title: Increased peritoneal dissemination after laparotomy versus pneumoperitoneum in a mouse cecal cancer model.
abstract: BACKGROUND
  The effect of carbon dioxide (CO(2)) pneumoperitoneum on the liberation of cancer cells from the primary tumor is not clear. This study investigated the influence of laparotomy versus CO(2) pneumoperitoneum on the progression of colon cancer with serosal invasion in a mouse model.
  
  
  METHODS
  Pieces of human colon adenocarcinoma (HT29) tumor were implanted in the cecal wall of 45 BALB/c nude mice. Each mouse underwent one of three procedures: laparotomy, CO(2) pneumoperitoneum, or anesthesia (control). Three weeks later, the size and weight of cecal tumors, the number of nodules, and the tumor volume score of peritoneal dissemination were examined. Another 45 mice were treated in the same way. The cecal tumor was resected on days 1, 3, or 5 after treatment. Total RNA was isolated from the resected tumors. The expression of E-cadherin and beta-1 integrin messenger RNA (mRNA) was examined by semiquantitative real-time reverse transcriptase-polymerase chain reaction assay.
  
  
  RESULTS
  Significantly more nodules of peritoneal dissemination were found in the laparotomy group than in the control group (p < 0.05). The tumor volume score of peritoneal dissemination in the laparotomy group was significantly higher than in the other two groups (p < 0.05). The expression of E-cadherin mRNA at day 5 in the laparotomy group was significantly less than in the other two groups (p < 0.05). There were no differences in beta-1 integrin among three groups.
  
  
  CONCLUSIONS
  Peritoneal dissemination was more extensive after laparotomy than after CO(2) pneumoperitoneum in a mouse model of cecal cancer with serosal invasion. Decreased expression of E-cadherin mRNA in tumors after laparotomy, but not after CO(2) pneumoperitoneum, may be associated with the increase in peritoneal dissemination.
authors.affiliation: Department of Surgery I, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama-machi, Oita, 879-5593, Japan. aaq29851@hkg.odn.ne.jp
authors.forename: H
authors.initials: H
authors.lastname: Takeuchi
authors.forename: M
authors.initials: M
authors.lastname: Inomata
authors.forename: K
authors.initials: K
authors.lastname: Fujii
authors.forename: S
authors.initials: S
authors.lastname: Ishibashi
authors.forename: N
authors.initials: N
authors.lastname: Shiraishi
authors.forename: S
authors.initials: S
authors.lastname: Kitano
mesh_terms: D000230:Adenocarcinoma / Q000556:secondary*; D000818:Animals; D002245:Carbon Dioxide / Q000009:adverse effects*; D002430:Cecal Neoplasms / Q000473:pathology*; D004195:Disease Models, Animal; D007813:Laparotomy / Q000009:adverse effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009361:Neoplasm Invasiveness; D009366:Neoplasm Seeding; D010534:Peritoneal Neoplasms / Q000556:secondary*; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects*
chemical_list: D002245:Carbon Dioxide