogenesis; D002278:Carcinoma in Situ / Q000175:diagnosis* / Q000473:pathology; D002291:Carcinoma, Papillary / Q000175:diagnosis / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000175:diagnosis / Q000473:pathology; D003138:Common Bile Duct Neoplasms / Q000175:diagnosis / Q000473:pathology; D003937:Diagnosis, Differential; D004502:Education, Medical, Continuing; D005706:Gallbladder Neoplasms / Q000175:diagnosis* / Q000473:pathology; D006801:Humans; D010190:Pancreatic Neoplasms / Q000175:diagnosis* / Q000473:pathology; D018300:Papilloma, Intraductal / Q000175:diagnosis / Q000473:pathology; D010338:Pathology, Clinical / Q000193:education / Q000379:methods* / Q000639:trends; D011230:Precancerous Conditions / Q000175:diagnosis* / Q000473:pathology; D000078329:Workforce