Study of the kinetics of local growth and metastatic diffusion of cancers is extremely important for increasing knowledge of the natural history of the tumors and for determination of appropriate surgical strategies and/or medical therapies.
Although experimental models are the best means for study of tumor kinetics, exposure of animals to carcinogenic agents results in excessive variability such as differences in differentiation, location and diffusion. On the contrary, implantation of cancer cells or solid tumor, directly into the site to be studied, it can reproduce a standard condition more suitable for this kind of studies [3–7].
Several experimental models of free cancer cell implantation into the wall of the colon have been described [3, 4]. The animal model used in our experiments is well-established, since it has been fully demonstrated that DHD/K12/TRb colonic cancer cells are able to grow when injected subcutaneously, intraperitoneally and in the wall of the colon [3–5]. Nevertheless, some of these studies used nude animals, in which unusual immunological status may result in great difficulty in interpretation of results.
In our study, the incidence of tumor growth after implantation was almost 65%; similar results have been reported by other studies [4, 7]. Incorrect parietal injection, low viability of tumor cells, intraluminar injection, or host immune response to cancer cells may be explanations of the 65% tumor growth incidence.
Garcia Almo et al, , injecting DHD/K12/TRb cells into the cecal wall of syngeneic rats, demonstrated progressive tumor growth from stage T1 to stage T4, as well as lymph node involvement and distant metastases, reproducing the same progressive development as occurs in human colon cancer. Nevertheless, with this kind of injection model, it seems to be extremely difficult to perform precise implantation into the mucosa and to enable progressive tumor growth corresponding to that observed clinically.
In order to avoid accidental spillage of tumor cells and induce true local growth, Balague et al,  developed a model in which solid tumors, derived from DHD/K12/TRb colonic cancer cells, were implanted into the wall of the colon. Nevertheless, variability in the number of viable cells contained in a single piece of implanted tumor may result in misinterpretation of results.
None of the above studies considered difference in tumor implantation side, mesenteric or antimesenteric, as affecting local growth and distant metastases.
This difference might be of clinical significance, since certain locations can result in more aggressive tumor behavior due to particular anatomical patterns of blood or lymphatic vessels. In our study, when injection of tumor cells was performed in the mesenteric site of the colon, cancer grew locally and spread to the regional mesenteric lymph nodes. On the other hand, with antimesenteric implantation, there was lymph node metastasis but a high incidence of peritoneal carcinomatosis.
Proximity to larger blood and lymphatic vessels of the mesenteric site of the colon could explain the tendency of implanted cells to spread to regional nodes. When cancer cells are injected into the antimesenteric wall, peritoneal diffusion appears to be promoted, probably due to direct contact of the tumor with loops of bowel and the peritoneum.
Another explanation may be related to differences in microvascular pattern of the wall of the colon. Preliminary results of an experimental vascular casting study that we are performing in collaboration with the Department of Human Anatomy, seem to support the theory that the antimesenteric side of the colon differs significantly from the mesenteric side in microvascular arterial density and distribution (unpublished data).
Since M and N stage are the most important prognostic factors in human colorectal cancer , differences in local and metastatic diffusion of cancers located on the mesenteric or antimesenteric sites of the colon may be of clinical importance .