title: A subgroup of intrahepatic cholangiocarcinoma with an infiltrating replacement growth pattern and a resemblance to reactive proliferating bile ductules: 'bile ductular carcinoma'.
abstract: OBJECTIVE
  The histogenesis and biological behaviour of peripheral intrahepatic cholangiocarcinoma (peripheral CC) remain unclarified. The aim of this study was to examine the growth pattern of peripheral CC (24 cases) in comparison with hepatocellular carcinoma (HCC, 27 cases) and metastatic colorectal adenocarcinoma (MCA, 24 cases).
  
  
  RESULTS
  Tumour/surrounding liver borders were classified as: (i) fibrous encapsulation, (ii) compressive growth, and (iii) infiltrating replacement. Nineteen of 24 peripheral CCs showed (iii), whereas 23 of 27 HCCs showed (i) and 17 of 24 MCAs showed (ii). In (iii), carcinoma cells infiltrated the surrounding liver without compression, and hepatic supporting vascular structures such as portal tracts were secondarily incorporated into the tumour. In (i) and (ii), the surrounding liver was compressed and no or few portal tracts were incorporated within the tumour. Fifteen of 24 peripheral CCs were composed of carcinoma cells resembling reactive bile ductules and these cells were positive for neural cell adhesion molecule (NCAM), a marker of proliferating bile ductules. The remaining nine peripheral CCs were composed of ordinary adenocarcinoma and negative for NCAM.
  
  
  CONCLUSIONS
  A subgroup of peripheral CCs with an infiltrating replacement growth pattern resembles reactive bile ductules and expresses NCAM. 'Bile ductular carcinoma' may be a better term for this subgroup.
authors.affiliation: Department of Human Pathology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kozaka
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
authors.forename: T
authors.initials: T
authors.lastname: Fujii
authors.forename: K
authors.initials: K
authors.lastname: Harada
authors.forename: Y
authors.initials: Y
authors.lastname: Zen
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: S
authors.initials: S
authors.lastname: Sawada
authors.forename: H
authors.initials: H
authors.lastname: Minato
authors.forename: O
authors.initials: O
authors.lastname: Matsui
authors.forename: Y
authors.initials: Y
authors.lastname: Nakanuma
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000556:secondary; D000368:Aged; D000369:Aged, 80 and over; D001344:Autopsy; D001650:Bile Duct Neoplasms / Q000378:metabolism / Q000473:pathology*; D001652:Bile Ducts / Q000378:metabolism / Q000473:pathology*; D001653:Bile Ducts, Intrahepatic / Q000737:chemistry / Q000473:pathology*; D019002:CD56 Antigen / Q000032:analysis; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000473:pathology; D018281:Cholangiocarcinoma / Q000378:metabolism / Q000473:pathology*; D015179:Colorectal Neoplasms / Q000378:metabolism / Q000556:secondary; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000032:analysis; D008099:Liver / Q000737:chemistry / Q000473:pathology; D008113:Liver Neoplasms / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D019006:Neural Cell Adhesion Molecules / Q000032:analysis; D009929:Organ Size; D014746:Vimentin / Q000032:analysis
chemical_list: D019002:CD56 Antigen; D019006:Neural Cell Adhesion Molecules; D014746:Vimentin; D007633:Keratins