MECHANISM AND PREVENTION OF PORT-SITE TUMOR RECURRENCE AFTER LAPAROSCOPY IN A MURINE MODEL

Citation
T. Iwanaka et al., MECHANISM AND PREVENTION OF PORT-SITE TUMOR RECURRENCE AFTER LAPAROSCOPY IN A MURINE MODEL, Journal of pediatric surgery, 33(3), 1998, pp. 457-461
Citations number
33
Categorie Soggetti
Pediatrics,Surgery
ISSN journal
00223468
Volume
33
Issue
3
Year of publication
1998
Pages
457 - 461
Database
ISI
SICI code
0022-3468(1998)33:3<457:MAPOPT>2.0.ZU;2-P
Abstract
Background/Purpose: Although minimally invasive surgery (MIS) has been broadly applied in patients with cancer of the gastrointestinal tract , the etiology of port-site tumor recurrence (PSR) after laparoscopic cancer surgery remains unclear. The authors report here an analysis of PSR in a model of murine neuroblastoma after laparoscopic tumor biops y and propose a mechanism for this complication as well as a potential treatment. Methods: Immature 5- to 7-week old male A/J mice (18-23 g) were subcutaneously inoculated with the minimally immunogenic TBJ-neu roblastoma (TBJ-NB) in the left flank and divided into three treatment groups. The following operations were performed 14 days after tumor i noculation: group 1, additional intraperitoneal or intravenous injecti on of TBJ-NB during CO2 pneumoperitoneum; group 2, simulated transperi toneal tumor biopsy using MIS techniques during either COP pneumoperit oneum or gasless suspension; Group 3, intraperitoneal (IF) or intraven ous (IV) administration of cyclophosphamide on postoperative days 0 an d 3 to prevent PSR after simulated tumor biopsy during CO2 pneumoperit oneum. Results: In group 1, the incidence of PSR was 0% in the intrave nously injected mice versus 63% in mice injected intraperitoneally wit h TBJ-NB. In group 2, no significant difference in the incidence of PS R was seen between simulated tumor biopsy (89%) animals with CO2 pneum operitoneum versus animals with gasless suspension (81%), In group 3. mice that did not receive any chemotherapy had an 89% incidence of PSR . Administration of cyclophosphamide via either the IP or IV route eff ectively prevented PSR, although there was no difference in the incide nce of PSR between the two routes (IP 12% versus IV 13%). Conclusions: The data suggest that PSR in tumor-bearing hosts may be caused by dir ect seeding of exfoliated tumor cell, and not by hematogenous metastas es. Contrary to the other reports, CO2 pneumoperitoneum was not found to be essential for the development of PSR. Furthermore, the authors c onclude that postoperative chemotherapy may be useful in preventing PS R after MIS in patients bearing chemotherapy-sensitive tumors such as neuroblastoma. Copyright (C) 1998 by W.B. Saunders Company.