title: Telangiectatic focal nodular hyperplasia: a variant of hepatocellular adenoma.
abstract: OBJECTIVE
  "Telangiectatic focal nodular hyperplasia" designate atypical lesions considered as variants of focal nodular hyperplasia (FNH). However, because "telangiectatic FNH" share several morphologic patterns with hepatocellular adenomas, classification of such lesions deserve further clarification. Therefore, the aim of the present study was to reconsider the classification of telangiectatic FNH with the help of a molecular approach.
  
  
  METHODS
  Ten telangiectatic FNH, 6 typical FNH, and 6 hepatocellular adenomas were studied. DNA, RNA, and protein from each lesion were extracted. Clonality was assessed by the study of the X chromosome inactivation pattern (HUMARA assay). Angiopoietin (ANGPT-1 and ANGPT-2) mRNA, genes the expression of which is typically modified in FNH, were quantified by a real-time RT-PCR procedure. Protein profiles were analyzed by SELDI-TOF PROTEINCHIP (Cyphergen Biosystem, Inc., Fremont, CA) technology.
  
  
  RESULTS
  Although all informative cases of FNH (5 of 6) and hepatocellular adenomas (6 of 6) were polyclonal and monoclonal, respectively, clonal analysis showed a nonrandom pattern of X chromosome inactivation consistent with a monoclonal lesion in 6 of 8 cases of telangiectatic FNH. The mean value of the ANGPT-1/ANGPT-2 mRNA ratio was 21.4 in FNH, 2.6 in adenomas, and 2.1 in telangiectatic FNH (P <or = 0.001 in telangiectatic FNH vs. FNH). SELDI-TOF PROTEINCHIP profiling and hierarchical clustering analysis showed that all except 1 telangiectatic FNH clustered within the group of hepatocellular adenomas.
  
  
  CONCLUSIONS
  These results show that telangiectatic FNH display a molecular pattern closer to that of hepatocellular adenomas than to FNH and suggest that these lesions should instead be referred to as "telangiectatic hepatocellular adenomas."
authors.affiliation: Service d'Anatomie Pathologique, Hôpital Beaujon, Clichy, France. vparadis@teaser.fr
authors.forename: Valerie
authors.initials: V
authors.lastname: Paradis
authors.forename: Asmae
authors.initials: A
authors.lastname: Benzekri
authors.forename: Delphine
authors.initials: D
authors.lastname: Dargère
authors.forename: Ivan
authors.initials: I
authors.lastname: Bièche
authors.forename: Ingrid
authors.initials: I
authors.lastname: Laurendeau
authors.forename: Valerie
authors.initials: V
authors.lastname: Vilgrain
authors.forename: Jacques
authors.initials: J
authors.lastname: Belghiti
authors.forename: Michel
authors.initials: M
authors.lastname: Vidaud
authors.forename: Claude
authors.initials: C
authors.lastname: Degott
authors.forename: Pierre
authors.initials: P
authors.lastname: Bedossa
mesh_terms: D018248:Adenoma, Liver Cell / Q000145:classification*; D000293:Adolescent; D000328:Adult; D042683:Angiopoietin-1 / Q000235:genetics; D042702:Angiopoietin-2 / Q000235:genetics; D002648:Child; D002999:Clone Cells / Q000473:pathology; D003199:Computer Systems; D005260:Female; D020518:Focal Nodular Hyperplasia / Q000145:classification* / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008113:Liver Neoplasms / Q000145:classification*; D008875:Middle Aged; D040081:Protein Array Analysis; D011506:Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013684:Telangiectasis / Q000145:classification* / Q000150:complications* / Q000378:metabolism / Q000473:pathology
chemical_list: C467630:ANGPT1 protein, human; D042683:Angiopoietin-1; D042702:Angiopoietin-2; D011506:Proteins; D012333:RNA, Messenger