Induction of B cell tumor dormancy by anti-idiotypic antibodies.
Induction of B cell tumor dormancy by anti-idiotypic antibodies.
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DOI：
10.1016/0952-7915(93)90130-k
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发表时间：
1993-10
影响因子：
7
通讯作者：
E. Yefenof;L. Picker;R. Scheuermann;E. Vitetta;N. Street;T. Tucker;J. Uhr
中科院分区：
文献类型：
--
作者：
E. Yefenof;L. Picker;R. Scheuermann;E. Vitetta;N. Street;T. Tucker;J. Uhr
通过用肿瘤上表达的独特型免疫宿主，可以实验诱导小鼠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和维持休眠状态。与抗独特型抗体相互作用的淋巴瘤细胞的生长被阻止，它们在形态、细胞周期状态和癌基因表达方面发生了巨大的变化。肿瘤在长期休眠后的再生长是由于出现了一种不再对生长抑制的抗体产生反应的肿瘤细胞变体。这些数据证明了通过特定的生长抑制信号逆转细胞恶性表型的可行性，并为癌症的治疗干预提供了新的方法。
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.