Molecular biology of chronic myelogenous leukemia.
Molecular biology of chronic myelogenous leukemia.
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慢性粒细胞白血病的分子生物学。
DOI：
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发表时间：
1988
期刊：
影响因子：
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通讯作者：
R. Gale
中科院分区：
文献类型：
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作者：
O. Dreazen;E. Canaani;R. Gale
在这篇综述中，我们描述了t（9;22）易位典型的CML和ALL的一些情况下的分子后果。这些数据表明abl和bcr的重要作用，并提出一些共同的机制激活c-abl相关的酪氨酸激酶活性。该数据还提供了对Ph 1阳性、Ph 1阴性CML和Ph 1阳性ALL之间关系的深入了解。虽然这些数据回答了一些问题，但也提出了其他问题，例如，t（9;22）易位的分子基础是什么？慢性粒细胞白血病中abl相关激酶活性的增加是如何发生的？最后，回顾这些数据表明，abl和bcr以外的因素在CML中一定发挥作用。这些因素的定义在未来将是重要的。
In this review we have described molecular consequences of the t(9;22) translocation typical of CML and some cases of ALL. This data indicates an important role for abl and bcr and suggest some common mechanisms of activation of c-abl related tyrosine kinase activity. This data also provides insight into the relationship between Ph1 positive, Ph1 negative CML and Ph1 positive ALL. Although this data answers some questions, they raise others; eg, what is the molecular basis of the t(9;22) translocation? How does increased abl related kinase activity eventuate in CML? Finally, this data reviewed suggests that factors other than abl and bcr must play a role in CML. Definition of these factors will be important in the future.