Yefenof E, Picker L J, Scheuermann R H, Vitetta E S, Street N E, Tucker T F, Uhr J W
Lautenberg Center for General and Tumor Immunology, Hebrew University Hadassah Medical School, Jerusalem, Israel.
Curr Opin Immunol. 1993 Oct;5(5):740-4. doi: 10.1016/0952-7915(93)90130-k.
Long-term dormancy of murine B-cell lymphomas can be experimentally induced by immunizing the host with the idiotype expressed on the tumor. Interaction of the cells with anti-idiotype antibodies is sufficient to induce and maintain the dormant state. The growth of lymphoma cells interacting with anti-idiotype antibodies is arrested and they undergo dramatic changes in their morphology, cell-cycle status and oncogene expression. Regrowth of a tumor after long-term dormancy results from the emergence of a tumor cell variant that no longer responds to the antibodies with growth inhibition. These data demonstrate the feasibility of reversing a malignant phenotype of cells by specific growth arrest signals and suggest new approaches for therapeutic intervention in cancer.
通过用肿瘤上表达的独特型免疫宿主，可在实验中诱导小鼠B细胞淋巴瘤的长期休眠。细胞与抗独特型抗体的相互作用足以诱导并维持休眠状态。与抗独特型抗体相互作用的淋巴瘤细胞生长停滞，其形态、细胞周期状态和癌基因表达发生显著变化。长期休眠后肿瘤的重新生长是由于出现了一种不再对抗体产生生长抑制反应的肿瘤细胞变体。这些数据证明了通过特定的生长停滞信号逆转细胞恶性表型的可行性，并为癌症治疗干预提出了新方法。
