title: Human telomerase reverse transcriptase, p53 and Ki-67 expression and apoptosis in colorectal serrated adenoma.
abstract: BACKGROUND
  Serrated adenoma (SA) has recently been proposed as a distinct histological lesion of the colorectum. However, no definite histopathologic criteria for SA have been established, and its histogenesis and natural history remain unclear.
  
  
  METHODS
  We analysed 25 hyperplastic polyps (HPs), 26 low-grade SAs (LG-SAs), 32 high-grade SAs (HG-SAs), 18 low-grade tubular adenomas (LG-TAs), 16 high-grade TAs (HG-TAs) and 20 carcinoma in situ (CIS). To clarify molecular features of SA, we used in situ hybridization to examine the expression of human telomerase reverse transcriptase (hTERT), immunohistochemistry to examine the expressions of p53 and Ki-67, and in situ DNA nick end labeling to detect apoptotic cells.
  
  
  RESULTS
  The incidence of hTERT expression was 1 (4.0%) of 25 for HP, 12 (46.2%) of 26 for LG-SA, 18 (56.3%) of 32 for HG-SA, 6 (33.3%) of 18 for LG-TA, 7 (43.8%) of 16 for HG-TA, 12 (80.0%) of 15 for CIS, respectively. The incidence of hTERT expression in SA was significantly higher than that in HP. Seventeen (29%) of the 58 SAs were regarded as positive for p53 protein, but none of the HPs showed p53 immunoreactivity. Ki-67 labeling index in SA, TA and CIS was significantly higher than that in HP. The apoptototic index was not significantly different between HP, SA, TA and CIS. In HG-SA, the incidence of hTERT expression in p53-positive lesions was significantly higher than that in p53-negative lesions.
  
  
  CONCLUSIONS
  These results suggest that hTERT and p53 expression increase in the early stages of carcinogenesis in SA and that SA has a malignant transformation similar to that of TA. It may be useful to investigate hTERT and p53 expression for differential diagnosis of SA from HP.
authors.affiliation: First Dept of Internal Medicine, Hiroshima University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Oka
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Hiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Kitadai
authors.forename: M
authors.initials: M
authors.lastname: Yoshihara
authors.forename: F
authors.initials: F
authors.lastname: Shimamoto
authors.forename: K
authors.initials: K
authors.lastname: Haruma
authors.forename: K
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000236:Adenoma / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D017209:Apoptosis / Q000235:genetics*; D002278:Carcinoma in Situ / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D003106:Colon / Q000473:pathology / Q000503:physiopathology; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D004268:DNA-Binding Proteins; D003937:Diagnosis, Differential; D015870:Gene Expression / Q000235:genetics*; D006801:Humans; D006965:Hyperplasia / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D017403:In Situ Hybridization; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000032:analysis* / Q000235:genetics*; D019098:Telomerase / Q000032:analysis* / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis* / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D019098:Telomerase