Does the immune reaction cause malignant transformation by disrupting cell-to-cell or cell-to-matrix communications?

Relatively low titers of specific immune reactants are known to stimulate, but cell-to-cell or cell-to-matrix interactions appear to be major inhibitors of tumor-growth. Therefore, it seems reasonable to hypothesize that the mechanism of immunostimulation may be an interference with cell-to-cell or cell-to-matrix communication by a sub-lethal immune-reaction.While the above hypothesis remains unproven, some evidence suggests that immunity may have a major facilitating effect on tumor growth especially at the time of malignant transformation. There is even some evidence suggesting that transformation in vivo may seldom occur in the absence of immunostimulation of the premalignant lesion. Positive selection by the immune reaction may be the reason that tumors are immunogenic.It is widely believed that each malignant tumor is a clone of abnormal cells. However, there is great phenotypic and genetic diversity within the cancer-cell population owing to an ongoing process of variation and selection. This continuing process results in "progression"; the term, as used by Foulds [1], describes the progressive changes in the biological attributes within a lesion, including dedifferentiation. The term, by definition, is not directly related to the tumor's physical growth or extent. I will first review some of the more notable observations that suggest that, during the course of progression, many (all?) malignancies pass through an earlier benign stage before they transform into the malignant state.Among breeding mice of the C3H/An strain, 100% of over 1500 females developed breast cancer [2]. There were numerous HAN (benign hyperplastic alveolar nodules) in each mammary gland as a result of the action of the MTV (milk agent – mammary tumor virus). However, an individual mouse seldom developed more than one carcinoma; the transformation from benign HAN to carcinoma was thus a rare event. The striking feature of the data was that the percentage of surviving mice that developed a