[Antitumor concomitant immunity: a possible metastasis control mechanism]

Concomitant immunity (CI) is defined as the lack or retardation or proliferation of a secondary tumor implant at a distant site; it has been given an immunological interpretation. Our experiments were designed to investigate CI in association with spontaneous tumors with or without metastases. In BALB/c mice, various syngeneic tumors, of undetectable immunogenicity, induced CI, preventing the development of a secondary implant of the same and occasionally of another tumor, indicating some degree of nonspecificity. This CI could also be observed in young and adult nude mice with high and low NK level, and in those treated with silica, discarding and participation of T lymphocytes, NK cells and macrophages, respectively. The lack of development of the secondary implant was not due to tumor rejection--contrarily to observations in allogeneic systems with immunogenic tumor--but to cytostasis. This "dormant tumor" state is observed together with the absence of host cell infiltration. The creation of a local inflammatory reaction abrogated CI, resulting in rapid tumor growth. On the other hand, an inflammatory reaction created by a foreign body inhibited the development of a tumor implant in the contralateral flank and tumor growth could be inhibited by piroxicam; furthermore, the tumor itself diminished the inflammatory reaction created by a foreign body at a distant site. Considering metastases as natural secondary implants, two mammary adenocarcinomas with a common origin were compared, one with 0 and the other with 100% metastatic incidence. The non-metastatic tumor induced stronger and earlier CI against both tumors and prevented the development of experimental and spontaneous metastases; moreover; its surgical extirpation led to the appearance of lung metastases.(ABSTRACT TRUNCATED AT 250 WORDS)