title: [Clinicopathological and immunohistochemical features of colorectal sessile serrated adenoma].
abstract: OBJECTIVE
  To investigate the clinicopathological characteristics and expression status of Ki67, p53, CEA, CDX, CK7 in colorectal sessile serrated adenoma (SSA).
  
  
  METHODS
  The clinicopathological data of 11 cases of SSA, 51 cases of hyperplastic polyp (HP) and one case with mixed HP/SSA were reviewed and analyzed retrospectively. The expression of Ki67, p53, CEA, CDX and CK7 were detected by immunohistochemistry.
  
  
  RESULTS
  The major histological features in SSA were architectural abnormality in crypts, dilatation of serrated crypt bases like an inverted "T" or "L" shape adjacent to muscularis mucosa. Atypical cells containing round to oval nuclei and nucleoli were also observed. The immunohistochemical staining showed that the expression of p53 increased gradually from HP to TA: 11.8% in HP, 20.0% in SSA, 41.2% in VTA and 75.0% in TA, with a significant difference among the groups (chi(2) = 17.996, P = 0.000). However, no significant difference in the expression of CDX and CK7 was observed between HP and SSA. Of the 10 SSA cases, positive expression of Ki67 was found in cells located in the base or middle part of crypt in 6 cases, positive cells index was 26% - 50% in 5 cases, and > 50% in 3. Compared with the expression of Ki67 in the HP, VTA and VA, SSA showed a significant difference in both the positive cell number and in the positive regions. (positive number: chi(2) = 34.601, P = 0.000; positive regions: chi(2) = 63.077, P = 0.000).
  
  
  CONCLUSIONS
  Morphological diagnosis of SSA was mainly based on crypt architectural and cellular abnormalities, and the crypt architectural abnormality may be more important than cellular features. Detection of p53 and Ki67 expression may be helpful in differential diagnosis and understanding the nature of SSA.
authors.affiliation: Department of Pathology, General Hospital of Beijing Military Command, Beijing 100700, China. BZWLP@yahoo.com
authors.forename: Lu-ping
authors.initials: LP
authors.lastname: Wang
authors.forename: Guang-zhi
authors.initials: GZ
authors.lastname: Yang
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Zhi-yong
authors.initials: ZY
authors.lastname: Zhou
authors.forename: Bao-lin
authors.initials: BL
authors.lastname: Gao
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Han
mesh_terms: D000236:Adenoma / Q000378:metabolism / Q000473:pathology*; D018253:Adenoma, Villous / Q000378:metabolism / Q000473:pathology; D000328:Adult; D000368:Aged; D000071616:CDX2 Transcription Factor; D002272:Carcinoembryonic Antigen / Q000378:metabolism; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology*; D003111:Colonic Polyps / Q000378:metabolism / Q000473:pathology; D003937:Diagnosis, Differential; D005260:Female; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D053552:Keratin-7 / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012004:Rectal Neoplasms / Q000378:metabolism / Q000473:pathology*; D012189:Retrospective Studies; D015534:Trans-Activators / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000071616:CDX2 Transcription Factor; D002272:Carcinoembryonic Antigen; D018398:Homeodomain Proteins; D053552:Keratin-7; D019394:Ki-67 Antigen; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53