Role of concomitant resistance in the development of murine lung metastases

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Abstract
An attempt was made to explain the distinct lung metastatic patterns of 2 mammary adenocarcinomas with a common BALB/c origin: M3, which does not induce spontaneous metastases, and MM3 with an almost 100% incidence. No difference between the 2 tumors was detected with respect to host mononuclear cell content, degree of immunogenicity or lung‐colony‐forming ability. Conversely, there was a marked difference in the capacity to induce concomitant resistance: M3‐bearing mice induced stronger and earlier resistance against i.v. challenge of both M3 and MM3 tumor cells than MM3‐bearing mice; this resistance was expressed as lower number of lung metastases and lower tumor‐cell proliferation in metastatic nodules. M3 was also able to control the development of spontaneous metastases: metastases developed in all M3‐excised mice, compared with none in M3‐bearing mice, while MM3‐bearing mice also bearing a secondary M3 tumor developed fewer metastases than mice bearing MM3 only. This anti‐metastatic effect does not appear to depend on classical immunological mechanisms since no difference could be detected between the 2 tumors in response to T cells, NK, macrophages or antibodies.