PubMed1998
The results from the majority of the reviewed studies support the hypothesis that abdominal surgery, performed via either a large incision or CO2 pneumoperitoneum, systemically encourages tumor growth in the postoperative period. A full laparotomy incision appears to have a significantly greater effect than CO2 pneumoperitoneum on postoperative tumor growth. Whether the large tumor observed in the surgical groups are the result of increased tumor cell proliferation or diminished tumor cell death remains unclear. There is some evidence pointing to both mechanisms. The loss of the postoperative tumor growth differences between the open and pneumo animals in the athymic mouse experiment suggests that cell-mediated immune function plays a role in tumor containment. The proliferation study results, however, suggest that other stimulatory influence(s) are also at work. Clearly, much research needs to be done regarding the etiology of these tumor growth differences. Other tumor cell lines need to be studied, and investigations regarding tumor growth in an intra-abdominal location need be performed as well. This body of research suggests that the manner in which the surgeon gains access to the abdominal cavity may have an impact on the propensity of tumor cells to implant, survive, and grow in the period immediately after surgery. If true, this may be the most compelling justification for the use of minimally invasive techniques for the curative resection of malignancies. However, it remains to be proven that human tumors will demonstrate differences in tumor growth similar to those noted in some of these animals models. Furthermore, it is not all clear that slight differences in tumor growth postoperatively will translate into significant differences in long-term survival or recurrence rates. At first glance, the existence of port-site tumors would appear to contradict totally the conclusions of many studies discussed in this synopsis. If laparoscopic methods are associated with decreased rates of tumor growth and establishment, then why do port-site tumors form? This is a complex issue calling for discussion that goes far beyond the scope of this article. However, several brief comment on this topic follow. The etiology of port tumors is unknown, although traumatization of the tumor during mobilization, resection, or removal is likely to play a significant role in the liberation of tumor cells from the primary. A relatively small protective benefit, in terms of slower tumor growth rates in laparoscopic patients, will likely not be sufficient to prevent a large inoculum of viable tumor cells in an abdominal wound from establishing a metastasis. Furthermore, as suggested earlier, the systemic effects on tumor growth may be different from the local (i.e., intra-abdominal or abdominal wound) effects. Finally, the true incidence of port tumors remains unknown. It has not been definitively established that the laparoscopic wound tumor incidence is significantly higher than the open rate, although this is the assumption of most surgeons. Several relatively large recently published laparoscopic series have reported port tumor incidences of 0 to 1.2%, which is in the same "ballpark" as the 0.6 1.0% abdominal wound tumor incidences mentioned in several open colectomy series. Clearly, much more research in this area is needed to understand port tumors better and to reconcile the port tumor results with the systemic tumor growth benefits that may be associated with minimally invasive methods.