Sachs L
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
Blood Cells. 1993;19(3):709-26; discussion 727-30.
Identification of normal viability-, growth-, and differentiation-inducing cytokines, the cells that produce them, and how cytokines interact in normal development, has made it possible to identify the cellular and molecular basis of normal development and changes in the developmental program that result in leukemia. When normal cells have been changed into leukemic cells, the malignant phenotype can again be suppressed in various ways. Results on the molecular control of growth, differentiation, and apoptosis in normal myeloid hematopoietic cells, changes in the normal developmental program in myeloid leukemia, and the suppression of malignancy in myeloid leukemia, have shown that (A) malignancy can be suppressed either with or without genetic changes in the tumor cells, (B) suppression of malignancy by inducing differentiation does not have to restore all the normal controls, and (C) genetic abnormalities which give rise to malignancy can be bypassed and their effects nullified by inducing differentiation and apoptosis which stop cells from multiplying.
对正常的活力诱导、生长诱导和分化诱导细胞因子、产生这些细胞因子的细胞以及细胞因子在正常发育过程中如何相互作用的鉴定，使得确定正常发育的细胞和分子基础以及导致白血病的发育程序变化成为可能。当正常细胞转变为白血病细胞时，恶性表型又可以通过多种方式被抑制。关于正常髓系造血细胞生长、分化和凋亡的分子控制、髓系白血病中正常发育程序的变化以及髓系白血病中恶性肿瘤的抑制的研究结果表明：（A）无论肿瘤细胞是否发生基因改变，恶性肿瘤都可以被抑制；（B）通过诱导分化抑制恶性肿瘤不一定需要恢复所有正常控制；（C）导致恶性肿瘤的基因异常可以被绕过，并且通过诱导分化和凋亡使细胞停止增殖可以消除其影响。
