title: Loss of Fhit protein expression in high-grade and advanced stage endometrial carcinomas.
abstract: BACKGROUND
  The fragile histidine triad (FHIT) gene is a candidate tumor suppressor gene located at 3p14.2, and the absence or reduction of Fhit protein expression has recently been reported in various carcinomas.
  
  
  METHODS
  We examined the expression of Fhit protein in 50 endometrial carcinomas and 19 normal endometrial tissues by immunohistochemistry, and this expression was correlated with clinicopathological parameters, p53 expression, sex steroid receptor status and abnormal FHIT transcripts.
  
  
  RESULTS
  All the specimens of normal endometrial gland in the proliferative phase exhibited relatively strong Fhit expression, while most of endometrial tissues in the secretory phase showed weak Fhit expression. In 50 endometrial carcinomas, immunoreactivity for Fhit protein was strong in 21 cases (42%), weak in 22 cases (44%) and partially or totally absent in the remaining 7 cases (14%). There were significant correlations of negative Fhit expression with high tumor grade (p = 0.033) and with advanced stage (p = 0.048). On the other hand, abnormal FHIT transcripts lacking several exons were found in 29% of cases. Neither p53 nor sex steroid receptor status were significantly related with the loss of Fhit expression.
  
  
  CONCLUSIONS
  The loss of Fhit protein expression may be associated with aggressive phenotype of endometrial carcinomas.
authors.affiliation: Department of Gynecology and Obstetrics, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
authors.forename: Yasuichiro
authors.initials: Y
authors.lastname: Yura
authors.forename: Masaki
authors.initials: M
authors.lastname: Mandai
authors.forename: Ikuo
authors.initials: I
authors.lastname: Konishi
authors.forename: Atia A
authors.initials: AA
authors.lastname: Hamid
authors.forename: Yuko
authors.initials: Y
authors.lastname: Tsuruta
authors.forename: Takashi
authors.initials: T
authors.lastname: Kusakari
authors.forename: Shingo
authors.initials: S
authors.lastname: Fujii
mesh_terms: D017766:Acid Anhydride Hydrolases; D016889:Endometrial Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics; D009367:Neoplasm Staging; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000235:genetics; D011980:Receptors, Progesterone / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics; D000099170:Bis(5'-adenosyl)triphosphatase
chemical_list: D017766:Acid Anhydride Hydrolases; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; D000099170:Bis(5'-adenosyl)triphosphatase