enocarcinoma. Nine months later the patient presented with implantation on the retraction port but not on the laparotomy incision. She subsequently died nine months later from liver metastases. Critics of the issue of port site implantation claim that all of these lesions are due to either technical ineptitude, direct traumatization by the tumor, or inadequate nodal sampling. In the first instance, they state that either the bowel was per­forated or mishandled. In the second instance, they claim that either intracorporeal vascular ligation was not performed therefore leading cells to be “milked” through the lympathics and blood vessels during specimen extrication or that the speci­men was evacuated directly through the wound without the use of a plastic bag. In the third argument, they note that many of these recurrences, claimed to have been in patients with Dukes’ A or Dukes’ B lesions, were truly in patients with Dukes’ C le­sions in whom an inadequate number of nodes was retrieved and sampled. Montorsi et al. (1995) reported a 65-year-old male with a right colon carcinoma who underwent a completely intracorporeal resection and anastomosis. The specimen was carefully delivered through a plastic bag and noted to be a Dukes’ B le­sion. Twenty-eight nodes were sampled. This number is clearly higher than any reported in the aforementioned laparoscopic literature. Despite all of these excellent technical skills and pre­cautions, the patient presented two months later with a 7 cm mass at the extraction site with no other metastases. To date, over 30 port site recurrences have been noted with incidences ranging from a low of 1.3% to 21% with a mean somewhere be­tween 3 and 4.5% (Berends et al. 1994). In the laparotomy litera­ture, only two series have reviewed this issue (Hughes et al. 1983, Reilly et al. 1996). Both of these series included patients with carcinomatosis and noted that the laparotomy incision contained tumor implants in between 0.6 and 0.8% of cases. However, if patients with carcinomatosis were excluded, the in­cidence appears to have been approximately 0.1%, much lower than in any of the laparoscopic reports. To date, several very provocative animal models have led sup­port to the port site implantation issue spectively randomized 92 hamsters in whom a human colon cancer was implanted. All animals underwent a midline la­parotomy and placement of four ports. Pathologists were blinded at the time of necropsy. It was determined that the ad­dition of pneumoperitoneum tripled the port site implantation rate from 26 to 75% (p < 0.0001). Jacobi and coworkers (1996) noted a significant increase in the number of tumor cells after carbon dioxide pneumoperitoneum compared to a control group in vitro and confirmed these findings in a rat model as well. Other authors have suggested that CO motes more growth than does gasless laparoscopy and that using a solid tumoral model direct contact enhances growth (Whelan 1996). Thomas and coworkers (1996) used a filter sys­tem to capture expelled carbon dioxide and failed to find any cells in the carbon dioxide. However, they found that all of the instruments and ports were contaminated. A similar study was undertaken by Köckerling (1996). Once again, they failed to find cells in the carbon dioxide, but did find cells contaminating the instruments and ports. In the United States, laparoscopy for benign disease is much more accepted than is laparoscopy for malignancy. In a survey of the American Society of Colon and Rectal Surgeons (Wexner et al. 1995) only 6% of colorectal surgeons would have their own rectal carcinoma laparoscopically treated. In order to try and address this issue, a prospective randomized, multicentered