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慢性粒细胞白血病的分子生物学

Molecular biology of chronic myelogenous leukemia.

作者信息

Dreazen O, Canaani E, Gale R P

机构信息

Department of Medicine, UCLA School of Medicine 90024.

出版信息

Semin Hematol. 1988 Jan;25(1):35-48.

PMID:3279514
Abstract

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.

摘要

在本综述中,我们描述了慢性粒细胞白血病(CML)以及部分急性淋巴细胞白血病(ALL)病例中典型的t(9;22)易位的分子后果。这些数据表明abl和bcr具有重要作用,并提示了c-abl相关酪氨酸激酶活性激活的一些共同机制。这些数据还为Ph1阳性、Ph1阴性CML与Ph1阳性ALL之间的关系提供了见解。尽管这些数据回答了一些问题,但也引发了其他问题;例如,t(9;22)易位的分子基础是什么?abl相关激酶活性增加如何导致CML?最后,本文综述的数据表明,除abl和bcr外的其他因素必定在CML中发挥作用。明确这些因素在未来将非常重要。

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