Abstract
Earlier studies have shown that pregnant and nonpregnant mammalian uteri respond differently to tumor cell invasion, colonization and metastasis, but the biological basis of such differential uterine response has not been clarified. In the present study we have investigated the role of the metastatic potential of the tumor in the differential response of different stages of mouse uteri, using a highly metastatic tumor. The results obtained were compared with earlier data obtained using low metastatic or nonmetastatic tumors. Lewis lung carcinoma (LLC) cells were infused nonsurgically into nonpregnant uteri of various estrus stages and into pregnant uteri on day 3 postcoitum. Response of the uteri and embryos was studied histologically on days 2, 5 and 18 posttreatment (p.t.). The embryonic development was severely inhibited resulting in extensive resorption. In the tumor cell-treated animals, despite an early and uniform invasion the patterns of tumor cell colonization and metastasis differed remarkably from the pregnant to nonpregnant uteri. On day 5 p.t. 66% of nonpregnant animals showed tumor cells in the endometrium and 40% had tumor metastasis in other organs. Though 40% of the pregnant animals had tumor cells in the uteri, none had metastasis in other organs. By day 18 p.t., despite the absence of tumor cells in the uteri, 75% of nonpregnant animals showed metastasis in lung and liver. In pregnant animals, tumor cells were seen neither in uteri nor in other organs studied. These results indicate the refractory nature of both the pregnant and nonpregnant mouse uteri to the survival and colonization of LLC cells, but the mechanisms by which the tumor cells are eliminated differ between these two types of uteri.
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