title: Growth patterns and genetic changes of colorectal carcinoma.
abstract: BACKGROUND
  Recent Japanese studies have shown that histogenesis of small colorectal carcinomas can be divided into two groups: polypoid growth arising from polypoid neoplasia, and nonpolypoid growth arising from flat or depressed neoplasia. This classification should be verified with genetic as well as morphologic characteristics.
  
  
  METHODS
  In order to classify our subject into polypoid growth and nonpolypoid growth types both histologically and endoscopically, we selected 42 colorectal carcinomas < 2 cm in size (35 submucosal and seven more advanced). Clinicopathological findings, presence or absence of Ki-ras gene mutation and overexpression of p53 protein were compared between the two types.
  
  
  RESULTS
  Histologically, the cases were divided into 27 of the polypoid growth type and 15 of the nonpolypoid growth type. None of the nonpolypoid growth cases contained adenomatous remnant, wheras this was found in 75% of the polypoid growth cases. No Ki-ras mutation was observed in any of the nonpolypoid growth cases, although it appeared in 44% of the polypoid growth cases. Regarding the overexpression of p53 protein, no significant difference was observed between the two types. The histological and the colonoscopic polypoid growth-nonpolypoid growth classifications correlated well with each other (agreement rate 98%), except for one lesion, which was classified as polypoid growth type endoscopically but as nonpolypoid growth type histologically.
  
  
  CONCLUSIONS
  The histologically defined polypoid growth-nonpolypoid growth classification may indicate a difference in pathway of colorectal carcinogenesis. Also, colonoscopic polypoid growth-nonpolypoid growth classification is available for preoperative estimation of the genetic characteristics of small carcinomas.
authors.affiliation: Department of Medicine, National Cancer Center Hospital East, Chiba, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Fujii
authors.forename: S
authors.initials: S
authors.lastname: Kato
authors.forename: N
authors.initials: N
authors.lastname: Boku
authors.forename: Y
authors.initials: Y
authors.lastname: Oda
authors.forename: I
authors.initials: I
authors.lastname: Koba
authors.forename: A
authors.initials: A
authors.lastname: Ohtsu
authors.forename: K
authors.initials: K
authors.lastname: Hosokawa
authors.forename: M
authors.initials: M
authors.lastname: Ono
authors.forename: T
authors.initials: T
authors.lastname: Shimoda
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
mesh_terms: D000236:Adenoma / Q000235:genetics / Q000473:pathology; D003111:Colonic Polyps / Q000235:genetics* / Q000473:pathology*; D003113:Colonoscopy; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology*; D015870:Gene Expression; D011905:Genes, ras; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D009154:Mutation; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D016159:Tumor Suppressor Protein p53